The Echo Manual [3 ed.] 1451156847, 9781451156843

Table of contents :
1. Front
1.2 Authors and Editors
J a e K . O h M D
J a m e s B . S e w a r d M D
A . J a m i l T a j i k M D
S e c o n d a r y E d i t o r s
F r a n D e S t e f a n o
J u l i a S e t o
B r i d g e t t D o u g h e r t y
B e n j a m i n R i v e r a
A n g e l a P a n e t t a
D o u g S m o c k
L a s e r w o r d s P r i v a t e L i m i t e d , C h e n n a i , I n
A l l i s o n C a b a l k a M D
F r a n k C e t t a J r . M D
R o g e r L . C l i c k M D
R a u l E . E s p i n o s a M D
D o n a l d J . H a g l e r M D
I f t i k h a r J . K u l l o M D
A . R a u o o f M a l i k M D
R R D o n n e l l e y
C o n t r i b u t o r s
P a t r i c k W . O ' L e a r y M D
B r i a n D . P o w e l l M D
G u y S . R e e d e r M D
C h e u k - M a n Y u M D
1.3 Dedication
D e d ic a t io n
1.4 Preface
2. TOC
1 - How to Obtain a Good Echocardiography Examination: Ultrasound Physi cs
2 - Transthoracic Echocardiography: M - mode, Two - Dimensional, and Three
3 - Transesophageal and Intracardiac Echocardiography
4 - Doppler Echocardiography and Color Flow Imaging: Comprehensive Noninva
5 - Tissue Doppler Imaging, Strain Imaging, and Dyssynchrony Assessment
6 - Contrast Echocardiography
7 - Assessment of Systolic Function and Quantification of Cardiac Cham ber
8 - Assessment of Diastolic Function and Diastolic Heart Failure
9 - Pulmonary Hypertension and Pulmonary Vein Stenosis
10 - Coronary Artery Disease and Acute Myocardial Infarction
11 - Stress Echocardiography
12 - Valvular Heart Disease
13 - Prosthetic Valve Evaluation
14 - I nfective Endocarditis
15 - Cardiomyopathies
16 - Cardiac Diseases Due to Systemic Illness, Genetics, Medication, or I
17 - Pericardial Diseases
18 - Tumors and Masses
19 - Diseases of the Aorta
20 - Echocardiography in Congenital Heart Disease: An Overview
21 - I ntraoperative Echocardiography
22 - Vascular Imaging and Tonometry
23 - Goal - Directed and Comprehensive Examination
Appendices
Appendix 1: Echocardiography laboratory, Mayo Clinic, Rochester, Minnesota—
Appendix 2: Normal values from M - mode echocardiography
Appendix 3: Reference limits and partition values of left ventricular size
Appendix 4: Reference limits and values and partition values of left ventricu
Appendix 5: Reference limits and partition values of left ventricular mass a
Appendix 6: Reference limi ts and partition values of right ventricular and p
Appendix 7: Reference limits and partition values of right ventricular size a
Appendix 8: Reference limits and partition values for left atrial dimensions
Appendix 9
Appendix 10: Reference ranges for diastolic function parameters by age
Appendix 11: Mitral inflow velocities in 117 normal subjects, stratified by p
Appendix 12: Pulmonary venous flow velocities in 85 normal subjects, stratifi
Appendix 13: Normal Doppler data in children (n = 223): mitral valve flow va
Appendix 14: Normal Doppler data in children (n = 223): pulmonary vein flow v
Appendix 15
Appendix 16: Velocity of individual segments determined with tissue Doppler e
Appendix 17: Strain rate of individual segments
Appendix 18: Displacement and systolic strain of individual segments
Appendix 19: Qualitative and quantitative parameters useful in grading mitr
Appendix 20: Qualitative and quantitative parameters use ful in grading aorti
Appendix 21: Echocardiographic and Doppler paramete rs used in grading tricus
Appendix 22: Echocardiographic and Doppler parameters used in grading pulmon
3. Abbreviations
A b b r e v i a t i o n s
A
A â € ²
Aa
Ao
C H F
CI
CO
D
DT
E
E â € ²
Ea
E/A
E C G
ERO
IVC
I V C T
I V R T
LA
LV
L V E F
L V O T
MV
P F O
PHT
P I S A
PW
RA
RV
S
S â € ²
SV
SVC
T E E
TTE
TVI
2D
VS
4. 1 - How to Obtain a Good Echocardiography Examination
H o w t o O b t a i n a G o o d E c h o c a r d i o g r a p h y E x
U l t r a s o u n d a n d T r a n s d u c e r
S c r e e n D i s p l a y a n d K n o b S e t t i n g s
G o a l - D i r e c t e d a n d C o m p r e h e n s i v e E x a m i n a
T a b l e 1 - 1 T r a i n i n g r e q u i r e m e n t s f o r
t h e p e r f o r m a n c e a n d i n t e r p r e t a t i o n
o f a d u l t t r a n s t h o r a c i c
e c h o c a r d i o g r a p h y e x a m i n a t i o n s
M i n i m u m
T o t a l N u m b e r
M i n i m u m
C u m u l a t i v e D u r a t i o n o f
o f
N u m b e r o f
T r a i n i n g ,
E x a m i n a t i o n s
mo
P e r f o r m e d
I n t e r p r e t e d
D i g i t a l E c h o c a r d i o g r a p h y
E c h o c a r d i o g r a p h y R e p o r t
5. 2 - Transthoracic Echocardiography
T w o - D i m e n s i o n a l E c h o c a r d i o g r a p h y
P a r a s t e r n a l P o s i t i o n
T a b l e 2 - 1 T r a n s d u c e r p o s i t i o n s a n d
c a r d i a c v i e w s
L o n g - A x i s V i e w o f t h e L e f t V e n t r i c l e
L o n g - A x i s V i e w o f R i g h t V e n t r i c u l a r I n f
S h o r t - A x i s V i e w s
A p i c a l P o s i t i o n
S u b c o s t a l P o s i t i o n
S u p r a s t e r n a l N o t c h P o s i t i o n
U n u s u a l I m a g i n g W i n d o w
M - M o d e E c h o c a r d i o g r a p h y
T h r e e - D i m e n s i o n a l E c h o c a r d i o g r a p h y
R e f e r e n c e s
6. 3 - Transesophageal and Intra cardiac Echocardiography
T r a n s e s o p h a g e a l a n d I n t r a c a r d i a c E c h o c a r
J a e K . O h
D o n a l d J . H a g l e r
A l l i s o n C a b a l k a
G u y S . R e e d e r
F r a n k C e t t a J r
J a m e s B . S e w a r d
T r a n s e s o p h a g e a l E c h o c a r d i o g r a p h y
I n d i c a t i o n s
T a b l e 3 - 1 I n d i c a t i o n s f o r
t r a n s e s o p h a g e a l e c h o c a r d i o g r a p h y a t
M a y o C l i n i c R o c h e s t e r f r o m
S e p t e m b e r 2 0 0 1 t o J u l y 2 0 0 4 : 8 , 5 3 5
p r o c e d u r e s
I n d i c a t i o n
P r o c e d u r e s , %
P r e p a r a t i o n a n d P o t e n t i a l C o m p l i c a t i o n s
I n s t r u m e n t a t i o n
T a b l e 3 - 2 P r e p a r a t i o n f o r
t r a n s e s o p h a g e a l e c h o c a r d i o g r a p h y
T r a i n i n g o f P h y s i c i a n s a n d t h e R o l e o f
T a b l e 3 - 3 S u m m a r y o f t h e r o l e o f t h e
s o n o g r a p h e r / a s s i s t a n t i n
t r a n s e s o p h a g e a l e c h o c a r d i o g r a p h y
( T E E )
M u l t i p l a n e T r a n s e s o p h a g e a l E c h o c a r d i o g r
P r i m a r y V i e w s
L o n g i t u d i n a l V i e w s
T r a n s g a s t r i c M u l t i p l a n e V i e w s
P u l m o n a r y A r t e r y B i f u r c a t i o n
P u l m o n a r y V e i n s
L e f t A t r i a l A p p e n d a g e
T h o r a c i c A o r t a
C o r o n a r y A r t e r i e s
C a v e a t s
I n t r a c a r d i a c E c h o c a r d i o g r a p h y
D e t a i l e d D e s c r i p t i o n o f a n I n t r a c a r d i a c
A p p l i c a t i o n s o f I n t r a c a r d i a c E c h o c a r d i o
E l e c t r o p h y s i o l o g y P r o c e d u r e s
D e v i c e C l o s u r e P r o c e d u r e s
P e r i v a l v u l a r L e a k
O t h e r A p p l i c a t i o n s
E x t r a c a r d i a c U s e o f t h e I n t r a c a r d i a c E c
R e f e r e n c e s
7. 4 - Doppler Echocardiography and Color Flow Imaging
D o p p l e r E c h o c a r d i o g r a p h y
C o l o r F l o w I m a g i n g
T a b l e 4 - 1 C o m p a r i s o n o f p u l s e d w a v e
a n d c o n t i n u o u s w a v e D o p p l e r
P u l s e d W a v e
C o n t i n u o u s W a v e
T a b l e 4 - 2 N o r m a l m a x i m a l v e l o c i t i e s
( m / s ) : D o p p l e r m e a s u r e m e n t s
C h i l d r e n
A d u l t s
M e a n
R a n g e
M e a n
R a n g e
T r a n s v a l v u l a r G r a d i e n t s
I n t r a c a r d i a c P r e s s u r e s
T a b l e 4 - 3 D o p p l e r e s t i m a t i o n o f
i n t r a c a r d i a c p r e s s u r e s
S t r o k e V o l u m e a n d C a r d i a c O u t p u t
T a b l e 4 - 4 A r e a c a l c u l a t i o n f r o m
d i a m e t e r ( D ) : a r e a = D 2 Ã — 0 . 7 8 5
A r e a
D i a m e t e
( c m 2
D i a m e t e
A r e a
D i a m e t e
A r e a
r ( c m )
( c m 2 )
r ( c m )
( c m 2 )
P u l m o n a r y â € “ S y s t e m i c F l o w R a t i o ( Q p / Q s )
C o n t i n u i t y E q u a t i o n
P r e s s u r e H a l f - T i m e
R e g u r g i t a n t V o l u m e , F r a c t i o n , a n d O r i f i
V o l u m e t r i c M e t h o d
P r o x i m a l I s o v e l o c i t y S u r f a c e A r e a ( P I S A
d p / d t
R e s i s t a n c e
R e f e r e n c e s
8. 5 - Tissue Doppler Imaging, Strain Imaging, and Dyssynchrony Assessment
T i s s u e D o p p l e r I m a g i n g , S t r a i n I m a g i n g ,
B r i a n D . P o w e l l
R a u l E . E s p i n o s a
C h e u k - M a n Y u
J a e K . O h
T i s s u e D o p p l e r I m a g i n g
A s s e s s m e n t o f M y o c a r d i a l R e l a x a t i o n
T a b l e 5 - 1 C o m p a r i s o n o f t w o-
d i m e n s i o n a l ( 2 D ) g r a y s c a l e a n d
t i s s u e d o p p l e r i m a g i n g ( T D I )
TDI
2 D G r a y
C o l o r
P u l s e d
V a r i a b l e
S c a l e
D o p p l e r
E s t i m a t i o n o f L e f t V e n t r i c u l a r F i l l i n g
E v a l u a t i o n o f R e g i o n a l a n d G l o b a l S y s t o
T i s s u e V e l o c i t y G r a d i e n t
C a r d i a c T i m e I n t e r v a l s
E v a l u a t i o n o f T h i c k W a l l s
P r o g n o s t i c a t i o n
S t r a i n a n d S t r a i n R a t e I m a g i n g
D e t e c t i o n o f M y o c a r d i a l I s c h e m i a
A s s e s s m e n t o f M y o c a r d i a l V i a b i l i t y
E v a l u a t i o n o f C a r d i o m y o p a t h y
S p e c k l e T r a c k i n g E c h o c a r d i o g r a p h y
D y s s y n c h r o n y A s s e s s m e n t
S y s t o l i c D y s s y n c h r o n y o f t h e V e n t r i c l e
C a r d i a c R e s y n c h r o n i z a t i o n T h e r a p y f o r H
P a t i e n t S e l e c t i o n f o r I m p l a n t a t i o n o f C
A s s e s s m e n t o f R e s p o n s e t o C R T
O p t i m i z a t i o n o f t h e A t r i o v e n t r i c u l a r I n
O p t i m i z a t i o n o f I n t e r v e n t r i c u l a r I n t e r v
T h e R o l e o f E c h o c a r d i o g r a p h y i n I d e n t i f
E c h o c a r d i o g r a p h i c T o o l s f o r t h e A s s e s s m
M - M o d e M e a s u r e m e n t
P u l s e d W a v e D o p p l e r M e a s u r e m e n t
T i s s u e D o p p l e r I m a g i n g
T a b l e 5 - 2 P u b l i s h e d c r i t e r i a o f
s y s t o l i c a s y n c h r o n y b y t i s s u e D o p p l e r
i m a g i n g t h a t p r e d i c t a f a v o r a b l e
e c h o c a r d i o g r a p h i c r e s p o n s e t o
c a r d i a c r e s y n c h r o n i z a t i o n t h e r a p y
C r i t e r i
D e f i n
F o l l
C u t o
S e n s i
S p e c i
m p l
a
i t i o n
ow-
ff
t i v i t y
f i c i t y
o f
u p ,
V a l u
S i z
R e s p
mo
e ,
e
o n d e
ms
S t u d y
rs
M e c h a n i c a l D y s s y n c h r o n y i n P a t i e n t s w i t
A s s e s s m e n t o f t h e M e c h a n i s m o f B e n e f i t
F u t u r e P e r s p e c t i v e s i n t h e E c h o c a r d i o g r
9. 6 - Contrast Echocardiography
C o n t r a s t E c h o c a r d i o g r a p h y
E v a l u a t i o n o f S h u n t s
A u g m e n t a t i o n o f t h e D o p p l e r V e l o c i t y S i
Gas - F i l l e d M i c r o b u b b l e s
E n h a n c e m e n t o f t h e D e f i n i t i o n o f t h e E n
M y o c a r d i a l P e r f u s i o n I m a g i n g
R e f e r e n c e s
10. 7 - Assessment of Systolic Function and Quantification of Cardiac Cham
A s s e s s m e n t o f S y s t o l i c F u n c t i o n a n d Q u a n
L e f t V e n t r i c u l a r a n d R i g h t V e n t r i c u l a r
A t r i a l S i z e a n d V o l u m e
L e f t V e n t r i c u l a r M a s s
V o l u m e
A u t o m a t e d B o r d e r D e t e c t i o n a n d C o l o r K i
S y s t o l i c F u n c t i o n V a r i a b l e s
F r a c t i o n a l S h o r t e n i n g
E j e c t i o n F r a c t i o n
S t r o k e V o l u m e
S y s t o l i c V e l o c i t y o f M y o c a r d i a l T i s s u e
V e n t r i c u l a r M e c h a n i c a l S y n c h r o n y
T i s s u e T r a c k i n g
R e g i o n a l W a l l M o t i o n A n a l y s i s
11. 8 - Assessment of Diastolic Function and Diastolic Heart Failure
A s s e s s m e n t o f D i a s t o l i c F u n c t i o n a n d D i a
T a b l e 8 - 1 P r i m a r y d i a s t o l i c h e a r t
f a i l u r e
D i a s t o l i c F u n c t i o n
T a b l e 8 - 2 F a c t o r s t h a t i n f l u e n c e
d i s t e n s i b i l i t y o f t h e l e f t v e n t r i c u l a r
( L V ) c h a m b e r d u r i n g d i a s t o l e
D o p p l e r F l o w V e l o c i t i e s
M i t r a l F l o w V e l o c i t i e s
M i t r a l I n f l o w V e l o c i t i e s w i t h V a l s a l v a
M i t r a l A n u l u s V e l o c i t i e s
M i t r a l I n f l o w P r o p a g a t i o n V e l o c i t y ( V p )
P u l m o n a r y V e i n F l o w V e l o c i t i e s
T r i c u s p i d F l o w V e l o c i t i e s
H e p a t i c V e i n F l o w V e l o c i t i e s
S u p e r i o r V e n a C a v a F l o w V e l o c i t i e s
L e f t A t r i u m
T e c h n i q u e s f o r D i a s t o l i c D o p p l e r P a r a m e
G r a d i n g o f D i a s t o l i c D y s f u n c t i o n ( o r D i
N o r m a l D i a s t o l i c F i l l i n g P a t t e r n
A b n o r m a l P a t t e r n s
G r a d e 1 D i a s t o l i c D y s f u n c t i o n ( I m p a i r e d
G r a d e 2 D i a s t o l i c D y s f u n c t i o n ( P s e u d o n o
G r a d e 3 â € “ 4 D i a s t o l i c D y s f u n c t i o n ( R e s t
V a r i a t i o n s i n M i t r a l I n f l o w P a t t e r n s
T a b l e 8 - 3 C l a s s i f i c a t i o n o f d i a s t o l i c
f i l l i n g
D i a s t o l i c F i l l i n g P a t t e r n i n A t r i a l F i b
C a r d i a c T i m e I n t e r v a l s
I n d e x o f M y o c a r d i a l P e r f o r m a n c e ( T e i I n
T i m e I n t e r v a l f r o m t h e O n s e t o f M i t r a l
A s s e s s m e n t o f I n t e r v e n t r i c u l a r a n d I n t r
C l i n i c a l A p p l i c a t i o n s o f t h e A s s e s s m e n t
E s t i m a t i o n o f F i l l i n g P r e s s u r e s a t R e s t
M a n a g e m e n t o f H e a r t F a i l u r e
T a b l e 8 - 4 D i a s t o l i c s t r e s s t e s t
T a b l e 8 - 5 N o r m a l v a l u e s f o r
d i a s t o l o g y s t r e s s t e s t
V a r i a b l e
B a s e l i n e
E x e r c i s e
P r o g n o s i s
D i a g n o s i s o f D i a s t o l i c H e a r t F a i l u r e , C
R e f e r e n c e s
12. 9 - Pulmonary Hypertension and Pulmonary Vein Stenosis
P u l m o n a r y H y p e r t e n s i o n a n d P u l m o n a r y V e
T w o - D i m e n s i o n a l E c h o c a r d i o g r a p h y
D o p p l e r E c h o c a r d i o g r a p h y
T a b l e 9 - 1 E t i o l o g i c c l a s s i f i c a t i o n o f
p u l m o n a r y h y p e r t e n s i o n
T r i c u s p i d R e g u r g i t a t i o n V e l o c i t y
T r i c u s p i d R e g u r g i t a t i o n V e l o c i t y w i t h E
T e c h n i c a l C a v e a t
P u l m o n a r y R e g u r g i t a t i o n V e l o c i t y
R i g h t V e n t r i c u l a r O u t f l o w T r a c t F l o w A c
P u l m o n a r y V a s c u l a r R e s i s t a n c e
M i t r a l I n f l o w V e l o c i t y P a t t e r n i n P u l m o
H e p a t i c V e i n V e l o c i t y P a t t e r n i n P u l m o n
C o r P u l m o n a l e a n d P u l m o n a r y E m b o l i s m
T r a n s t h o r a c i c E c h o c a r d i o g r a p h y
T r a n s e s o p h a g e a l E c h o c a r d i o g r a p h y
C h r o n i c T h r o m b o e m b o l i c P u l m o n a r y H y p e r t
E v a l u a t i o n o f t h e P u l m o n a r y V e i n s
P u l m o n a r y V e i n S t e n o s i s
13. 10 - Coronary Artery Disease and Acute Myocardial Infarction
C o r o n a r y A r t e r y D i s e a s e a n d A c u t e M y o c a
E v a l u a t i o n o f M y o c a r d i a l W a l l M o t i o n
T e c h n i c a l C a v e a t s
E v a l u a t i o n o f C h e s t P a i n S y n d r o m e
A c u t e M y o c a r d i a l I n f a r c t i o n
M e c h a n i c a l C o m p l i c a t i o n s a n d C a r d i o g e n i
L e f t V e n t r i c u l a r F a i l u r e a n d R e m o d e l i n g
T a b l e 1 0 - 1 C o m p l i c a t i o n s o f
m y o c a r d i a l i n f a r c t i o n
R i g h t V e n t r i c u l a r I n f a r c t
F r e e W a l l R u p t u r e a n d P s e u d o a n e u r y s m
T a b l e 1 0 - 2 D i f f e r e n t i a l d i a g n o s i s o f a
n e w m u r m u r i n p a t i e n t s w i t h a c u t e
m y o c a r d i a l i n f a r c t i o n
V e n t r i c u l a r
P a p i l l a r y
L V O T
S e p t a l
M u s c l e
O b s t r u c t i o
R u p t u r e
n
V e n t r i c u l a r S e p t a l R u p t u r e
P a p i l l a r y M u s c l e R u p t u r e
I s c h e m i c M i t r a l R e g u r g i t a t i o n
A c u t e D y n a m i c L e f t V e n t r i c u l a r O u t f l o w
P e r i c a r d i a l E f f u s i o n a n d T a m p o n a d e
T r u e V e n t r i c u l a r A n e u r y s m a n d T h r o m b u s
A c u t e M y o c a r d i a l I n f a r c t i o n w i t h N o r m a l
D i a s t o l i c F u n c t i o n
R i s k S t r a t i f i c a t i o n
E v a l u a t i o n o f t h e C o r o n a r y A r t e r i e s a n d
I n t r a v a s c u l a r U l t r a s o n o g r a p h y
T a b l e 1 0 - 3 C l a s s i f i c a t i o n o f c o r o n a r y
a n o m a l i e s o b s e r v e d i n ( n o r m a l )
h u m a n h e a r t s
R e f e r e n c e s
14. 11 - Stress Echocardiography
S t r e s s E c h o c a r d i o g r a p h y
T y p e s o f S t r e s s E c h o c a r d i o g r a p h y
T a b l e 1 1 - 1 E x e r c i s e
e c h o c a r d i o g r a p h y p r o t o c o l
W h a t t o L o o k f o r a s a M a r k e r o f C o r o n a r
T a b l e 1 1 - 2 D o b u t a m i n e
e c h o c a r d i o g r a p h y p r o t o c o l
T a b l e 1 1 - 3 I n t e r p r e t a t i o n b y r e g i o n a l
w a l l m o t i o n ( W M ) a n a l y s i s
R e s t
S t r e s s
I n t e r p r e t a t i o n
T a b l e 1 1 - 4 I s c h e m i c m a n i f e s t a t i o n s
o f s e v e r e c o r o n a r y a r t e r y d i s e a s e
E x e r c i s e
D o b u t a m i n e
T a b l e 1 1 - 5 I n d i c a t i o n s f o r w h i c h
e x e r c i s e a n d d o b u t a m i n e s t r e s s
e c h o c a r d i o g r a p h i c s t u d i e s w e r e
p e r f o r m e d a t M a y o C l i n i c i n 2 0 0 4
E x e r c i s e
D o b u t a m i n e
% o f
S t u d i e
I n d i c a t i o n
s
I n d i c a t i o n
s
M a y o C l i n i c E x p e r i e n c e
D i a g n o s t i c A c c u r a c y
S t r e s s E c h o c a r d i o g r a p h y a s a P r o g n o s t i c
C a v e a t s f o r T e c h n i c a l a n d I n t e r p r e t a t i o
A s s e s s m e n t o f M y o c a r d i a l V i a b i l i t y
D o p p l e r S t r e s s H e m o d y n a m i c s i n V a l v u l a r
D i a s t o l i c S t r e s s T e s t
R e f e r e n c e s
15. 12 - Valvular Heart Disease
V a l v u l a r H e a r t D i s e a s e
A o r t i c S t e n o s i s
T w o - D i m e n s i o n a l a n d M - M o d e E c h o c a r d i o g r
D o p p l e r E c h o c a r d i o g r a p h y
D e f i n i t i o n o f S e v e r e A o r t i c S t e n o s i s
D o b u t a m i n e E c h o c a r d i o g r a p h y i n S e v e r e A
C a v e a t s
D i a s t o l i c F u n c t i o n i n A o r t i c S t e n o s i s
S e v e r e P u l m o n a r y H y p e r t e n s i o n w i t h S e v e
N a t u r a l P r o g r e s s i o n a n d R o l e o f E x e r c i s
T r a n s e s o p h a g e a l E c h o c a r d i o g r a p h y
C l i n i c a l I m p l i c a t i o n s
M i t r a l S t e n o s i s
T w o - D i m e n s i o n a l a n d M - M o d e E c h o c a r d i o g r
D o p p l e r a n d C o l o r F l o w I m a g i n g
T a b l e 1 2 - 1 E c h o c a r d i o g r a p h i c s c o r e
u s e d t o p r e d i c t o u t c o m e o f m i t r a l
b a l l o o n v a l v u l o p l a s t y a
S u b v a l v u l
a r
G r a d
T h i c k e n i n
C a l c i f i c a t i
e
M o b i l i t y
g
T h i c k e n i n g
on
D e f i n i t i o n o f M i t r a l S t e n o s i s S e v e r i t y
C a v e a t s
E x e r c i s e H e m o d y n a m i c s
T r a n s e s o p h a g e a l E c h o c a r d i o g r a p h y
Cl i n i c a l I m p l i c a t i o n s
T r i c u s p i d S t e n o s i s
P u l m o n a r y S t e n o s i s
A o r t i c R e g u r g i t a t i o n
T w o - D i m e n s i o n a l a n d M - M o d e E c h o c a r d i o g r
D o p p l e r a n d C o l o r F l o w I m a g i n g
M i t r a l R e g u r g i t a t i o n
T w o - D i m e n s i o n a l a n d M - M o d e E c h o c a r d i o g r
M i t r a l V a l v e P r o l a p s e
F u n c t i o n a l M i t r a l R e g u r g i t a t i o n
D o p p l e r a n d C o l o r F l o w I m a g i n g
V o l u m e t r i c M e t h o d
P r o x i m a l I s o v e l o c i t y S u r f a c e A r e a M e t h o
S i m p l i f i c a t i o n o f t h e P I S A M e t h o d
V e n a C o n t r a c t a W i d t h
T r a n s e s o p h a g e a l E c h o c a r d i o g r a p h y
T r i c u s p i d R e g u r g i t a t i o n
T w o - D i m e n s i o n a l a n d M - M o d e E c h o c a r d i o g r
D o p p l e r a n d C o l o r F l o w I m a g i n g
D r u g - I n d u c e d V a l v u l a r H e a r t D i s e a s e
V a l v u l a r R e g u r g i t a t i o n i n N o r m a l S u b j e c
C l i n i c a l I m p a c t
T i m i n g o f S u r g e r y f o r V a l v u l a r D i s e a s e
R e f e r e n c e s
16. 13 - Prosthetic Valve Evaluation
P r o s t h e t i c V a l v e E v a l u a t i o n
T w o - D i m e n s i o n a l E c h o c a r d i o g r a p h y
D o p p l e r a n d C o l o r F l o w I m a g i n g
T a b l e 1 3 - 1 D o p p l e r h e m o d y n a m i c
p r o f i l e s o f 6 0 9 n o r m a l a o r t i c v a l v e
p r o s t h e s e s
T y p e o f
N o . o f
P e a k
M e a n
L V O T
G r a d i e n t ( m m H g )
P r o s t h e s i
P r o s t h e s
V e l o c i t y
T V I / A V
s
es
( m / s )
TVI
T a b l e 1 3 - 2 D o p p l e r h e m o d y n a m i c
p r o f i l e s o f 4 5 6 n o r m a l m i t r a l v a l v e
p r o s t h e s e s
M e a n
N o . o f
P e a k
G r a d i e n t
E f f e c t i v
T y p e o f P r o s t h e s i s
P r o s t h e s
V e l o c i t y
( m m
e A r e a
es
( m / s )
H g )
( c m 2 )
O b s t r u c t i o n
T a b l e 1 3 - 3 D o p p l e r h e m o d y n a m i c
p r o f i l e s o f 8 2 n o r m a l t r i c u s p i d v a l v e
p r o s t h e s e s
P r e s s u r
N o . o f
P e a k
M e a n
e H a l f-
T y p e o f P r o s t h e s i s
P r o s t h e s e
V e l o c i t y
G r a d i e n t
T i m e
s
( m / s )
( m m H g )
( m s )
T a b l e 1 3 - 4 D o p p l e r
e c h o c a r d i o g r a p h i c d a t a f o r
p u l m o n a r y v a l v e p r o s t h e s e s
T r i v i a l / M i
l d
P e a k
M e a n
P r o s t h e t i
T y p e o f
V e l o c i t
G r a d i e n
P r o s t h e
S i z e
t ( m m
R e g u r g i t a
sis
( m m )
( m / s )
H g )
t i o n ( n o . )
T a b l e 1 3 - 5 I n t e r p r e t a t i o n o f
i n c r e a s e d p r o s t h e s i s f l o w v e l o c i t y
P r o s t h e s i s - P a t i e n t M i s m a t c h
C a l c u l a t i o n o f E f f e c t i v e P r o s t h e t i c O r i
T h r o m b o l y t i c T h e r a p y f o r O b s t r u c t i o n o f
T a b l e 1 3 - 6 E f f i c a c y o f t h r o m b o l y t i c
a g e n t s u s e d f o r v a l v e o b s t r u c t i o n ,
s t r a t i f i e d b y v a l v e p o s i t i o n
A g e n t
T i s s u e - T y p e
P l a s m i n o g e
S t r e p t o k i n a s e
U r o k i n a s e
n A c t i v a t o r
P o s i t i o n
N o . a
T a b l e 1 3 - 7 M o r t a l i t y a n d m o r b i d i t y
w i t h t h r o m b o l y t i c t h e r a p y f o r v a l v e
o b s t r u c t i o n , s t r a t i f i e d b y v a l v e
p o s i t i o n
E m b o l i s
N o n d i s a b l i
D e a t h
m
S t r o k e
n g B l e e d
N o .
o f
P o s i t i o
V a l v
n
es
N o .
R e g u r g i t a t i o n
T r a n s e s o p h a g e a l E c h o c a r d i o g r a p h y
H e m o l y s i s A f t e r M i t r a l V a l v e R e p a i r o r
C l i n i c a l I m p a c t
C a v e a t s
R e f e r e n c e s
17. 14 - Infective Endocarditis
I n f e c t i v e E n d o c a r d it i s
N e w D i a g n o s t i c C r i t e r i a
T a b l e 1 4 - 1 D e f i n i t i o n o f t e r m s u s e d
i n t h e p r o p o s e d d i a g n o s t i c c r i t e r i a
T a b l e 1 4 - 2 N e w c r i t e r i a f o r d i a g n o s i s
o f i n f e c t i v e e n d o c a r d i t i s
E c h o c a r d i o g r a p h i c A p p e a r a n c e
C o m p l i c a t i o n s
T a b l e 1 4 - 3 C o m p l i c a t i o n s o f
e n d o c a r d i t i s
T r a n s e s o p h a g e a l E c h o c a r d i o g r a p h y
T r a n s e s o p h a g e a l E c h o c a r d i o g r a p h y o r N o
N o n b a c t e r i a l T h r o m b o t i c E n d o c a r d i t i s
C l i n i c a l C a v e a t s
R e f e r e n c e s
18. 15 - Cardiomyopathies
C a r d i o m y o p a t h i e s
D i l a t e d C a r d i o m y o p a t h y
T w o - D i m e n s i o n a l E c h o c a r d i o g r a p h y
T a b l e 1 5 - 1 C l a s s i f i c a t i o n o f
c a r d i o m y o p a t h i e s b y
p a t h o p h y s i o l o g i c m e c h a n i s m o r
e t i o l o g i c / p a t h o g e n i c f a c t o r a n d b y
a s s o c i a t e d s p e c i f i c d i s o r d e r
B y M e c h a n i s m
B y D i s o r d e r
D o p p l e r ( P u l s e d W a v e , C o n t i n u o u s W a v e ,
E c h o c a r d i o g r a p h y i n t h e M a n a g e m e n t o f D
H y p e r t r o p h i c C a r d i o m y o p a t h y
T w o - D i m e n s i o n a l a n d M - M o d e E c h o c a r d i o g r
D o p p l e r ( P u l s e d W a v e , C o n t i n u o u s W a v e )
L V O T O b s t r u c t i o n
M i t r a l R e g u r g i t a t i o n
D i a s t o l i c F i l l i n g P a t t e r n a n d T i s s u e D o
D y n a m i c L V O T O b s t r u c t i o n i n O t h e r Diseases
A l c o h o l A b l a t i o n T h e r a p y
T r a n s e s o p h a g e a l E c h o c a r d i o g r a p h y a n d T h
C a v e a t s
A t h l e t e ' s H e a r t V e r s u s H y p e r t r o p h i c C a r
R e s t r i c t i v e C a r d i o m y o p a t h y
A r r h y t h m o g e n i c R i g h t V e n t r i c u l a r D y s p l a
N o n c o m p a c t i o n C a r d i o m y o p a t h y ( I s o l a t e d
P e d i a t r i c C a r d i o m y o p a t h y
R e f e r e n c e s
19. 16 - Cardiac Diseases Due to Systemic Illness, Genetics, Medication,
C a r d i a c D i s e a s e s D u e t o S y s t e m i c I l l n e s
A m y l o i d o s i s a n d I n f i l t r a t i v e C a r d i o m y o p
T a b l e 1 6 - 1 E c h o c a r d i o g r a p h i c
f e a t u r e s o f c a r d i a c m a n i f e s t a t i o n s o f
s y s t e m i c i l l n e s s es
C a r c i n o i d
D r u g - I n d u c e d C a r d i a c D i s e a s e s
H e m o c h r o m a t o s i s
H y p e r e o s i n o p h i l i c S y n d r o m e
R a d i a t i o n - I n d u c e d C a r d i a c D i s e a s e s
R e n a l F a i l u r e
S a r c o i d o s i s
W e g e n e r G r a n u l o m a t o s i s
S c l e r o d e r m a
S e p s i s
C h a g a s D i s e a s e
S p o n d y l o a r t h r o p a t h i e s a n d V a s c u l i t i s
S y s t e m i c L u p u s E r y t h e m a t o s u s
G e n e t i c D i s e a s e s
R e f e r e n c e s
20. 17 - Pericardial Diseases
P e r ic a r d i a l D i s e a s e s
C o n g e n i t a l l y A b s e n t P e r i c a r d i u m
P e r i c a r d i a l C y s t
P e r i c a r d i a l E f f u s i o n a n d T a m p o n a d e
E c h o c a r d i o g r a p h i c a l l y G u i d e d P e r i c a r d i o
P e r i c a r d i a l E f f u s i o n V e r s u s P l e u r a l E f f
C o n s t r i c t i v e P e r i c a r d i t i s
P i t f a l l s a n d C a v e a t s
R e s t r i c t i o n V e r s u s C o n s t r i c t i o n
T a b l e 1 7 - 1 T r a d i t i o n a l h e m o d y n a m i c
c r i t e r i a f o r c o n s t r i c t i o n v e r s u s
r e s t r i c t i o n
C r i t e r i o n
C o n s t r i c t i o n
R e s t r i c t i o n
E f f u s i v e - C o n s t r i c t i v e P e r i c a r d i t i s
T r a n s i e n t C o n s t r i c t i v e P e r i c a r d i t i s
P e r i c a r d i a l E f f u s i o n A s s o c i a t e d w i t h M a
T r a n s e s o p h a g e a l E c h o c a r d i o g r a p h y
C l i n i c a l I m p a c t
R e f e r e n c e s
21. 18 - Tumors and Masses
T u m o r s a n d M a s s e s
T u m o r s
M y x o m a
T a b l e 1 8 - 1 R e l a t i v e i n c i d e n c e o f
t u m o r s o f t h e h e a r t
T y p e o f T u m o r
N o .
F i b r o m a
R h a b d o m y o m a
P a p i l l a r y F i b r o e l a s t o m a
T a b l e 1 8 - 2 S u m m a r y o f s u r g i c a l l y
e x c i s e d b e n i g n c a r d i a c t u m o r s a t
M a y o C l i n i c , 1 9 5 7 t h r o u g h M a r c h
M e a n
S e x
A g e
T u m o r S i t e
T u m o r T y p e
N o .
( F : M )
( y r )
a n d N o .
P h e o c h r o m o c y t o m a
M a l i g n a n t T u m o r s o f t h e H e a r t
O t h e r M a s s e s
P s e u d o t u m o r a n d P i t f a l l s
22. 19 - Diseases of the Aorta
D i s e a s e s o f t h e A o r t a
A o r t i c A n e u r y s m
A n e u r y s m o f t h e S i n u s o f V a l s a l v a
A t h e r o s c l e r o s i s a n d A o r t i c D e b r i s
A o r t i c D i s s e c t i o n a n d I n t r a m u r a l H e m a t o
T r a n s t h o r a c i c E c h o c a r d i o g r a p h y
T r a n s e s o p h a g e a l E c h o c a r d i o g r a p h y
A o r t i c P e n e t r a t i n g U l c e r
A o r t i c R u p t u r e
A o r t i t i s
C o a r c t a t i o n o f t h e A o r t a
F r a n k C e t t a J r .
J a m e s B . S e w a r d
P a t r i c k W . O ' L e a r y
23. 20 - Echocardiography in Congenital Heart Disease - An Overview
E c h o c a r d i o g r a p h y i n C o n g e n i t a l H e a r t D is
S e g m e n t a l A p p r o a c h t o C o n g e n i t a l H e a r t
I m a g e O r i e n t a t i o n i n C o n g e n i t a l H e a r t D
P r e n a t a l a n d N e o n a t a l P r e s e n t a t i o n s o f
P e d i a t r i c a n d A d u l t P r e s e n t a t i o n s o f C o
M a l f o r m a t i o n s A s s o c i a t e d w i t h S h u n t P h y
A t r i a l S e p t a l D e f e c t s
A t r i o v e n t r i c u l a r S e p t a l D e f e c t s â € ” C o m p l
V e n t r i c u l a r S e p t a l D e f e c t s
T a b l e 2 0 - 1 N o m e n c l a t u r e o f
a t r i o v e n t r i c u l a r s e p t a l d e f e c t s
I m a g i n g N o t e s
A n o m a l o u s P u l m o n a r y V e n o u s C o n n e c t i o n s
I m a g i n g N o t e s
A n o m a l o u s S y s t e m i c V e i n s
P a t e n t D u c t u s A r t e r i o s u s
C l i n i c a l N o t e s
I m a g i n g N o t e s
O b s t r u c t i o n t o B l o o d F l o w
C o a r c t a t i o n o f t h e A o r t a
C l i n i c a l N o t e s
I m a g i n g N o t e s
D o p p l e r E v a l u a t i o n
V e n t r i c u l a r O u t f l o w T r a c t O b s t r u c t i o n
C o m p l e x C o n g e n i t a l C a r d i a c M a l f o r m a t i o n
E b s t e i n A n o m a l y
T e t r a l o g y o f F a l l o t
C o m p l e t e T r a n s p o s i t i o n o f t h e G r e a t A r t
C o n g e n i t a l l y C o r r e c t e d T r a n s p o s i t i o n o f
U n i v e n t r i c u l a r A t r i o v e n t r i c u l a r C o n n e c t
R e f e r e n c e s
R o g e r L . C l i c k
J a e K . O h
24. 21 - Intraoperative Echocardiography
I n t r a o p e r a t i v e E c h o c a r d i o g r a p h y
I o t e e A p p l i c a t i o n
I m p l e m e n t a t i o n
I n d i c a t i o n s
I m p a c t o f I o t e e
M i t r a l V a l v e R e p a i r
H y p e r t r o p h i c O b s t r u c t i v e C a r d i o m y o p a t h y
M e a s u r e m e n t o f H o m o g r a f t S i z e
D e t e c t i o n o f A t h e r o m a t o u s P l a q u e i n t h e
A o r t i c D i s s e c t i o n
I n t r a o p e r a t i v e M o n i t o r i n g
M i s c e l l a n e o u s A p p l i c a t i o n s
U n s t a b l e H e m o d y n a m i c s
C o n c l u s i o n
R e f e r e n c e s
25. 22 - Vascular Imaging and Tonometry
V a s c u l a r I m a g i n g a n d T o n o m e t r y
A . R a u o o f M a l i k
I f t i k h a r J . K u l l o
B r a c h i a l A r t e r y R e a c t i v i t y T e s t i n g
C a r o t i d I n t i m a - M e d i a T h i c k n e s s
A r t e r i a l T o n o m e t r y f o r A s s e s s m e n t o f A r
A o r t i c P u l s e W a v e V e l o c i t y
A o r t i c A u g m e n t a t i o n I n d e x
O t h e r M e a s u r e s o f A r t e r i a l S t i f f n e s s
R e f e r e n c e s
26. 23 - Goal - Directed and Comprehensive Examination
G o a l - D i r e c t e d a n d C o m p r e h e n s iv e E x a m i n a t
E v a l u a t i o n o f V e n t r i c u l a r F u n c t i o n a n d
T a b l e 2 3 - 1 R e a s o n s f o r r e f e r r a l t o
e c h o c a r d i o g r a p h y : 1 0 , 0 0 0
c o n s e c u t i v e p a t i e n t s a
R e a s o n
P a t i e n t s , n o .
E v a l u a t i o n o f D y s p n e a o r H e a r t F a i l u r e
S y s t e m i c H y p e r t e n s i o n
M u r m u r o r M i t r a l V a l v e P r o l a p s e
A t r i a l F i b r i l l a t i o n
I d e n t i f i c a t i o n o f U n d e r l y i n g C a u s e a n d
E v a l u a t i o n o f S y s t o l i c a n d D i a s t o l i c F u
P r e c a r d i o v e r s i o n T r a n s e s o p h a g e a l E c h o c a
L e f t A t r i a l A p p e n d a g e F l o w V e l o c i t i es
B e f o r e a n d A f t e r a R a d i o f r e q u e n c y A b l a t
C h e s t P a i n
N o n s p e c i f i c E l e c t r o c a r d i o g r a p h i c A b n o r m
C a r d i a c S o u r c e o f E m b o l i o r S y n c o p e
H y p o t e n s i o n , S y n c o p e , o r C a r d i o g e n i c S h
C a r d i a c C o n t u s i o n , D o n o r H e a r t E v a l u a t i
E v a l u a t i o n o f L e f t V e n t r i c u l a r A s s i s t D
E v a l u a t i o n o f C a n c e r P a t i e n t s
27. Appendices
27.1 1. Echocardiography laboratory, Mayo Clinic, Rochest er, Minnesota -
A p p e n d ix 1 : E c h o c a r d i o g r a p h y l a b o r a t o r y ,
R e f e r r a l d i a g n o s i s
H e m o d y n a m i c s H e a r t r a t e : 1 0 7 B P M
F i n a l i m p r e s s i o n s
F i n d i n g s
M e a s u r e m e n t s ( E x a m p l e s )
27.2 2. Normal values from M - mode echocardiography
27.3 3. Reference limits and partition values of left ventricular size
A p p e n d ix 3 : R e f e r e n c e l i m i t s a n d p a r t i t i
W o m e n
M e n
R e f e r e n c e Ran ge
M i l d l y Abn o r m al
M o d e r a t e l y Abn o r m al
S e v e r e l y Abn o r m al
R e f e r e n c e Ran ge
M i l d l y Abn o r m al
M o d e r a t e l y Abn o r m al
S e v e r e l y Abn o r m al
V a r i a b le
L V d i a s t o l ic v o l u m e / B S A , m L / m 2
35â € “ 7
76â € “ 8
87â€
35â € “ 7
76â € “ 8
87â€
L V s y s t o l i c v o l u m e / B S A , m L / m 2
12â € “ 3
31â € “ 3
37â€
12â € “ 3
31â € “ 3
37â€
27.4 4. Reference limits and values and partition values of left ventricular
A p p e n d ix 4 : R e f e r e n c e l i m i t s a n d v a l u e s
W o m e n
M e n
R e f e r e n c e Ran ge
M i l d l y Abn o r m al
M o d e r a t e l y A b n o r m a l
S e v e r e l y Abn o r m al
R e f e r e n c e Ran ge
M i l d l y Abn o r m al
M o d e r a t e l y A b n o r m a l
S e v e r e l y Abn o r m al
V a r i a b l e
E j e c t i o n f r a c t i o n ,
45â € “ 5
30â€
< 3 0 ≠¥55
45â € “ 5
30â€
27.5 5. Reference limits and partition values of left ventricular mass and g
A p p e n d ix 5 : R e f e r e n c e l i m i t s a n d p a r t i t i
W o m e n
M e n
R e f e r e n c e Ran ge
M i l d l y Abn o r m al
M o d e r a t e l y Abn o r m al
S e v e r e l y Abn o r m al
R e f e r e n c e Ran ge
M i l d l y Abn o r m al
M o d e r a t e l y Abn o r m al
S e v e r e l y Abn o r m al
V a r i a b l e
L V m a s s / B S A , g / m 2
43â€
96â€
109â € “ 1 2
49â€
116â € “ 1 3
132â € “ 1 4
Se p t a l t h i c k n e s s , c m
0.6â € “ 0 .
1.0â € “ 1 .
1.3â € “ 1 .
0.6â € “ 1 .
1.1â € “ 1 .
1.4â € “ 1 .
0.6â € “ 0 .
1.0â € “ 1 .
1.3â € “ 1 .
0.6â € “ 1 .
1.1â € “ 1 .
1.4â € “ 1 .
Po s t e r i o r w a l l t h i c k n e s s , c m
L V m a s s / B S A , g / m 2
44â€
89â€
101â € “ 1 1
50â€
103â € “ 1 1
117â € “ 1 3
27.6 6. Reference limits and partition values of right ventricular and pulmon
A p p e n d ix 6 : R e f e r e n c e l i m i t s a n d p a r t i t i
R e f e r e n c e R a n g e
M i l d l y A b n o r m a l
M o d e r a t e l y A b n o r m a l
S e v e r e l y A b n o r m a l
V a r i a b l e
27.7 7. Reference limits and partition values of right ventricular size and
A p p e n d ix 7 : R e f e r e n c e l i m i t s a n d p a r t i t i
R e f e r e n c e R a n g e
M i l d l y A b n o r m a l
M o d e r a t e l y A b n o r m a l
S e v e r e l y A b n o r m a l
V a r i a b l e
27.8 8. Reference limits and partition values for left atrial dimensions and
A p p e n d ix 8 : R e f e r e n c e l i m i t s a n d p a r t i t i
W o m e n
M e n
R e f e r e n c e Ran ge
M i l d l y Abn o r m al
M o d e r a t e l y A b n o r m a l
S e v e r e l y Abn o r m al
R e f e r e n c e Ran ge
M i l d l y Abn o r m al
M o d e r a t e l y A b n o r m a l
S e v e r e l y Abn o r m al
L A v o l u m e / B S A , m L / m
29â € “ 3
34â€
29â € “ 3
34â€
27.9 9. Appendix 9
27.10 10. Reference ranges for diastolic function parameters by age
A p p e n d ix 1 0 : R e f e r e n c e r a n g es f o r d i a s t o l
A g e G r o u p s , y
P a r a m e t e r
45–
50–
55–
60–
65–
≥7 0
27.11 11. Mitral inflow velocities in 117 normal subjects, stratified by phas
A p p e n d ix 1 1 : M i t r a l i n f l o w v e l o c i t i e s i n
V a r i a b l e I n s p i r a t i o n E x p i r a t i o n A p n e a
27.12 12. Pulmonary venous flow velocities in 85 normal subjects, stratified
A p p e n d i x 1 2 : P u lm o n a r y v e n o u s f l o w v e l o c
V a r i a b l e I n s p i r a t i o n E x p i r a t i o n A p n e a
27.13 13. Normal Doppler data in children, n = 223 - mitral valve flow var
A p p e n d ix 1 3 : N o r m a l D o p p l e r d a t a i n c h i l
3 â € “ 8 Y e a r s ( n = 7 5 )
9 â € “ 1 2 Y e a r s ( n =
1 3 â € “ 1 7 Y e a r s ( n =
F a c t o r M e a n
27.14 14. Normal Doppler data in children, n = 223 - pulmonary vein flow v
A p p e n d ix 1 4 : N o r m a l D o p p l e r d a t a i n c h i l
3 â € “ 8 Y e a r s ( n = 7 5 )
9 â € “ 1 2 Y e a r s ( n =
1 3 â € “ 1 7 Y e a r s ( n =
F a c t o r M e a n
27.15 15. Appendix 15
27.16 16. Velocity of individual segments determined with tissue Doppler ech
A p p e n d ix 1 6 : V e l o c i t y o f i n d i v i d u a l s e g m
S e p t u m L a t e r a l I n f e r i o r A n t e r i o r
27.17 17. Strain rate of individual segments
27.18 18. Displacement and systolic strain of individual segments
27.19 19. Qualitative and quantitative parameters useful in grading mitral r
A p p e n d ix 1 9 : Q u a l i t a t i v e a n d q u a n t i t a t i v
P a r a m e t e r M i l d
M o d e r a t e
S e v e r e
27.20 20. Qualitative and quantitative parameters useful in grading aortic r
A p p e n d ix 2 0 : Q u a l i t a t i v e a n d q u a n t i t a t i v
A o r t i c R e g u r g i t a t i o n
P a r a m e t e r M i l d M o d e r a t e S e v e r e
27.21 21. Echocardiographic and Doppler parameters used in grading tricuspid
A p p e n d ix 2 1 : E c h o c a r d i o g r a p h i c a n d D o p p l
T r i c u s p i d R e g u r g i t a t i o n
27.22 22. Echocardiographic and Doppler parameters used in grading pulmonary
A p p e n d ix 2 2 : E c h o c a r d i o g r a p h i c a n d D o p p l
P u l m o n a r y R e g u r g i t a t i o n
P a r a m e t e r M i l d M o d e r a t e S e v e r e

Citation preview

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Table of Contents 1. Front ................................................................................................................................................ 3 1.1 Cover ......................................................................................................................................... 3 1.2 Authors and Editors ................................................................................................................ 61 1.3 Dedication ............................................................................................................................... 63 1.4 Preface .................................................................................................................................... 63 2. TOC ................................................................................................................................................ 65 3. Abbreviations ................................................................................................................................ 68 4. 1 - How to Obtain a Good Echocardiography Examination .......................................................... 71 5. 2 - Transthoracic Echocardiography ............................................................................................. 86 6. 3 - Transesophageal and Intracardiac Echocardiography ........................................................... 122 7. 4 - Doppler Echocardiography and Color Flow Imaging ............................................................. 179 8. 5 - Tissue Doppler Imaging, Strain Imaging, and Dyssynchrony Assessment ............................. 223 9. 6 - Contrast Echocardiography.................................................................................................... 267 10. 7 - Assessment of Systolic Function and Quantification of Cardiac Chambers ........................ 286 11. 8 - Assessment of Diastolic Function and Diastolic Heart Failure ............................................. 309 12. 9 - Pulmonary Hypertension and Pulmonary Vein Stenosis ..................................................... 364 13. 10 - Coronary Artery Disease and Acute Myocardial Infarction ............................................... 388 14. 11 - Stress Echocardiography .................................................................................................... 435 15. 12 - Valvular Heart Disease ....................................................................................................... 469 16. 13 - Prosthetic Valve Evaluation ............................................................................................... 549 17. 14 - Infective Endocarditis ........................................................................................................ 583 18. 15 - Cardiomyopathies .............................................................................................................. 603 19. 16 - Cardiac Diseases Due to Systemic Illness, Genetics, Medication, or Infection .................. 652 20. 17 - Pericardial Diseases ........................................................................................................... 684 21. 18 - Tumors and Masses ........................................................................................................... 729 22. 19 - Diseases of the Aorta ......................................................................................................... 752 23. 20 - Echocardiography in Congenital Heart Disease - An Overview ......................................... 774 24. 21 - Intraoperative Echocardiography ...................................................................................... 844 25. 22 - Vascular Imaging and Tonometry ...................................................................................... 871 26. 23 - Goal-Directed and Comprehensive Examination ............................................................... 887 27. Appendices................................................................................................................................ 915 27.1 1. Echocardiography laboratory, Mayo Clinic, Rochester, Minnesota - example of a final report .......................................................................................................................................... 915 27.2 2. Normal values from M-mode echocardiography............................................................ 917 27.3 3. Reference limits and partition values of left ventricular size ......................................... 918 27.4 4. Reference limits and values and partition values of left ventricular function................ 920 27.5 5. Reference limits and partition values of left ventricular mass and geometry ............... 922 27.6 6. Reference limits and partition values of right ventricular and pulmonary artery size ... 924 27.7 7. Reference limits and partition values of right ventricular size and function as measured in the apical four-chamber view ................................................................................................. 925 27.8 8. Reference limits and partition values for left atrial dimensions and volumes ............... 926 27.9 9. Appendix 9 ...................................................................................................................... 928

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techom 27.10 10. Reference ranges for diastolic function parameters by age ....................................... 929 27.11 11. Mitral inflow velocities in 117 normal subjects, stratified by phase of respiration ... 933 27.12 12. Pulmonary venous flow velocities in 85 normal subjects, stratified by phase of respiration ................................................................................................................................... 934 27.13 13. Normal Doppler data in children, n = 223 - mitral valve flow variables and left ventricular isovolumic relaxation time, stratified by age group ................................................. 935 27.14 14. Normal Doppler data in children, n = 223 - pulmonary vein flow variables, stratified by age group .................................................................................................................................... 937 27.15 15. Appendix 15 ................................................................................................................ 938 27.16 16. Velocity of individual segments determined with tissue Doppler echocardiography 939 27.17 17. Strain rate of individual segments .............................................................................. 940 27.18 18. Displacement and systolic strain of individual segments ........................................... 941 27.19 19. Qualitative and quantitative parameters useful in grading mitral regurgitation severity .................................................................................................................................................... 941 27.20 20. Qualitative and quantitative parameters useful in grading aortic regurgitation severity .................................................................................................................................................... 944 27.21 21. Echocardiographic and Doppler parameters used in grading tricuspid regurgitation severity........................................................................................................................................ 946 27.22 22. Echocardiographic and Doppler parameters used in grading pulmonary regurgitation severity........................................................................................................................................ 948

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1.2 Authors and Editors Jae K. Oh MD Codirector Echocardiography Laboratory; Consultant, Division of Cardiovascular Diseases, Mayo Clinic; Professor of Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota James B. Seward MD Consultant Division of Cardiovascular Diseases, Mayo Clinic; John M. Nasseff, Sr., Professor in Cardiology in Honor of Dr. Burton Onofrio; Professor of Medicine and of Pediatrics, Mayo Clinic College of Medicine, Rochester, Minnesota A. Jamil Tajik MD Consultant Division of Cardiovascular Diseases, Mayo Clinic, Scottsdale, Arizona; Thomas J. Watson, Jr., Professor in Honor of Dr. Robert L. Frye; Professor of Medicine and of Pediatrics, Mayo Clinic College of Medicine, Rochester, Minnesota

Secondary Editors Fran DeStefano Acquisitions Editor Julia Seto Managing Editor Bridgett Dougherty Production Manager Benjamin Rivera Senior Manufacturing Manager Angela Panetta Marketing Manager Doug Smock Design Coordinator Laserwords Private Limited, Chennai, India

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Contributors Allison Cabalka MD Consultant Division of Pediatric Cardiology, Mayo Clinic; Professor of Pediatrics, Mayo Clinic College of Medicine; Rochester, Minnesota Frank Cetta Jr. MD Chair Division of Pediatric Cardiology, Mayo Clinic; Professor of Medicine and of Pediatrics, Mayo Clinic Colle ge of Medicine; Rochester, Minnesota Roger L. Click MD Consultant Division of Cardiovascular Diseases, Mayo Clinic; Associate Professor of Medicine, Mayo Clinic College of Medicine; Rochester, Minnesota Raul E. Espinosa MD Consultant Division of Cardiovascular Diseases, Mayo Clinic; Assistant Professor of Medicine, Mayo Clinic College of Medicine; Rochester, Minnesota Donald J. Hagler MD Consultant Division of Pediatric Cardiology, Mayo Clinic; Professor of Pediatrics, Mayo Clinic College of Medic ine; Rochester, Minnesota Iftikhar J. Kullo MD Consultant Division of Cardiovascular Diseases, Mayo Clinic; Associate Professor of Medicine, Mayo Clinic College of Medicine; Rochester, Minnesota A. Rauoof Malik MD

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techom Research Fellow in Cardiovascular Diseases Mayo School of Graduate Medical Education, Mayo Clinic College of Medicine; Rochester, Minnesota Patrick W. O'Leary MD Consultant Divisions of Cardiovascular Diseases and Pediatric Cardiology, Mayo Clinic; Associate Professor of Pediatrics, Mayo Clinic College of Medicine; Rochester, Minnesota Brian D. Powell MD Fellow in Cardiovascular Diseases Mayo School of Graduate Medical Education, Mayo Clinic College of Medicine; Rochester, Minnesota Guy S. Reeder MD Consultant Division of Cardiovascular Diseases, Mayo Clinic; Professor of Medicine, Mayo Clinic College of Medicine; Rochester, Minnesota Cheuk-Man Yu MD Head Division of Cardiology, The Chinese University of Hong Kong Prince of Wales Hospital, Shatin, N.T. Hong Kong

1.3 Dedication Dedication To our patients

1.4 Preface “When is your next edition going to come out?” We began hearing this question 3 years ago and realized that the second edition of the Echo Manual had been published 7 years ago. Echocardiography is now firmly established as the single most useful diagnostic test for evaluation of patients with cardiovascular diseases because it provides reliable structural, functional, and hemodynamic information a bout the cardiovascular system. Echocardiography continues to evolve, and the development of new modalities improves its diagnostic capability. The echocardiography examination is continuously being refined through better display of cardiac anatomy, more r eliable quantitation, and more precise

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techom assessment of cardiac function. Therefore, the appropriate clinical application of this versatile diagnostic technique requires continuing education and training of physicians and sonographers. At an echocardiography meeting, the daughter of a cardiologist attending the meeting pleaded, “Please, do not come up with too many new things in echocardiography. My father is very stressed about keeping up with new stuff and does not have much time to spend with us.” It is our hope that this third edition of the Echo Manual will provide an enjoyable learning experience, rather than stress, for cardiologists, internists, anesthesiologists, critical care physicians, emergency room physicians, and sonographers as well as for residents and fellows in training. When we wrote the first edition of the Echo Manual, our main purpose was to foster the proper clinical use of echocardiography as a diagnostic tool by sharing our extensive experience in evaluating patients who had various cardiovascular diseases. The main goal of this third edition remains the same as for previous editions: to help readers learn new applications as well as established practices. The Echo Manual is unique in that the entire contents of the first two editions we re written initially by the first author and then revised by coauthors, who are pioneers in echocardiography. For the third edition, several colleagues were invited to revise chapters or to write new ones. New chapters and sections added to this edition in clude the following topics: tissue Doppler and strain imaging, evaluation of mechanical dyssynchrony, three -dimensional echocardiography, intracardiac echocardiography, diastolic stress testing, congenital echocardiography, and vascular imaging. The chapte r on diastolic function has been greatly expanded. All other chapters have been revised, with many new figures and references added. The first chapter describes how to obtain not only clinically valuable echocardiographic images but also beautifully displa yed images, which we believe requires knowledge of cardiovascular diseases and ultrasound physics as well as good technique. Bruce K. Daniel, a staff sonographer, reviewed the first chapter and provided valuable suggestions. There are numerous other persons for us to thank. Dr. O. Eugene Millhouse edited the book, and Roberta Schwartz (supervisor), Kristin M. Nett (editorial assistant), and Ann Lemke (proofreader), as members of the Section of Scientific Publications, assisted with the production. Mar k A. Zangs, Vernon P. Weber, and Jeffrey R. Stelley (Echocardiography Laboratory) created beautiful still frame images from patients' echocardiography studies. Paul W. Honermann (Illustration and Design) put a final artistic touch on all 64

techom the figures. Julie L. Griffin and Kelly M. Wilson (medical secretaries) assisted with the revision. A book -grant from Lippincott Williams & Wilkins, provided us with some quiet time so we were able to concentrate our efforts on this edition. Also, many individuals at Lippin cott Williams & Wilkins helped and encouraged us to produce this beautifully designed book with the dark green biplane cover. A project of this magnitude is not possible without support and understanding from our families. The development of echocardiograp hy and the accumulation of extensive clinical material at Mayo Clinic are a product of the efforts of our physician colleagues and sonographers. (There are 45 echocardiography physicians and more than 90 sonographers at Mayo Clinic Rochester.) Finally, our patients are the ultimate reason for our interest in echocardiography, and they provided all the educational images in the Echo Manual. We will be most gratified if this book helps improve the care of patients. Jae K. Oh on behalf of all authors

2. TOC ↑ Table of Contents

[+]

1 - How to Obtain a Good Echocardiography Examination: Ultrasound Physics, Technique, and Medical Knowledge [+]

2 - Transthoracic Echocardiography: M-mode, Two-Dimensional, and Three-Dimensional [+]

3 - Transesophageal and Intracardiac Echocardiography [+]

4 - Doppler Echocardiography and Color Flow Imaging: Comprehensive Noninvasive Hemodynamic Assessment [+]

5 - Tissue Doppler Imaging, Strain Imaging, and Dyssynchrony Assessment [+]

6 - Contrast Echocardiography [+]

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7 - Assessment of Systolic Function and Quantification of Cardiac Chambers [+]

8 - Assessment of Diastolic Function and Diastolic Heart Failure [+]

9 - Pulmonary Hypertension and Pulmonary Vein Stenosis [+]

10 - Coronary Artery Disease and Acute Myocardial Infarction [+]

11 - Stress Echocardiography [+]

12 - Valvular Heart Disease [+]

13 - Prosthetic Valve Evaluation [+]

14 - Infective Endocarditis [+]

15 - Cardiomyopathies [+]

16 - Cardiac Diseases Due to Systemic Illness, Genetics, Medication, or Infection [+]

17 - Pericardial Diseases [+]

18 - Tumors and Masses [+]

19 - Diseases of the Aorta [+]

20 - Echocardiography in Congenital Heart Disease: An Overview [+]

21 - Intraoperative Echocardiography [+]

22 - Vascular Imaging and Tonometry [+]

23 - Goal-Directed and Comprehensive Examination ↑ Back of Book

[-]

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Appendices -

Appendix 1: Echocardiography laboratory, Mayo Clinic, Rochester, Minnesota—example of a final report -

Appendix 2: Normal values from M-mode echocardiography -

Appendix 3: Reference limits and partition values of left ventricular size -

Appendix 4: Reference limits and values and partition values of left ventricular function -

Appendix 5: Reference limits and partition values of left ventricular mass and geometry -

Appendix 6: Reference limits and partition values of right ventricular and pulmonary artery size -

Appendix 7: Reference limits and partition values of right ventricular size and function as measured in the apical four-chamber view -

Appendix 8: Reference limits and partition values for left atrial dimensions and volumes [+]

Appendix 9 -

Appendix 10: Reference ranges for diastolic function parameters by age -

Appendix 11: Mitral inflow velocities in 117 normal subjects, stratified by phase of respiration -

Appendix 12: Pulmonary venous flow velocities in 85 normal subjects, stratified by phase of respiration -

Appendix 13: Normal Doppler data in children (n = 223): mitral valve flow variables and left ventricular isovolumic relaxation time, stratified by age group -

Appendix 14: Normal Doppler data in children (n = 223): pulmonary vein flow variables, stratified by age group [+]

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Appendix 15 -

Appendix 16: Velocity of individual segments determined with tissue Doppler echocardiography -

Appendix 17: Strain rate of individual segments -

Appendix 18: Displacement and systolic strain of individual segments -

Appendix 19: Qualitative and quantitative parameters useful in grading mitral regurgitation severity -

Appendix 20: Qualitative and quantitative parameters useful in grading aortic regurgitation severity -

Appendix 21: Echocardiographic and Doppler parameters used in grading tricuspid regurgitation severity -

Appendix 22: Echocardiographic and Doppler parameters used in grading pulmonary regurgitation severity

3. Abbreviations Abbreviations A late diastolic filling due to atrial contraction A′ late diastolic velocity of the mitral anulus Aa (same as A′) Ao aorta CHF congestive heart failure CI cardiac index CO

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techom cardiac output D diastolic forward flow velocity DT deceleration time E peak velocity of early diastolic filling of mitral inflow E′ peak early diastolic velocity of the mitral anulus Ea mitral anulus early diastolic velocity (same as Eâ €²) E/A ratio of E and A velocities ECG electrocardiogram ( -graphy) ERO effective regurgitant orifice IVC inferior vena cava IVCT isovolumic contraction time IVRT isovolumic relaxation time LA left atrium ( -ial) LV left ventricle ( -icular) LVEF left ventricular ejection fraction LVOT left ventricular outflow tract

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techom MV mitral valve PFO patent foramen ovale PHT pressure half-time PISA proximal isovelocity surface area PW posterior wall RA right atrium ( -ial) RV right ventricle ( -icular) S systolic forward flow velocity S′ systolic velocity of the mitral anulus SV stroke volume SVC superior vena cava TEE transesophageal echocardiography TTE transthoracic echocardiography TVI time velocity integral 2D two-dimensional VS

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techom ventricular septum

4. 1 - How to Obtain a Good Echocardiography Examination > Table of Contents > 1 - How to Obtain a Good Echocardiography Examination: Ultrasound Physics, Technique, and Medical Knowledge

1 How to Obtain a Good Echocardiography Examination: Ultrasound Physics, Technique, and Medical Knowledge The burgeoning technologic revolution of the past two decades has produced a continuous evolution in the definition of a complete and comprehensive echocardiographic evaluation ( Fig. 1-1). Echocardiography is now a fully grown tree. It has numerous clinical applications, with various forms of ultrasound technology being used throughout the entire field of cardiovascular medicine. This mature ultrasound tree has grown from a seed planted more than 50 years ago. Since then, the tree has been trimmed and nourished carefully by many pioneers to serve the needs of patients and clinicians. In 1954, Edler and Hertz ( 1) of Sweden were the first to record movements of cardiac structures, in particular, the mitral valve, with ultrasound. In the early 1960s in the United States, Joyner and Reid (2) at the University of Pennsylvania were the first to use ultrasound to examine the heart. Shortly afterward, in 1965, Feigenbaum and colleagues ( 3) at Indiana University reported the first detection of pericardial effusion with ultrasound and were responsible for introducing echocardiography into the clinical practice of cardiology. However, M -mode echocardiography produced only an “ice pick† view of the heart; two dimensional (2D) sector scanning, developed in the mid -1970s, allowed real -time tomographic images of cardiac morphology and function (4). The first phased array 2D sector scan at Mayo Clinic was made on March 17, 1977. Although the development of Doppler echocardiography paralle led that of M-mode and 2D echocardiography from the early 1950s, it was not used clinically until the late 1970s. Pressure gradients across a fixed orifice could

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techom be obtained reliably with blood -flow velocities recorded by Doppler echocardiography. Two grou ps, Holen and colleagues ( 5) and Hatle and colleagues ( 6, should be credited for introducing Doppler echocardiography into clinical practice. Numerous validation studies subsequently confirmed the accuracy of Doppler echocardiography in the assessment of c ardiac pressures. Therefore, the Doppler technique made echocardiography not only an imaging but also a hemodynamic technique. On the basis of the Doppler concept, color flow imaging was developed in the early 1980s so that blood flow could also be visuali zed noninvasively ( 7). P.2

Another ingenious modification of Doppler echocardiography was tissue Doppler imaging (TDI), which allows echocardiographers to record myocardial tissue velocity and to measure the extent of myocardial deformation as strain ( 8, 9). These measurements provide a sensitive assessment of systolic and diastolic function and are becoming a standard component of a comprehensive echocardiography examination. Widespread clinical use of transesophageal echocardiography (TEE) began in 1987 (10, and the subsequent development of intravascular and intracardiac high frequency transducers has permitted extraordinarily detailed imaging and hemodynamic assessment of the cardiovascular system. Most recently, three -dimensional (3D) echocardiography has become a reality. It provides a more realistic depiction of cardiovascular structures and more accurate volumetric quantitation ( 11, 12).

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Figure 1-1 Echocardiography has become a mature tree that has numerous branches and is still growing. CFI, color flow imaging; ICUS, intracardiac ultrasonography; I-Op, intraoperative echocardiography; IVUS, intravascular ultrasonography; TEE, transesophageal echocardiography; 3D/4D, three- and four-dimensional echocardiography.

With these technologic advances, the application of echocardiography has been spreading into numerous clinical areas, including the evaluation of diastolic function, stress echocardiography, intraoperative echocardiography, fetal echocardiography, contrast echocardiography, intr acardiac imaging, and vascular imaging. The size of the ultrasound unit is becoming smaller, and some units can be hand -carried to the patient's bedside ( 13, 14). We are fortunate to have this versatile diagnostic modality to provide reliable structural, f unctional, and hemodynamic information about the cardiovascular system of our patients.

Ultrasound and Transducer Echocardiography uses ultrasound to create real -time images of the cardiovascular system in action. Ultrasound represents sound waves with a frequency of 20,000 Hz or more. All sound waves (Fig. 1-2) are characterized by the following seven variables ( 15: frequency (f), wavelength (λ), period (p), speed (sp), amplitude (A), power, and intensity. 

f = the number of cycles per second; 1 cps is 1 H z.



λ = the length of one complete cycle of the sound; its usual unit of measure is millimeters (mm).



sp = the speed or velocity of sound waves through a medium is equal to the product of f and λ (sp = f • λ) and is determined by the characteristics of the medium. Speed is not affected by the frequency of sound. The average speed of sound in soft tissue is 1,540 m/s.



p = the time duration of 1 cycle; hence, 1 second/ f = p or f • p = 1.



A = the magnitude of a sound wave, the maximum change from the baseline.



Power is the rate at which energy is transferred from a sound beam, in watts (W), and is proportional to the amplitude squared (15).

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Intensity is the concentration of energy in a sound beam and equals power divided by its cross -sectional area.

Figure 1-2 Diagram of a sound wave. A, amplitude.

Sound waves can be combined to create one wave. Thus, two in phase (or superimposed) waves create a wave with a larger amplitude, and two out -of-phase (or mirror -image) waves create a wave with a smaller a mplitude or the two waves cancel each other if they have the same amplitude. This phenomenon is called interference ( 15). It is used in pulse -inversion and pulse modulation techniques for harmonic imaging and contrast echocardiography. At the start of an e chocardiography examination, the appropriate transducer is selected according to the type of examination and patient's body habitus. A higher frequency transducer provides better resolution, but it has a shallower depth of penetration. For the pediatric po pulation, the transducer frequency is usually 5 to 7.5 MHz (1 MHz = 1 million cps), but for adults the transducer frequency at the start of an examination is usually 2 to 2.5 MHz and occasionally 5 MHz for patients with a thin chest wall. The transducer co nsists of piezoelectric elements that convert electrical energy to ultrasound and vice versa. Electrical energy is applied to the transducer in pulses with a defined pulse repetition frequency (PRF in kilohertz [kHz]), producing ultrasound waves at defined, regular intervals of pulsed repetition period. The wavelength of the ultrasound generated is related to the thickness of the piezoelectric elements. The thinner the elements, the shorter the wavelength. Because the product of wavelength P.3

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(λ) and sound frequency ( f) is the speed of the sound in the tissue (λ • f = 1,540 m/s), sound frequency is related inversely to the thickness of the piezoelectric elements. These transducer elements need to move to generate multidirectional ultrasound beams. T his movement can be achieved mechanically or electronically. Although a mechanical transducer can produce multiple imaging lines from a small transducer area, the ultrasound beam diverges more the deeper it penetrates tissue. In an electronic transducer, m ultiple piezoelectric elements are arranged in a straight line and sound beams are steered and focused electronically. Most of the current ultrasound units have electronic steering, with phased stimulation of the piezoelectric elements. Because image resol ution is better with shorter wavelengths, a higher frequency transducer produces an image with better resolution but shallower penetration. Technology has advanced to the point that a transducer contains 3,000 piezoelectric elements to create a matrix tran sducer, which allows real -time 3D imaging. In fundamental imaging, echocardiographic images are created when the transducer receives reflected beams of the same frequency as the transmitted beam, but the interface between tissue and blood can be delineated better with the reception of harmonic frequencies. Harmonic imaging has developed directly from arduous attempts to improve the ultrasound imaging of contrast microbubbles. When contrast microbubbles are imaged, the bubbles resonate and produce harmonic f requencies (i.e., equivalent to multiple of the transmitted frequency). When the only reflected frequency received to create the ultrasound image is equal to a multiple (2 f, 3f, …) of the transmitted frequency, images of contrast microbubbles are prefere ntially produced (contrast harmonic imaging). Like microbubbles, myocardial tissues are able to generate harmonic frequencies, and harmonic imaging improves the delineation of the endocardial border (tissue harmonic imaging). As a result, harmonic imaging is usually the imaging modality of choice not only for contrast echocardiography but also for a standard echocardiography examination. Additional modifications of harmonic imaging include pulse inversion and power modulation imaging, which improved resolut ion in contrast imaging. A limitation of harmonic imaging in routine 2D echocardiography is the increased sparkling quality to the ultrasound image and the increased thickness of the endocardial border. If the image quality is not optimal in spite of all m easures, including harmonic imaging, then a contrast agent should be 75

techom injected intravenously to improve the definition of the endocardial border. Because intravenous access is required, a qualified member of an intravenous team should be available to start an intravenous line as soon as contrast echocardiography is needed.

Screen Display and Knob Settings How best to display echocardiographic images on the screen is a personal choice and should be choreographed according to the clinical objectives of the examiner. The following should be shown on the screen: the patient's identification, blood pressure at the time of the examination, and a sharp electrocardiographic tracing with prominent R and P waves ( Fig. 1-3 and 1-4). Depth, size, and gain settings of the ultrasound images need to be adjusted frequently during the examination. To develop an initial impression of the overall cardiac structure and P.4

function, the examination of an adult patient usually begins with a depth of 20 to 25 cm and a wide sec tor (90 degrees). This also gives an idea about any unusual extracardiac structures ( Fig. 1-4). After the initial view, adjust the field depth to use the entire screen to demonstrate the intended cardiovascular images. A zoom or regional expansion selectio n (RES) function should be used frequently to visualize a region of interest in more detail. The zoomed image is also better for making quantitative measurements, with less intraobserver and interobserver variability. When quantitative measurements are mad e, review the acquired image in a cine loop format to identify a frame at a specific timing of a cardiac cycle. Examples are a mid -systolic frame to measure the diameter of the left ventricular outflow tract, an end-systolic frame to measure the size of th e left atrium, and an end-diastolic frame to measure the wall thickness of the left ventricle. After an overview, specific areas need to be imaged and it may be necessary to decrease the sector size, which will improve temporal resolution by increasing the frame rate. The gain of the image is controlled by overall gain and regional gain (by time gain compensation [TGC]).

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Figure 1-3 Still frame of a typical echocardiography monitor screen. It is essential for the screen to display the patient's identification, blood pressure ( BP), and cardiac rhythm. The type of transducer, field depth, color map, and other machine settings are also displayed. In the example here, the BP was 120/52 mm Hg, with a wide pulse pressure. Aortic valve shows doming (arrow) during systole (a break in the ECG at the bottom indicates the timing of the image on the screen), with moderately severe aortic regurgitation that explains the wide pulse pressure. “H3.5 MHz† indicates harmonic imaging with a 3.5-MHz transducer. Field depth is 160 mm (this information is important in stress echocardiography and other quantitative studies for which the same depth is des ired for all images). “MI† indicates mechanical index, which is an essential function in contrast echocardiography. “Store in progress” indicates that the echocardiographic images are stored digitally while the phrase is shown on the screen; thus, desired images need to be maintained during this period. HR, heart rate.

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Figure 1-4 Initial parasternal long -axis view with an imaging depth of 24 cm (240 mm on screen) demonstrating a large pleural effusion ( PL) and pericardial effusion ( PE). The descending aorta (*) can also be appreciated with a long imaging depth. LA, left atrium; LV, left ventricle; RV, right ventricle.

As sound waves travel through a medium (e.g., tissue or blood), the intensity weakens or attenuates. The degree of att enuation is expressed in decibels (dB). Absorption represents a conversion of sound energy to another form of energy and is the major reason for attenuation. Therefore, attenuation is determined by ultrasound frequency and tissue depth. Attenuation is also greater for highfrequency sounds, which result in higher absorption and more scatter. Total attenuation is calculated by multiplying the attenuation coefficient by the length of imaged tissue. TGC allows amplification of ultrasound beams from deeper dept hs because different amplitudes of ultrasound signals are produced when received from different depths. More TGC is required for higher frequency transducers, which create more attenuation. Compression also reduces the differences between the smallest and largest amplitudes of ultrasound images by reducing the total range without altering the signal ratio. Once 2D images are optimized, color flow imaging is turned on to visualize the intracardiac blood flow characteristics and to identify any turbulent flow within the heart. Occasionally, color flow imaging demonstrates hemodynamic or structural abnormalities

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techom that are not readily apparent with 2D echocardiography alone. When color flow imaging is used to show a regurgitant jet, the color map aliasing velocit y should be set as high as possible (by moving the velocity scale up as far as possible). The color gain should be increased to the point that it just begins to create background noise and then decreased to the level that optimizes color flow imaging of bl ood flow. The size of the color flow sector should be optimized because the frame rate for color flow imaging is inversely proportional to the area of imaging. The location and size of color flow imaging can be adjusted according to the objectives of the e xamination. If 2D or color flow imaging (or both) identifies an area of concern, a further quantitative assessment is made, such as measuring the size of the lesion, calculating the area of the stenotic or regurgitant orifice, or calculating the pressure gradient. Even without the presence of obvious structural or functional abnormalities, several areas of the heart need to be interrogated to assess systolic and diastolic function. Therefore, a pulsed wave Doppler examination follows and complements color flow imaging. A pulsed wave Doppler examination of the left ventricular outflow tract and the mitral leaflet tips is routinely performed to calculate stroke volume and to assess diastolic function, respectively. Other relatively routine pulsed Doppler examinations include the right ventricular outflow tract, pulmonary vein, hepatic vein, upper descending aorta, and abdominal aorta. A comprehensive echocardiography examination should include a continuous wave Doppler examination of the descending aorta to assess for the presence of coarctation, especially in patients who have hypertension or a bicuspid aortic valve. Another important area of a pulsed wave Doppler examination is the mitral anulus, but the Doppler mode needs to be changed to TDI. Pulsed wave Dop pler has been modified to record velocity from the tissues which is lower in absolute velocity but higher in amplitude. When TDI or myocardial imaging is selected, higher tissue velocities are filtered out and only lower tissue velocities, usually 5 to 20 cm/s, are recorded. Because of the higher amplitude, the gain needs to be decreased when the examination is switched from regular pulsed wave Doppler imaging to TDI. TDI has numerous applications (see Chapter 4). It is essential in evaluating cardiac function (systolic and diastolic) and the timing of cardiac events, and it is useful in assessing mechanical dyssynchrony among different regions of the left ventricle ( 16, 17). Myocardial strain and strain rate can be derived from TDI ( 18). Tissue tracking and tissue synchronization imaging (TSI) have been developed to allow 79

techom echocardiographers to assess the pattern and timing of myocardial contraction readily with color imaging of tissue Doppler velocities. During a Doppler examination, the recording of velocit y is optimized by selecting or adjusting the velocity scale, gain, baseline position, sweep speed, sample volume size, and respiratory cycle. Recording space should be used fully by selecting the highest velocity to be about 25% higher than the obtained velocity. For example, if aortic stenosis velocity is 4 m/s, it is better to have the highest velocity scale set at 5 m/s instead of 7 m/s. If pulmonary vein peak velocity is 80 cm/s, it is better to have the Nyquist limit or aliasing velocity at 120 cm/s in stead of 200 cm/s. The baseline can be shifted accordingly to demonstrate fully the obtained or desired recorded velocity. Initial Doppler gain should be increased to the point of background noise and then decreased to produce optimal contrast with the rec orded signal. Colorization of the Doppler signal frequently makes the velocity sharper and is available on most machines by pushing or selecting that option. The smallest possible sample volume size (1–2 mm) usually is selected to record P.5

the pure velocity signal from the region of interest when a slight variation in sample volume location can produce different velocities, as in the left ventricular outflow tract or mitral leaflet tips. However, a larger sample volume size (3–5 mm) may be necessary to obtain a good velocity signal from an area of interest that is small, as in a pulmonary vein, or hepatic vein, or during tissue Doppler imaging of the mitral anulus. Color flow imaging is helpful as a guide for locating the ideal site for placing a sam ple volume. When the region of interest moves with the cardiac cycle or with respiration, a signal may be obtained by instructing the patient to hold his or her breath or by slightly changing the location of the sample volume during several attempts to obt ain the signal. The sweep speed is usually set at 50 mm/s for recording Doppler velocities, but when time intervals are measured, it may be increased to 100 mm/s. When multiple cardiac cycles need to be recorded together, the sweep speed is reduced to 25 mm/s, especially when the respiratory variation of Doppler velocity is assessed. Because contrast can dramatically enhance weak Doppler signals, it should be considered for improving the accuracy of the examination of patients who have weak tricuspid regurgitation or an aortic stenosis jet.

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Goal-Directed and Comprehensive Examination by Well-Trained Personnel To perform a clinically pertinent echocardiography examination, it is important to have a strategy to determine which of the numerous echocardiographic views and parameters will provide the optimal information for assessing the patient being examined. A strategy is best formulated after the examiner (sonographer or physician) has a clear understanding of the clinical problem or problems to be evaluated. An echocardiography examination is highly useful clinically and cost -effective when sound medical knowledge is combined with sound technical skills, including an understanding of ultrasound physics ( 15, 19) and the instrumentation, and interpretive skills. Some start echocardiographic training by developing technical expertise, and others approach this training after medical school or residency. The miniaturization and portability of echocardiographic machines may provide a strong incentive for physicians t o learn technical and interpretive skills of ultrasonography during medical school ( 13) or residency, akin to learning about heart sounds by using a stethoscope. Sonographers take a different road to sonography, approaching echocardiography by learning and perfecting technical skills. When a sonographer understands which echocardiographic parameters are important for a specific clinical diagnosis or for the patient's symptoms and why, he or she is truly an accomplished echocardiographer. Therefore, the echo cardiography examination should integrate the medical and sonographic skills to produce clinically relevant and visually attractive echocardiograms. Physician training requirements for the performance and interpretation of adult transthoracic echocardiogra phy examinations have been developed by the ACC/AHA Task Force on competence in collaboration with the American Society of Echocardiography, the Society of Cardiovascular Anesthesiologists, and the Society of Pediatric Echocardiography ( Table 1-1) (20). There are three levels of physician training: 

Level 1 training is defined as the minimal introductory training that must be achieved by all trainees in adult cardiovascular medicine. This includes a basic understanding of the physics of ultrasound, the funda mental technical aspects of the examination, cardiovascular anatomy and physiology related to echocardiographic and Doppler imaging,

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techom and recognition of simple and complex cardiac abnormalities and their pathophysiology. 

Level 2 training is the minimum reco mmended training for a physician to perform echocardiography and to interpret echocardiograms independently.



Level 3 training requires at least 12 months of training that provides a level of expertise sufficient to enable a physician to serve as director o f an echocardiography laboratory and to be directly responsible for quality P.6

control and for training sonographers and physicians in echocardiography.

Table 1-1 Training requirements for the performance and interpretation of adult transthoracic echocardiography examinations Minimum Cumulative

Total Number

Minimum

Duration of

of

Number of

Training,

Examinations

Examinations

mo

Performed

Interpreted

Level 1

3

75

150

Level 2

6

150 (75

300 (150

additional)

additional)

300 (150

750 (450

additional)

additional)

Level 3

12

Digital Echocardiography

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techom Digital echocardiography has profoundly changed and improved the practice of echocardiography ( 21). It is extremely convenient to acquire, transmit, and review echocardiographic images digitally. However, because only a limited number of cardiac cycles usually are acquired, it is essential for examiners to capture the most representative cardiac cycles. The number of cardiac cycles for image acquisition can be adjusted. One cycle is most economical for storage space, but it may not be representative, especially if the underlying rhythm is not regular. Acquisition of more cardiac cycles increases the time and storage space of the study. If the patient has normal sinus rhythm, a good compromise is to capture two or three cardiac cycles. However, one cardiac cycle is better for stress echocardiography because each view is compared with other images simultaneously side by side. If the patient has atrial fibrillation, three to five cardiac cycles should be acquire d. Digital imaging exposes the ultrasound system to the risk of viruses, worms, and parasites of the electronic system. To maintain the function of the machine and the security of patient information, the ultrasound unit needs to be protected against these electronic hazards.

Echocardiography Report Ideally, the echocardiographic reporting system should be integrated with the digital imaging system. With this integrated system, measured echocardiographic data are transferred automatically to the echocardiographic report and a still frame or even small clip of a real -time image can be included. The echocardiography report is the medium through which an echocardiographer conveys not only the descriptive findings of echocardiography but, more importantly, the c linical implications and diagnostic considerations in the context of the patient's clinical presentation. A report should do the following three things: 1) answer referral questions; even if echocardiography does not demonstrate any abnormality to explain the patient's symptoms, the absence of positive findings should be stated; 2) describe unsuspected, but clinically important, findings; and 3) provide basic data for all patients. The basic data include the following: left ventricular systolic and diastoli c function, left ventricular cavity size, wall thickness, right ventricular size and function, valvular structure and function, left atrial volume, anatomy of the great vessels, and pulmonary artery systolic pressure. Typical

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References 1. Edler I, Hertz xsCH. The use of ultrasonic reflectoscope for the continuous recording of the movements of heart walls. 1954. Clinical Physiology and Functional Imaging, 2004;24:118–136. 2. Joyner CR Jr, Reid JM. Applications of ultrasound in cardiology and cardiovascular physiology. Progress in Cardiovascular Diseases, 1963;5:482–497. 3. Feigenbaum H, Waldhausen JA, Hyde LP. Ultrasound diagnosis of pericardial effusion. JAMA: the Journa l of the American Medical Association, 1965; 191:711–714. 4. Tajik AJ, Seward JB, Hagler DJ, et al. Two -dimensional real -time ultrasonic imaging of the heart and great vessels: Technique, image orientation, structure identification, and validation. Mayo Clinic Proceedings, 1978;53:271–303. 5. Holen J, Aaslid R, Landmark K, et al. Determination of pressure gradient in mitral stenosis with a non -invasive ultrasound Doppler technique. Acta Medica Scandinavica, 1976;199:455–460. 6. Hatle L, Brubakk A, Tro msdal A, et al. Noninvasive assessment of pressure drop in mitral stenosis by Doppler ultrasound. British Heart Journal, 1978; 40:131–140. 7. Omoto R, Kasai C. Physics and instrumentation of Doppler color flow mapping. Echocardiography, 1987;4:467–483. 8. McDicken WN, Sutherland GR, Moran CM, et al. Colour Doppler velocity imaging of the myocardium. Ultrasound in Medicine and Biology, 1992;18:651–654. 9. Heimdal A, Stoylen A, Torp H, et al. Real -time strain rate imaging of the left ventricle by ultrasound. Journal of the American Society of Echocardiography, 1998;11:1013–1019. 10. Seward JB, Khandheria BK, Oh JK, et al. Transesophageal echocardiography: Technique, anatomic correlations, implementation, and clinical applications. Mayo Clinic Pro ceedings, 1988;63:649–680. 11. Zamorano J, Cordeiro P, Sugeng L, et al. Real -time threedimensional echocardiography for rheumatic mitral valve stenosis evaluation: An accurate and novel approach. Journal of the American College of Cardiology, 2004;43:20 91–2096. 84

techom 12. Kuhl HP, Schreckenberg M, Rulands D, et al. High -resolution transthoracic real -time three-dimensional echocardiography: Quantitation of cardiac volumes and function using semi -automatic border detection and comparison with cardiac magnetic r esonance imaging. Journal of the American College of Cardiology, 2004;43:2083–2090. 13. Wittich CM, Montgomery SC, Neben MA, et al. Teaching cardiovascular anatomy to medical students by using a handheld ultrasound device. JAMA: the Journal of the Americ an Medical Association, 2002;288:1062–1063. 14. Seward JB, Douglas PS, Erbel R, et al. Hand -carried cardiac ultrasound (HCU) device: Recommendations regarding new technology: A report from the Echocardiography Task Force on New Technology of the Nomencla ture and Standards Committee of the American Society of Echocardiography. Journal of the American Society of Echocardiography, 2002;15:369–373. 15. Edelman SK, ed. Understanding Ultrasound Physics: Fundamentals and Exam Review, 2nd ed. Woodlands, TX: ESP , 1994. 16. Ommen SR, Nishimura RA, Appleton CP, et al. Clinical utility of Doppler echocardiography and tissue Doppler imaging in the estimation of left ventricular filling pressures: A comparative simultaneous Doppler -catheterization study. Circulation, 2000;102:1788–1794. 17. Oh JK, Tajik J. The return of cardiac time intervals: The phoenix is rising. Journal of the American College of Cardiology, 2003;42:1471–1474. 18. Urheim S, Edvardsen T, Torp H, et al. Myocardial strain by Doppler echocardiograp hy: Validation of a new method to quantify regional myocardial function. Circulation, 2000;102:1158–1164. 19. Kremkau FW, ed. Diagnostic Ultrasound: Principles and Instruments, 6th ed. Philadelphia: W.B. Saunders, 2002. 20. Quinones MA, Douglas PS, Foste r E, et al. American College of Cardiology, American Heart Association, American College of Physicians-American Society of Internal Medicine, American Society of Echocardiography, Society of Cardiovascular Anesthesiologists, Society of Pediatric Echocardio graphy. ACC/AHA clinical competence statement on echocardiography: A report of the American College of Cardiology/American Heart Association/American College of Physicians -American Society of

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techom Internal Medicine Task Force on Clinical Competence. Journal of the American College of Cardiology, 2003;41:687–708. 21. Hansen WH, Gilman G, Finnesgard SJ, et al. The transition from an analog to a digital echocardiography laboratory: The Mayo experience. Journal of the American Society of Echocardiography, 2004;17: 1214–1224.

5. 2 - Transthoracic Echocardiography > Table of Contents > 2 - Transthoracic Echocardiography: M -mode, Two-Dimensional, and Three -Dimensional

2 Transthoracic Echocardiography: M-mode, Two-Dimensional, and Three-Dimensional Two-Dimensional Echocardiography An echocardiography examination begins with transthoracic two dimensional (2D) scanning from four standard transducer positions: the parasternal, apical, subcostal (subxiphoid), and suprasternal windows. The parasternal and apical views us ually are obtained with the patient in the left lateral decubitus position ( Fig. 2-1A) and the subcostal and suprasternal notch views, with the patient in the supine position ( Fig. 2-1B). An examiner may sit at the left or right side of a patient and scan with the right or left hand, respectively. From each transducer position, multiple tomographic images of the heart relative to its long and short axes are obtained by manually rotating and angulating the transducer (Table 2-1); hence, a multiplane examinat ion is performed ( Fig. 22) (1, 2, 3, 4). The long-axis view represents a sagittal or coronal section of the heart, bisecting the heart from the base to the apex. The short axis view is perpendicular to the long -axis view and is equivalent to sectioning the heart like a loaf of bread (“bread -loafing”). Real-time 2D echocardiography provides high -resolution images of cardiac structures and their movements so that detailed anatomic and functional information about the heart can be obtained. Therefore, 2D echocardiography is the basis of morphologic and functional assessments of the heart. Quantitative measurements of cardiac dimensions, area, and volume are derived from 2D images

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techom or 2D-derived M-mode. In addition, 2D echocardiography provides the framework for Doppler and color flow imaging. These standard long and short tomographic imaging planes are acquired as described in the following sections ( 1). Newer matrix transducers allow visualization of multiple tomographic views from a single three-dimensional (3D) or multidimensional image of the heart. Biplane imaging allows visualization of two tomographic views from the same acquisition. This shortens the duration of the examination and minimizes variation in the acquisition of cardiovascular images. With more advances and clinical experiences in 3D or multidimensional echocardiographic imaging, visualization and quantitation of cardiovascular structure, function, and hemodynamics will improve. (3D echocardiography is discussed in more detail at the end o f this chapter.)

Parasternal Position The examination is begun by placing the transducer in the left parasternal region, usually in the third or fourth left intercostal space, with the patient in the left lateral P.8

decubitus position ( Fig. 2-1A). From this position, sector images can be obtained of the heart along its long and short axes.

Figure 2-1 Four standard transthoracic transducer positions. A: The parasternal ( 1) and apical ( 2) views usually are obtained with the patient in the left lateral decubitus position. The parasternal view usually is obtained by placing the transducer at the left parasternal area in the third or fourth intercostal space. The apical view is obtained with the

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transducer at the maximal apical impulse (usually slightly lateral and inferior to the nipple, but it may be substantially displaced laterally and inferiorly because of cardiac enlargement or rotation or both). These views may be imaged best during he ld expiration, especially in patients who have chronic obstructive lung disease. The apical view can be difficult to obtain in a thin young person, and the transducer may need to be tilted superiorly. B: The subcostal ( 3) and suprasternal notch ( 4) views are obtained with the patient in the supine position. For subcostal imaging, relaxing the abdominal muscles by flexing the patient's knees and forced inspiration frequently improve the views. For suprasternal notch imaging, the patient's head needs to be ex tended and turned leftward so the transducer can be placed comfortably in the suprasternal notch without rubbing the patient's neck.

Table 2-1 Transducer positions and cardiac views

Parasternal position Long-axis view LV in sagittal section RV inflow LV outflow Short-axis view LV apex Papillary muscles (midlevel) Mitral valve (basal level) Aortic valve–RV outflow Pulmonary trunk bifurcation Apical position Four-chamber view Five-chamber (or long-axis) view Two-chamber view Subcostal position Inferior vena cava and hepatic vein RV and LV inflow LV-aorta

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RV outflow Suprasternal notch position Long-axis aorta–short -axis pulmonary artery Short-axis aorta–long-axis pulmonary artery Long-axis aorta and superior vena cava

LV, left ventricle; RV, right ventricle.

Long-Axis View of the Left Ventricle The long-axis view of the left ventricle (LV) is recorded with the transducer groove facing toward the patient's right flank and the transducer positioned in the third or fourth left intercostal interspace so that the ultrasound beam is parallel with a line joining the right shoulder to the left flank. The image obtained represents a section through the long axis of the LV (Fig. 2-3A). The image is oriented so the aorta is displayed on the right, the cardiac apex on the left, the chest wall and right ventricle (RV) anteriorly, and posterior structures posteriorly ( Fig. 2-3B). Therefore, the long -axis view of the LV is displ ayed as a sagittal section of the heart viewed from the left side of a supine patient. The long-axis view of the LV allows visualization of the aortic root and aortic valve leaflets. With the onset of systole, the leaflets open abruptly and come to lie nea rly parallel with the aortic walls. The chamber behind the aortic root is the left atrial (LA) cavity. Usually, the left inferior pulmonary vein, appearing as a round structure, also can be seen immediately posterior to the lower part of the LA. The long -axis view allows good visualization of the anterior and posterior leaflets of the mitral valve and their chordal and papillary muscle attachments ( Fig. 2-4A). The coronary sinus appears as a small, circular echo -free structure and usually can be recorded in the region of the posterior atrioventricular groove ( Fig. 2-3A). If the coronary sinus is enlarged, a persistent left -sided superior vena cava or increased right atrial (RA) pressure should be suspected ( Fig. 2-4B). The left-sided superior vena cava can b e confirmed by opacification of the coronary sinus with the administration of agitated saline through a vein in the left arm. The LV outflow tract (LVOT), bounded by the ventricular septum anteriorly and the anterior

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techom leaflet of the mitral valve posteriorly , is well seen and normally is widely patent during systole. Systolic anterior motion P.9

of the mitral valve has a characteristic appearance (see Chapter 15). The LVOT diameter, which is used to calculate stroke volume, is measured from this view. In this view, the descending thoracic aorta appears as a circular structure behind the LA. RV enlargement or RV pressure overload may be recognized in this view (Fig. 2-4C). With this view, color flow imaging is useful for screening for aortic and mitral valv e regurgitation.

Figure 2-2 A: Drawings of the longitudinal views from the four standard transthoracic transducer positions. Shown are the parasternal long -axis view (1), parasternal right ventricular inflow view ( 2), apical four-chamber view ( 3), apical fivechamber view ( 4), apical two-chamber view ( 5), subcostal four chamber view ( 6), subcostal long -axis (five-chamber) view ( 7), and suprasternal notch view ( 8). B: Drawings of short -axis views. These views are obtained by rotating the transducer 9 0 degrees clockwise from the longitudinal position. Drawings 1 to 6 show parasternal short -axis views at different levels by angulating the transducer from a superomedial position (for imaging the aortic and pulmonary valves) to an inferolateral position, tilting toward the apex (from level 1 to level 6 short -

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axis views). Shown are short -axis views of the right ventricular outflow tract and pulmonary valve ( 1), aortic valve and left atrium (2), right ventricular outflow tract ( 3), and short-axis views at the left ventricular basal (mitral valve level) ( 4), the left ventricle midlevel (papillary muscle) ( 5), and the left ventricle apical level ( 6). A good view to visualize the right ventricular outflow tract is the subcostal short -axis view (7). Also shown is the suprasternal notch short -axis view of the aorta (8). Ao, aorta; LA, left atrium; LV, left ventricle; MV, mitral valve; RA, right atrium; RPA, right pulmonary artery; RV, right ventricle; RVO, right ventricular outflow. ( B From Tajik et al [1]. By permission of Mayo Foundation for Medical Education and Research.)

Long-Axis View of Right Ventricular Inflow With the transducer in the same intercostal interspace (third or fourth), a long -axis view of the RV and RA is obtained by tilting the transducer inferomedially and rotating it slightly clockwise. In this view, the image is oriented with the chest wall anterior, the RA on the right and posterior, and the RV apex anterior and to the left. This view shows the RA cavity, tricuspid valve, coronary sinu s entry into the RA, and the RV inflow up to the apex of the RV ( Fig. 2-5). This view is good for recording the velocity of tricuspid regurgitation. The entry of the coronary sinus into the RA is seen clearly in this view.

Short-Axis Views With the transdu cer placed in the parasternal position (third or fourth left intercostal space), short -axis views of the heart are obtained by rotating the transducer clockwise so the plane of the ultrasound beam is approximately perpendicular to the plane of the long axi s of the LV. The groove on the transducer is pointed superiorly to face the right supraclavicular fossa, and the beam is roughly parallel with a line joining the left shoulder and right flank. With the transducer pointed directly posteriorly, a cross secti on P.10

is obtained of the LV at the level of the mitral leaflets. From this position, the transducer is tilted inferiorly toward the LV apex to 91

techom obtain a transverse section of the ventricular apex. The images are displayed as if viewed from below (lookin g from the apex of the heart up toward the base). In this format, the cross -sectional view of the LV is displayed posteriorly and to the right side of the image and the RV is displayed anteriorly and to the left.

Figure 2-3 A: Anatomic section ( left) and drawing (right) of the heart. B: Corresponding still frame of 2D echocardiographic image of the parasternal long -axis view. The parasternal long axis view allows visualization of the right ventricle ( RV), ventricular septum ( VS), posterior wall ( PW) aortic valve cusps, left ventricle ( LV), mitral valve, left atrium ( LA), and ascending thoracic aorta ( Ao). * Pulmonary artery. ( A from Tajik et al [1]. By permission of Mayo Foundation for Medical Education and Research.)

A cross section of the cardiac apex can be obtained also by placing the transducer directly over the point of maximal (apical) impulse (apical short -axis view). This view is helpful in the assessment of apical wall motion, apical hypertrophic cardiomyopathy, noncompaction of the apex, a nd apical mass. As the ultrasound beam is tilted superiorly, a cross section is obtained at the level of the papillary muscles. The papillary muscles, namely, the anterolateral and posteromedial muscles, project into the LV cavity

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techom at approximately the 3 - and 8-o'clock positions, respectively ( Fig. 2-6). By tilting the transducer further superiorly so it is nearly perpendicular to the chest wall, the ultrasound beam transects the body of the LV at the level of the mitral leaflets. In this view, the mitral anterior and posterior leaflets are seen in cross section and, during diastole, look like a fish mouth. This view is good for measuring the mitral valve area in a patient who has mitral stenosis, and it is the best view to identify a cleft mitral valve. By tilting the transducer further superiorly, the great arteries are sectioned transversely. At this level in normal subjects, the aorta appears as a circle with a trileaflet aortic valve that has the appearance of the letter “Y” during diastole ( Fig. 2-7). The RV outflow tract (RVOT) crosses anterior to the aorta from the left to the right of the image, wrapping around the aorta; in cross section, it has a sausage -like appearance anterior to the circular aorta. The pulmonary valve is observed anterior and to the right of the aortic valve. The origins of the right (anteriorly) and left main coronary arteries also can be seen in this view.

Apical Position This view is obtained with the patient turned in the left lateral decubitus position ( Fig. 2-1A). The apical impulse is localized and the transducer is placed at or in the immediate P.11

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vicinity of the point of maximal impulse. With the apical transducer position, a four -chamber view of the heart or a right anterior oblique equivalent view of the LV usually is recorded. The notch on the transducer is placed pointing up or down, depending on whether the goal is to display the LV on the right or on the left side of the image, respectively ( Fig. 2-8). Because the views obtained with the apical transducer position represent long -axis views of the heart, particularly of the LV, it is desirable that the orientation of the image of these views be similar to that of the long-axis view of the LV. For this reason, we have chosen to display the apical views with the LV on the left side and the RV on

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techom the right side of the image. For the four -chamber view, the ultrasound beam is directed superiorly and medially toward the patient's right scapula. This view displays all four chambers of the heart, the vent ricular and atrial septa, and the crux of the heart (Fig. 2-8A). While recording the apical four -chamber view, we usually tilt the beam in a slightly anterior and posterior direction to scan a greater portion of the atrial septum. The image is oriented so the apex is at the top and the atria at the bottom. In this image, the RA and RV are on the right and the LA and LV are on the left, with the groove of the transducer pointing down ( Fig. 2-8B). The ventricular and atrial septa are connected by a membranous septum. The left ( mitral) atrioventricular groove normally is slightly higher (more toward the atria) than the right (tricuspid) atrioventricular groove. The anterior leaflet of the mitral valve inserts into the left atrioventricular sulcus and near the P.13

cephalic end of the membranous septum, whereas the septal leaflet of the tricuspid valve inserts near the midportion of the membranous septum. Therefore, the insertion of the septal leaflet of the tricuspid valve is somewhat inferior (5–10 mm in th e hearts of older children and adults) to the insertion of the anterior mitral leaflet. This is an important anatomic distinction because it can be useful in identifying ventricular chambers. In Ebstein anomaly, the insertion of the septal tricuspid leafle t is displaced more apically.

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Figure 2-4 A: Parasternal long-axis view from a 64 -year-old patient with acute pulmonary edema demonstrating a flail posterior mitral leaflet ( arrow). Also, the left atrium ( LA) is enlarged. A round structure posterior to the LA is the descending thoracic aorta of normal dimension. B: Another parasternal long -axis view demonstrating a large coronary sinus (*). Because of a persistent left superior vena cava, the coronary sinus i s quickly opacified after agitated saline is injected into a left -arm vein. C: Young patient with pulmonary hypertension. The most prominent finding from this parasternal long-axis view is a dilated right ventricle ( RV). The ventricular septum ( VS) is flattened toward the left ventricle. Ao, ascending aorta; LA, left atrium; LV, left ventricle; RV, right ventricle.

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Figure 2-5 A: Right ventricular ( RV) inflow view demonstrating a tricuspid leaflet ( arrow) during systole. The coronary sinus (CS) enters the right atrium ( RA). This RV inflow view is good for visualizing tricuspid leaflet morphology and for obtaining tricuspid regurgitation velocity. B: Right ventricular inflow view during systole demonstrating inadequate coaptation of the tricuspid leaflets (arrow). The RA and CS are dilated. This is a good view to guide a catheter into the CS. LV, left ventricle; VS, ventricular septum.

Figure 2-6 Parasternal short -axis views. Multiple tomographic planes have been obtained by angulating the transducer from the level of the aortic and pulmonary valves to the left ventricular apex. A: Anatomic section ( left) and drawing ( right) of a parasternal short -axis view at the papillary muscle level. B: Corresponding still frame of a 2D echocardiographic image in the parasternal short -axis view at the papillary muscle level (AL, anterolateral papillary muscle; PM, posteromedial papillary muscle). This view is p articularly useful in measuring left ventricular (LV) cavity dimension and wall thickness and in assessing wall motion. C: Superior and rightward tilting of the transducer obtains a parasternal short -axis view at the basal

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level showing the mitral valve ( MV). RV, right ventricle; VS, ventricular septum. ( A from Tajik et al [1]. By permission of Mayo Foundation for Medical Education and Research.)

Figure 2-7 By tilting the transducer further superiorly, the short-axis view of the aortic valve is obtained. In this view, the right ventricular outflow tract and pulmonary valve are visualized. Below the aortic valve lies the left atrium; the connection of all fou r pulmonary veins with the left ventricle is usually seen. A: Anatomic section ( left) of the heart and drawing (right) of this view. B: Corresponding 2D echocardiographic image. LA, left atrium; PV, pulmonary valve; RA, right atrium; RVOT, right ventricula r outflow tract. ( A from Tajik et al [1]. By permission of Mayo Foundation for Medical Education and Research.)

In the apical view, the atrial septum usually can be seen in its entirety without any thinning or dropout if the ultrasound beam is directed sl ightly anteriorly; however, echoes do drop out in its midportion, which is the region of the fossa ovalis, if the ultrasound beam is directed further posteriorly. This view also allows visualization of the emptying of the right and left inferior pulmonary veins into the LA.

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techom With a slight clockwise rotation of the transducer ( Fig. 2-8C), the aortic root and valve are imaged in addition to the four chambers (apical long-axis or five-chamber view). The aortic root occupies the region where the crux of the hear t was recorded in the previous section. In this view, color flow imaging allows quantitative assessment by the proximal isovelocity area method as well as qualitative assessment of aortic regurgitation. Pulsed wave Doppler echocardiography from this view a t the aortic anulus region measures velocity and time velocity integral of the LVOT required for calculating stroke volume. With further clockwise rotation of the transducer, the apical two chamber view is obtained ( Fig. 2-8D). All three apical views are essential for analysis of regional myocardial contractility and, hence, for stress echocardiography. Apical views provide another opportunity to visualize all 16 LV segments. The aortic, mitral, and tricuspid valves are seen from the apical views. The LV apex harbors diagnostic clues for cardiomyopathy, apical thrombus, hypereosinophila, and aneurysm (Fig. 2-9). Apical views P.14

also are important for obtaining two quantitative measurements and basic Doppler echocardiographic recordings. LV volumes are quantified with the biplane Simpson method from apical four - and two-chamber views of the LV. LA volume is measured from the apical four-chamber and apical long -axis views. LVOT velocity, which is used to calculate stroke volume, is recorded from the apical long-axis view. Mitral inflow, pulmonary vein, and mitral anulus velocities, essential measurements for the assessment of diastolic function, also are obtained from the apical view. Mechanical dyssynchrony is determined with tissue Doppler imaging or strain imaging in apical views.

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Figure 2-8 A: Anatomic section ( left) and drawing ( right) of apical four-chamber view. B: Corresponding 2D echocardiographic image of the apical four -chamber view. The apical view is obtained by placing the transducer in the immediate vicinity of or at the point of maximal apical impulse. This view displays all four cardiac chambers, the ventr icular

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and atrial septa, and the crux of the heart. Note that the insertion of the septal leaflet of the tricuspid valve ( arrow) is slightly inferior to the insertion of the anterior mitral leaflet; this is an important anatomic distinction in the evaluati on of congenital heart disease. C: By rotating the transducer clockwise, the five -chamber, or long -axis apical, view allows visualization of the left ventricular ( LV) outflow tract and aortic valve (AV). Ao, aorta; AS, anteroseptum; AV, aortic valve; IL, inferolateral wall; LA, left atrium; LV, left ventricle; MV, mitral valve; RA, right atrium; RV, right ventricle. ( A from Tajik et al [1]. By permission of Mayo Foundation for Medical Education and Research.). D: Further rotation of the transducer clockwise produces the two -chamber view, which is useful for visualizing the entire posterior or inferior ( Inf) wall and in analyzing anterior (Ant) wall motion. E: The option #1 display ( left) of the apical four -chamber view from a patient with dilated cardiomyopathy. The left ventricle ( LV) is markedly dilated with notably reduced systolic function in real time view. The right ventricle (RV) and right atrium ( RA) are of relatively normal size. The option #2 display ( right) of the apical four -chamber view from the same patient as in option #1. LV is displayed on the right of the screen and RV, on the left.

Subcostal Position In certain patients, especially those who have chronic obstructive lung disease and emphysema, the usual precordial P.15

ultrasonic window may become obliterated because of hyperinflated lungs. This necessitated a search for other locations for imaging the heart and led to the discovery of the subcostal region, a good ultrasonic window in these patients. The subcostal examination is performed by placing the transducer in the midline or slightly to the patient's right, with the transducer groove pointed down toward the patient's spine ( Fig. 2-1B). The transducer head is tilted inferiorly and slightly toward the patient's right. With this positi on, the liver parenchyma, hepatic vessels, and inferior vena cava are visualized ( Fig. 2-10). With a slight superior tilt of the transducer, the drainage of the hepatic veins into the inferior vena cava can be identified. To record the inferior

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techom vena cava along its long axis, the transducer is rotated so that its groove points toward the patient's right flank. The hepatic veins again can be recognized by their draining into the inferior vena cava. Color flow imaging and pulsed wave Doppler recording of the hepatic veins ( Fig. 2-11) should be a routine part of the echocardiography study in all patients because severe tricuspid regurgitation, pulmonary hypertension, restrictive right -side filling, and constrictive pericarditis produce distinct Doppler signals i n the hepatic veins. The transducer is tilted further superiorly so that it points roughly between the patient's suprasternal notch and the left supraclavicular fossa. The tomographic view of the heart that is obtained is nearly similar to the four -chamber view obtained from the parasternal position ( Fig. 2-12), except that in this view the apices of the two ventricles can be visualized by tilting the transducer head slightly toward the patient's left. The two atria, and especially the atrial septum, are vi sualized best in this section. Although dropout of echoes of the atrial septum in the region of the fossa ovalis may be noted from the parasternal and apical transducer positions, the atrial septum can be seen in its P.16

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entirety from the subcostal position. Therefore, this is the best view to visualize abnormalities of the atrial septum with transthoracic echocardiography. To identify the sinus venosus portion of the atrial septum, the transducer needs to be rotated clockwise slightly to t he continuity between the atrial septum and the superior vena cava. Also, atrial septal motion can be well evaluated in this view. For orientation of the image in this view, we have followed the same format as for the similar view from the parasternal posi tion, that is, the atria are displayed on the right and the cardiac apex on the left.

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Figure 2-9 Various lesions seen in apical views. A: Apical fourchamber view ( left) showing noncompaction cardiomyopathy characterized by prominent noncompacted trabeculations (arrowheads) resulting in deep recesses ( arrows). Color flow imaging (right) shows flow within the recesses. B: Apical longaxis view showing mobile apical thrombus ( arrow) in left ventricle (LV) with an apical infarction. C: A large echo-free space (*) outside the LV and right ventricle ( RV) from a patient who had a surgical restoration procedure at the apex. A leak in the apical patch resulted in a pseudoaneurysm. D: Apical twochamber view of apical ballooning ( arrows). LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

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Figure 2-10 A: Subcostal view with the transducer angulated toward the liver and normal inferior vena cava ( IVC). The IVC is small and collapses with inspiration. The hepatic vein is small (arrow). B: In this patient, the hepatic vein ( HV) and IVC are markedly dilated because of venous congestion in a patient with increased right atrial ( RA) pressure. Both the left atrium (LA) and RA are dilated. The entry of the IVC into RA is well seen in this v iew.

From this position, the transducer is rotated clockwise and tilted slightly superiorly to visualize the ascending aorta and its relation to the mitral valve and LV. In this tomographic section, a foreshortened view of the LV long axis is recorded. Both leaflets of the mitral valve and the aortic leaflets as well as the LVOT usually can be well visualized.

Figure 2-11 A and B: Color flow imaging of the hepatic vein shows antegrade (blue) and reversal (orange -red) flow.

Further clockwise rotation and superior tilting of the transducer show a cross section of the heart ( Fig. 2-12C and D). In this view,

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techom the LV is visualized in the short axis, with portions of the mitral valve in its cavity. More importantly, this view is used to show the long axis of the entire RVOT. The orifice of the tricuspid valve usually appears directly end on. On the video monitor, the heart appears upside down, with RV inflow and RVOT along the right side of the image, the cross section of LV to the left, liver tissue anterior, and the pulmonary valve inferior. Another important structure to scan routinely from the subcostal view is the abdominal aorta, which can be imaged accurately in most patients ( Fig. 2-13 and 2-14). A prospective study showed that the screening examination detected an occult abdominal aortic aneurysm in 6.5% of hypertensive patients older than 50 years ( 5). A pulsed wave Doppler examination of the abdominal aorta in this P.18

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view is also helpful in identifying coarctation of the aorta by demonstrating persistent diastolic flow. Coarctation of the aorta and severe aortic regurgitation produce a characteristic pulsed wave Doppler recording in the abdominal aorta ( Chapters 12 and 20).

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Figure 2-12 Subcostal view. A: Anatomic sectio n (left) and drawing (right) of the heart in the long -axis view. B:

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Corresponding 2D echocardiographic image. C: Anatomic section (left) and drawing (right) of the heart in the short -axis view. The subcostal view allows better definition of certain cardiac structures, including the atrial septum ( arrows in B), left atrium ( LA), right atrium ( RA), right ventricular free wall, right ventricular outflow tract and pulmonary valve ( arrow in D), hepatic vein, and abdominal aorta. This view may be the only satisfactory echocardiographic window for patients who have chronic obstructive lung disease and emphysema. AV, aortic valve; LV, left ventricle; PA, pulmonary artery; RV, right ventricle. (A and C from Tajik et al [1]. By permission of Mayo Foundation for Medica l Education and Research.). D: Corresponding 2D echocardiographic image.

Figure 2-13 A: Normal abdominal aorta ( Ao) from the subcostal view. LA, left atrium; RA, right atrium. B: Normal pulsed wave Doppler recording from the abdominal aorta.

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Figure 2-14 A: Long-axis view of the abdominal aorta ( Ao) from the subcostal view demonstrating a large abdominal aortic aneurysm, half of which is filled with thrombus (*). This was not suspected clinically. B: Short-axis view of the Ao demonstrating a la rge abdominal aortic aneurysm with intramural thrombus (*).

Suprasternal Notch Position For visualization of the left aortic arch in the long axis, the transducer head is positioned in the suprasternal notch ( Fig. 2-1B), with the long axis of the transducer to the left and parallel with the trachea and the transducer groove directed toward the right supraclavicular region. With this transducer position ( Fig. 2-15A), the ascending aorta, aortic arch, origin of the brachiocephalic vessels, and descen ding thoracic aorta are visualized. Occasionally, leaflets of the aortic valve also can be seen in the aortic root. The orientation of the image of this view is similar to that of a lateral view of an angiogram; thus, the ascending aorta is on the left of the figure and the descending aorta on the right. The right pulmonary artery is visualized in the short axis posterior to the ascending aorta and beneath the aortic arch. Inferior to the right pulmonary artery, the LA can be seen. For visualization of the long axis of the aorta in the presence of a right aortic arch, the transducer is rotated counterclockwise, with the groove directed toward the right breast. The short-axis view of the aortic arch is obtained by rotating the transducer clockwise so the transducer groove faces posteriorly toward the patient's trachea ( Fig. 2-15B). In this view, the cross section of the ascending aorta is superior and the right pulmonary artery, in its long axis, is inferior. Occasionally, the first bifurcation of the righ t pulmonary artery can be visualized on the left of the image. By rotating the transducer slightly clockwise and tilting it toward the patient's left and slightly anteriorly, the distal main pulmonary artery can be visualized. From this position, the left pulmonary artery can be seen occasionally by tilting the transducer posteriorly and to the left. Inferior to the pulmonary artery is the LA cavity. Immediately beneath the distal part of the right pulmonary artery, the right superior pulmonary vein connect s with the LA. The superior vena cava also can be recorded in this view, appearing as an echo -free

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techom space alongside the aorta on the left of the image. The left innominate vein can be visualized traversing superior to the aorta to its junction with the supe rior vena cava. With a slight counterclockwise rotation and anterior tilt of the transducer, the long axis of the superior vena cava can be recorded alongside the long axis of the ascending aorta. In this view, the superior vena cava can be scanned to its junction with the RA. This same view of the superior vena cava occasionally can be obtained also with the transducer placed along the upper right sternal border.

Unusual Imaging Window When there is a sizable pleural effusion, echocardiographic imaging is possible from the back through the effusion. In some patients, this may be the only available ultrasound window ( Fig. 2-16).

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Figure 2-15 Drawing (left) and corresponding 2D echocardiographic image ( right) of suprasternal notch long axis, A, and short -axis, B, views. A (right): This transducer position allows visualization of the ascending aorta ( Asc), aortic arch (Arch), origin of the brachiocephalic vessels (arrows), descending thoracic aorta ( Dsc), and right pulmonary artery (*). B (right): The short-axis view of the aortic arch is obtained by rotating the transducer clockwise, which also allows visualization of the right pulmonary artery ( RPA) in its long-axis format, located inferiorly to the aortic arch ( Arch). Inferior to RPA is the le ft atrial (LA) cavity with connections of the four pulmonary veins ( arrows). The superior vena cava (SVC) is visualized by further clockwise rotation; it appears

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along the right side of the aorta or can be imaged separately from the right supraclavicular a rea, as in C

Figure 2-16 A and B: 2D echocardiographic imaging of the heart from the back through a large pleural effusion ( PL). Ao, aorta; LA, left atrium; LV, left ventricle; RV, right ventricle; VS, ventricular septum.

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M-Mode Echocardiography M-mode echocardiography complements 2D echocardiography by recording detailed motions of cardiac structures. It is best derived with guidance from a 2D echocardiographic image by placing a cursor through the desired structure ( Fig. 2-17). M-mode is used for the measurement of dimensions and is essential for the display of subtle motion abnormalities of specific cardiac structures. Methods for measuring cardiac dimensions from M -mode are shown in Figure 2-18. Normal values for cardiac dimens ions in adults are well established. Sex -specific reference M -mode values in adults were determined from a healthy subset of the Framingham Heart Study (6, 7). These values are given in the Appendix. For these measurements, the M -mode cursor is drawn as a straight line from the transducer position to any direction in the sector to record the

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techom movement of the cardiac structure of interest. Typical M -mode recordings of various cardiac lesions are shown in Figure 2-19. Some of these findings are of historical i nterest only because the diagnosis is usually made from 2D and Doppler echocardiographic information. However, subtle motion of cardiac structures can be appreciated from M -mode recordings. In some ultrasound units, the M-mode cursor can be adjusted ( Fig. 2-20) to obtain a more anatomically correct measurement. In anatomical M -mode, the cursor does not have to originate from the transducer location.

Figure 2-17 A: An M-mode cursor is placed along different levels (1, ventricular; 2, mitral valve; 3, aortic valve level) of the heart, with parasternal long -axis 2D echocardiographic guidance. B-D: Representative normal M -mode echocardiograms at the, B, midventricular, C, mitral valve, and D, aortic valve levels, respectively. B: EDd and ESd are end diastolic and end -systolic dimensions, respectively, of the left ventricle (LV). C: M-mode echocardiogram of the anterior mitral leaflet: A, peak of late opening with atrial systole; C, closure of the mitral valve; D, end-systole before mitral valve opening; E, peak of early opening; F, mid-diastolic closure. D: Double-headed arrow indicates the dimension of the left atrium

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(LA) at end-systole. Ao, aorta; AV, aortic valve; LA, left atrium; LV, left ventricle; PW, posterior wall; RV, right ventricle; RVOT, right ventricular outflow tract; VS, ventricular septum.

Figure 2-18 Diagram of M -mode echocardiogram of the left ventricle, aortic root, and left atrium ( LA). The left ventricular internal dimension ( LVD) at end-diastole (D) was measured at the onset of the QRS complex, and the systolic internal dimension [LVD(S)] was measured at the maximal excursion of the ventricular septum, which normally occurs before the maximal excursion of the posterior wall. These measurements correspond, respectively, to the max imal (max) and minimal (min) internal dimensions between the ventricular septum and the posterobasal LV free wall endocardium. Septal thickness (ST) and posterior wall thickness ( PWT) were measured at end diastole (D) at the onset of the QRS complex. The a ortic root dimension (AO) was measured at the onset of the QRS complex from the leading edge to the leading edge of the aortic walls. The LA dimension was measured at end -systole as the largest distance between the posterior aortic wall and the center of t he line denoting the posterior LA wall. Their normal values are given in the Appendix. ECG, electrocardiogram. (From

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Gardin JM, Henry WL, Savage DD, et al. Echocardiographic measurements in normal subjects: Evaluation of an adult population without clinic ally apparent heart disease. Journal of Clinical Ultrasound , 1979;7:439–447 . Used with permission.)

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Figure 2-19 A: M-mode echocardiogram of mitral valve prolapse. Mitral leaflets are thickened and there is late systolic posterior motion (prolapse) of the posterior mitral leaflet below the C-D line (arrows). B: M-mode echocardiogram of hypertrophic obstructive cardiomy opathy showing systolic anterior motion ( SAM, arrowheads ) of mitral valve responsible for obstruction of the LV outflow tract. C: M-mode echocardiogram of typical mitral stenosis ( MS). The mitral leaflet is thickened, and the E – F slope (arrows) is prolonged. D: M-mode echocardiogram of the mitral valve with fluttering ( arrowheads) from aortic regurgitation. However, this M-mode sign may not be present if the aortic regurgitation jet is eccentric toward the ventricular septum rather than toward the mitral valve. The left ventricle ( LV) is enlarged and systolic function is reduced. E: M-mode echocardiogram of left atrial myxoma recorded from the parasternal transducer position. During diastole, the mitral orifice is filled with increased echodensity ( arrows) representing protruding atrial myxoma. F: The maximal opening tapers off during mid -systole (arrowheads) when cardiac output is severely reduced. G: Aortic valve opening is only 4 mm, with thickened cusps. Also, multiple dense echoes ( arrow) are noted i n the aortic root during systole and diastole. These findings suggest severe aortic stenosis, but a Doppler study is required to determine how severe the stenosis is. H: In a 40-year-old patient with hypertrophic obstructive cardiomyopathy and endocarditis , the aortic valve (AV) opening is interrupted because of dynamic left ventricular outflow tract obstruction during mid -systole (midsystolic closure [ large arrow]) but reopens again at late systole. There is increased echodensity at the aortic cusps (small arrows) during diastole because of vegetation. I: Normal pulmonary valve ( PV) M-mode echocardiogram with prominent “a” wave (a). The valve closure is smooth ( arrowheads). J: Mid-systolic closure ( arrows) of PV, producing a W shape in pulmonary hypertension. There is no “a† wave. Ao, aorta; AV, aortic valve; LA, left atrium; LV, left ventricle; MS, mitral stenosis; PV, pulmonary valve; RV, right ventricle.

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Three-Dimensional Echocardiography Numerous attempts have been made to produce 3D images using echocardiography. Initially, 3D images were created as a reconstruction of multiple 2D images by a “freehand† scanning method or by “gated sequential imaging† in a linear, fanlike, or rotational format ( 8). All these met hods required multiple 2D images that were digitally reformatted into rectangular pixels. Therefore, this type of 3D echocardiographic reconstructed image relied on 2D echocardiographic images and the interpolation of missing data. However, 3D transducer t echnology has improved so that now real -time 3D images can be generated. Both 3D transducer and computer technology have advanced to create matrix transducers with 3,000 elements that can acquire a pyramidal image containing most cardiac structures. three dimensional image data sets (up to a 93 - × 80-degree pyramid) are obtained from several cardiac cycles while the patient holds his or her breath. During each cardiac cycle, a wedge -shaped subvolume is acquired, and the combined subvolumes from four cardiac cycles provide a full volume set. When 3D color flow images are obtained, data sets are gathered from more cardiac cycles. Currently, 3D echocardiography is performed after 2D echocardiographic imaging, using the same transducer positions (Fig. 2-20–2-23). A 3D matrix transducer can also scan two dimensionally and 2D images can be changed instantaneously into 3D images by selecting the 3D function. Multiple 2D images can be displayed simultaneously with live 3D real -time images. Also, with the use of cr opping controls, 3D images of the heart can be dissected from a full -volume pyramid containing the heart: 1) top to bottom (elevation control or coronal section), 2) left to P.26

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right (lateral control or sagittal section), and 3) front to back (depth control or transverse section). The auto crop function suppresses the front half of the 3D images, which can be a starting point of further cropping. The 3D images can be rotated to any direction for viewing. These capabilities provide optimal perspective for visualizing structural abnormalities and allow anatomically correct views for quantitative measurements.

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Figure 2-20 A: Drawing demonstrating the parasternal long axis tomographic plane ( gray plane) and two other standard imaging planes obtained with two -dimensional (2D) echocardiography. B: In three-dimensional (3D) echocardiography, a matrix transducer is able to image a pyramidal wedge of the heart from the same transducer position as 2D echocard iography; this wedge can be rotated and cropped to visualize the area of interest. C: In some

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instruments, the autocrop function removes 50% of the imaged section. In this drawing, half of the heart was removed from a 3D image in the parasternal long -axis view to provide a view similar to the 2D parasternal long -axis view, but with more depth and better delineation of the anatomical relations among various structures. D: Two 3D images from the parasternal long-axis viewed from different perspectives. LA, left atrium; LV, left ventricle; PW, posterior wall; RV, right ventricle; VS, ventricular septum.

Figure 2-21 A: Drawing demonstrating the parasternal short axis plane (gray plane), a standard two -dimensional echocardiographic tomographic plane. B: A pyramidal wedge is obtained with three -dimensional (3D) echocardiography from the parasternal short -axis transducer position. C: The apical portion of the 3D image was removed (cropped) to show the left ventricular short -axis view at the papillary muscle leve l. This provides more depth and better delineation of the anatomical relations of cardiac structures. D: Threedimensional image from the parasternal short -axis view rotated clockwise to demonstrate the “fish -mouth” appearance of a rheumatic mitral val ve (arrows).

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Figure 2-22 A: Drawing of the apical four -chamber view tomographic plane (gray plane) obtained with two -dimensional echocardiography. B: A pyramidal wedge section from the apical four-chamber view. C: The upper half of the wedge section was removed to show the four cardiac chambers, which can be rotated and cropped as needed. D: Apical four-chamber three-dimensional image showing the four chambers and an abnormal mitral valve (arrows). LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

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Figure 2-23 A: Three-dimensional long -axis image from the subcostal transducer position showing the abdominal aorta with a large aneurysm ( Ao) and intraluminal thrombi ( arrows). B: Three-dimensional short -axis image of an abdominal aortic aneurysm (Ao) with intraluminal thrombi ( arrows).

The clinical applications of 3D echocardiography are expanding and include the following: quantitative measurement of ventricular volume and mass (9, 10) simultaneous analysis of regional wall motion in multiple segments, evaluation of congenital heart disease, 3D display of valvular lesions ( 11, 12, demonstration of the spatial relation between abnormal and normal cardiac structure, and determination of ventricular mechanical dyssynchrony (13).

References 1. Tajik AJ, Seward JB, Hagler DJ, et al. Two -dimensional real -time ultrasonic imaging of the heart and great vessels: Technique, image orientation, structure identification, and validat ion. Mayo Clinic Proceedings, 1978;53:271–303. 2. Bansal RC, Tajik AJ, Seward JB, et al. Feasibility of detailed two dimensional echocardiographic examination in adults: Prospective study of 200 patients. Mayo Clinic Proceedings, 1980;55:291–308. 3. Edwards WD, Tajik AJ, Seward JB. Standardized nomenclature and anatomic basis for regional tomographic analysis of the heart. Mayo Clinic Proceedings, 1981;56:479–497.

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techom 4. Henry WL, DeMaria A, Gramiak R, et al. Report of the American Society of Echocardio graphy Committee on Nomenclature and Standards in Two -dimensional Echocardiography. Circulation, 1980;62:212–217. 5. Spittell PC, Ehrsam JE, Anderson L, et al. Screening for abdominal aortic aneurysm during transthoracic echocardiography in a hypertensiv e patient population. Journal of the American Society of Echocardiography, 1997;10:722–727. 6. Lauer MS, Larson MG, Levy D. Gender -specific reference M -mode values in adults: Population -derived values with consideration of the impact of height. Journal o f the American College of Cardiology, 1995;26:1039–1046. 7. Vasan RS, Larson MG, Benjamin EJ, et al. Echocardiographic reference values for aortic root size: The Framingham Heart Study. Journal of the American Society of Echocardiography, 1995;8:793–80 0. 8. Houck RC, Cooke J, Gill EA. Three -dimensional echo: Transition from theory to real -time, a technology now ready for prime time. Current Problems in Diagnostic Radiology, 2005;34:85–105. 9. Caiani EG, Corsi C, Zamorano J, et al. Improved semiautomat ed quantification of left ventricular volumes and ejection fraction using 3-dimensional echocardiography with a full matrix -array transducer: Comparison with magnetic resonance imaging. Journal of the American Society of Echocardiography, 2005;18:779–788 . 10. Mor-Avi V, Sugeng L, Weinert L, et al. Fast measurement of left ventricular mass with real -time three-dimensional echocardiography: Comparison with magnetic resonance imaging. Circulation, 2004 Sep 28;110:1814–1818. Epub 2004 Sep 20. 11. Schwalm SA, Sugeng L, Raman J, et al. Assessment of mitral valve leaflet perforation as a result of infective endocarditis by 3 dimensional real -time echocardiography. Journal of the American Society of Echocardiography, 2004;17:919–922. 12. Xie MX, Wang XF, Cheng TO, et al. Comparison of accuracy of mitral valve area in mitral stenosis by real -time, three-dimensional echocardiography versus two -dimensional echocardiography versus Doppler pressure half -time. American Journal of Cardiology, 2005;95:1496–1499. 13. Kapetanakis S, Kearney MT, Siva A, et al. Real -time three dimensional echocardiography: A novel technique to qualify global

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6. 3 - Transesophageal and Intracardiac Echocardiography 3 Transesophageal and Intracardiac Echocardiography Jae K. Oh Donald J. Hagler Allison Cabalka Guy S. Reeder Frank Cetta Jr James B. Seward

Transesophageal Echocardiography In 1987, clinical transesophageal echocardiography (TEE) was introduced at Mayo Clinic Rochester ( 1). This technology has inexorably changed the diagnostic strategy for numerous cardiovascular diseases and, in many circumstances, has become the diagnostic procedure of choice. The principal reason for this change in practice is that TEE provides superb clarity and resolution and easily interpretable images, which are uniquely suited to the clinical circumstance. After some initial trepidation, it is now appreciated that TEE is a procedure that is relatively easy to perform, uncomplicated, and capable of providing unique insight into cardiothoracic structures, even in critically ill patients. TEE incorporates all the functionality of transthoracic echocardiography (TTE), including three -dimensional imaging, which ca n reliably interrogate cardiovascular anatomy, function, hemodynamics, and blood flow. Before the introduction of TEE, echocardiography was frequently used as a screening tool that had to be complemented by other diagnostic modalities. Currently, definitiv e management of valvular disease, aortic dissection, endocarditis, atrial fibrillation, congenital heart disease, and intracardiac masses and tumors can be accomplished on the basis of a complete echocardiography examination, including TEE ( 2, 3, 4, 5). In this clinical context, TEE

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techom will continue to have a major role in the management of virtually all cardiovascular diseases. Approximately 5% to 10% of patients who have a TTE examination require the addition of TEE. Also, TEE has become an integral part of cardiovascular surgery for identifying a previously unrecognized abnormality that may affect the surgical procedure or the patient's outcome and for assessing the result of the operation (see Chapter 21). As in the first two editions of The Echo Manual , TEE is discussed throughout the text in relation to the diagnosis and management of specific cardiovascular diseases.

Indications The indications for referral for 8,535 TEE procedures from September 2001 to July 2004 at Mayo Clinic Rochester are listed in Table 3-1. The distribution of indications for TEE varies from institution to institution, depending on the patient population. The most common indication has been for evaluation of a potential cardiac source of embolism (35%) and atrial fibrillation (34%). Besides these pervasive and somewhat controversial indications, TEE is now considered essential in the evaluation of the mitral valve lesions, left atrial (LA) or LA appendage thrombus, intracardiac mass, atrial septal defect (in particular, aortic dissection), and critically ill patients ( 6, 7, 8, 9, 10, 11). Because of 1) an increasing number of patients with atrial fibrillation, 2) a new practice model for TEE -guided cardioversion, and 3) ablation procedures, atrial fibrillation has become one of the mor e common reasons for referral for TEE.

Table 3-1 Indications for transesophageal echocardiography at Mayo Clinic Rochester from September 2001 to July 2004: 8,535 procedures

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Indication

Procedures, %

Source of embolism

35

Atrial fibrillation

34

Suspected endocarditis

10

Valvular disease

6

Native

5

Prosthetic

1

Evaluation of aorta

2

Congenital heart disease

3

Intracardiac mass

2

Critically ill patient

1

Pulmonary hypertension

1

Others

6

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Preparation and Potential Complications

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techom TEE is a semi -invasive procedure that can be uncomfortable in unprepared patients. Patients should be informed about why TEE is performed, and the entire procedure should be explained, including rare side effects (70% methemoglobin), exchange transfusion or dialysis may be needed. A drying agent, glycopyrrolate (Robinul, 0.2 mg), can be used to minimize oral secretions and decrease the possibility of aspiration during the exam ination. Because glycopyrrolate is an atropine -like

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techom drug, it may increase heart rate, especially in patients with atrial fibrillation. A short -acting sedative or amnestic agent such a midazolam (Versed), 1 to 10 mg (mean dose, 3.6 ± 2.3 mg), and fentanyl, 25 to 100 mg intravenously, are used almost routinely to make the TEE examination more comfortable and accepted by the patient. These agents should be used with caution in debilitated or elderly patients because of potential respiratory suppression. However, midazolam can be rapidly reversed in about 60 seconds with flumazenil, 0.2 to 0.4 mg intravenously. In young patients, meperidine (Demerol), 25 to 50 mg, also may be used to help alleviate the gag reflex, relieve pain sensation, and enhance sedation. Prophylaxis for subacute bacterial endocarditis is not necessary or generally used even in patients with a prosthetic valve (16). Occasionally, it has been necessary to paralyze an agitated critically ill patient. A nasogastric or endotracheal tube usually does not interfere substantially with esophageal intubation with the TEE probe or prohibit the acquisition of satisfactory images. Esophageal perforation is a rare but disastrous complication of TEE ( 12). TEE should not be performed in patients with dyspha gia without further evaluation of the esophagus. Intubation of a TEE probe should not be forced. Prolonged intubation of a TEE probe during an operation may increase the risk of perforation. When the TEE probe is not used intraoperatively, it may be discon nected from the machine to reduce thermal injury. Also, the TEE probe should not be left in the esophagus or the stomach in a locked position.

Instrumentation The TEE probe is a modified gastroesophageal endoscopy probe, typically with a 3 - to 7-MHz ultrasound transducer at the tip. It can be maneuvered to various positions in the esophagus and stomach, from which the heart and other cardiovascular and surrounding structures can be visualized. The diameter of the adult transducer tip P.31

is 9 to 14 mm, and this is miniaturized to less than 3 mm for pediatric and neonatal and even fetal use. All adult probes use multiplane transducers that can be rotated 180 degrees. The transducer usually is rotated by a finger -pressure–sensitive switch at the proximal operator end. The tip of the probe also can

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techom be anteflexed or retroflexed or moved side to side by larger knobs at the proximal end. When performed electively, the examination begins with the patient in the left lateral decubitus position. The procedure ro om is equipped with oral suction, oxygen supply, pulse oximeter, and cardiopulmonary resuscitation capabilities. In critically ill patients for whom transfer is difficult, the examination is performed at the bedside. If the patient is mechanically ventilated, the TEE probe is often introduced with the patient supine.

Table 3-2 Preparation for transesophageal echocardiography

Preparation Inquiry about history of dysphagia or esophageal abnormality Reduce risk of pulmonary aspiration For healthy patients undergoing elective procedures 6 hours fasting (light meal consisting of toast and clear liquids) 6 hours milk 2 hours clear liquids No restriction if patient is tracheally intubated In very urgent situations , tracheal intubation and/or upper esophageal suction is necessary Local anesthesia spray Intravenous access with three -way stopcock Medications Drying agent (optional) to reduce salivation Glycopyrrolate (Robinul), 0.2 mg intravenous 2–3 min before examination Sedation Midazolam hydrochloride (Versed), 1–10 mg (low doses in older patients) Reversal: flumazenil (Romazicon), 0.2–0.4 mg, if needed for rapid reversal of midazolam hydrochloride Analgesia Fentanyl, 25–100 mg intraven ous (lower dosage in older patients)

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or Meperidine hydrochloride (Demerol), 25–50 mg intravenous Reversal: naloxone (Narcan) (1 mg/mL vial), up to 0.1 mg/kg For treatment of methemoglobinemia (most often associated with benzocaine products us ed for local anesthesia) Methylene blue, 1–2 mg/kg intravenously Muscle relaxant (occasional use in special circumstances) Paralyzing agent in conjunction with sedation for agitated patient on mechanical ventilator

We use a bite guard to protect the TEE scope, unless the patient is edentulous. When the scope is introduced, the imaging surface of the transducer faces the tongue, which directs the ultrasound beam from the posteriorly located esophagus anteriorly toward the hear t. A digital technique generally is used for esophageal intubation. When the probe is introduced, the posterior portion of the tongue is depressed with the left index finger to minimize tongue movement, and the tip of the transducer is placed over the left index finger to a position at the center of the tongue. After the transducer is in the correct position, the left index finger is placed over the distal shaft or tip of the probe and depressed directly downward onto the tongue. This places the tip of the probe in direct alignment with the posteriorly located esophagus and away from the anteriorly located trachea. The tip of the transducer is advanced smoothly and slowly posteriorly toward the esophagus. At this time, the patient is asked to swallow. The ti p of the TEE transducer should be advanced into the esophagus without force or notable resistance. The distance from the incisors to the part of the esophagus behind the mid LA is approximately 30 cm.

Training of Physicians and the Role of Sonographers TEE complements the TTE examination. Therefore, it is advised that a physician who performs TEE has competency P.32

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in TTE, which includes personally performing more than 300 documented surface echocardiograms before performing TEE. The physician also needs to learn the technique of esophageal intubation under the supervision of an endoscopist or other echocardiologist experienced in TEE procedure. We consider a minimum of 50 esophageal intubations necessary to provide adequate training in intubation.

Table 3-3 Summary of the role of the sonographer/assistant in transesophageal echocardiography (TEE)

Before procedure Preparation of equipment and supplies Assemble supplies Medications, normal saline flushes, and contrast medium Intravenous supplies (angiocatheter, three -way stopcock) Lidocaine spray and tongue blade Scope lubricant: lubricating jelly or viscous lidocaine Gloves, safety glasses, TEE probe, and bite block Maintain and check suction, oxygen, and basic life support equipment Patient preparation Confirm that patient has had no oral intake for 4–6 hours before TEE Obtain brief history of drug allergies and current medications Explain procedure to patient Obtain baseline vital signs and monitor rhythm Remove patient's dentures, oral prostheses, and eyeglasses Establish intravenous catheter for administration of medications Place patient in the left lateral decubitus position with

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wedge support and safety restraints Assist patient during esophageal intubation, such as head position, breathing, and reassurance Drugs Endocarditis prophylaxis: American Heart Association recommendations Pharyngeal anesthesia (see Table 3-2) Drying agent (optional ) Sedation and/or analgesia (see Table 3-2) During procedure Position and maintain bite block Monitor vital signs: rhythm, respiration, blood pressure, and oxygen saturation Use oral suction if necessary Have basic life-support equipment available After procedure Optional reversal of midazolam sedation with flumazenil (see Table 3-2) Assist patient during recovery period (patient must be fully awake and/or accompanied at departure) Remove intravenous catheter Instruct patient not to drive for 12 hours if sedation was used Record vital signs and patient's condition on dismissal Arrange for escort if patient is not completely recovered Clean scope with enzyme solution and glutaraldehyde disinfectant

The sonographer or trained assistant has an essential role in preparing patients for TEE and in assisting the physician during the examination. The role of the sonographer or assistant in TEE is summarized in Table 3-3. In our laboratory, a registered nurs e or nurse sonographer coordinates and assists with TEE examinations. Because TEE is semi -invasive, the skills of a registered nurse are preferred for closely monitoring the patient, that is, for obtaining vital signs, administering medications, inserting intravenous catheters, and using suction, oxygen, or other emergency equipment. A properly trained assistant can perform these functions except for intravenous administration of medications. Because TEE has a small but definite risk for the patient, it generally is considered necessary for the procedure to be

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techom performed by a physician. Also, physicians and allied health personnel involved in performing TEE are required to have annual training in conscious or moderate sedation. P.33

Multiplane Transesophageal Echocardiography Imaging Views The multiplane TEE transducer consists of a single array of crystals that can be rotated electronically or mechanically around the long axis of the ultrasound beam in an arc of 180 degrees ( Fig. 3-1). With rotation of the transducer array, multiplane TEE produces a continuum of transverse and longitudinal image planes ( 17). Multiplane images are identified by an icon to indicate the degree of transducer rotation ( Fig. 3-2). This designation helps the operator to understand the orientation of the ultrasound beam and to conduct the TEE examination more efficiently. The transverse esophageal plane, which is in the short axis of the body, is designated as 0 degrees. The longitudinal esophageal plane, which is in the long axis of the body, is designated as 90 degrees. The TEE transducer can be rotated in a continuum throughout 180 degrees, resulting in versatility of the examination and ease of understanding. Normally, from the midesophagus, the short axis of the heart is imaged a t 45 degrees of rotation and its long axis at 135 degrees. Almost all views obtained with surface echocardiography can be duplicated by TEE. Because the same cardiovascular structures are imaged by both TTE and TEE, the anatomic correlations and image orientations should be consistent for both examinations. To replicate the identical transthoracic (TTE) image format, we usually keep the electronic transducer artifact of TEE predominantly at the bottom of the display screen throughout the TEE examination ( 17). However, if preferred, the opposite orientation, with the transducer at the top of screen, may also be used.

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Figure 3-1 Array rotations of selected degrees (0, 45, 90, 135, and 180 degrees) permit a logical sequence of standard transducer orientations and resultant images. Such a display helps the examiner acquire the desired views:0 -degree transverse orientation, which is horizontal to the chest at the midesophageal level; 45 -degree short -axis orientation to the base of the heart from the midesophagus; 90 -degree longitudinal orientation, which is in the sagittal plane of the body; 135-degree long-axis orientation to the he art from the midesophagus; and 180 -degree rotation, which produces a mirror-image transverse plane. (From Seward et al [17]. Used with permission of Mayo Foundation for Medical Education and Research.)

Primary Views Four primary multiplane TEE views can b e obtained (Fig. 3-3 and 34) by rotating the transducer array from 0 degrees to 135 degrees:1) 0 degrees (transverse plane):oblique view of basal structures; the four -chamber view or transgastric short -axis view can be obtained from this position by retro flexion and anteflexion of the transducer tip, respectively; 2) 45 degrees:short -axis view; this image is similar to the TTE parasternal short -axis view at the level of the aortic valve; 3) 90 degrees:longitudinal transducer orientation; this produces imag es oblique to the long axis of the heart; 4) 135 degrees:the true long axis of the LA and left ventricular outflow tract (LVOT); this is analogous to the parasternal long -axis view.

Longitudinal Views 132

techom With the transducer array at 90 degrees, the plane is sagittal to the body and oblique to the long axis of the heart. Sequential leftward (counterclockwise rotation) and rightward (clockwise rotation) rotations of the probe shaft will develop a series of longitudinal TEE views ( Fig. 3-5 and 3-6). These views include the following:1) counterclockwise rotation of the scope, producing a two-chamber left ventricular (LV) inflow view; 2) slight rightward rotation of the scope from the first view, producing a long axis of the right ventricular outflow tract (RVOT); 3) further rightward rotation, producing a long -axis view of the proximal ascending aorta; and 4) still further rightward rotation of the scope, producing a long -axis view of the venae cavae and atrial septum.

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Figure 3-2 Four multiplane transesophageal echocardiographic (TEE) images obtained by rotating the transducer array from 0 degrees to 135 degrees. The icon (in the corner) indicates the position of the transducer. A: Four-chamber view (0 degrees with retroflexion of the transducer tip); two different image

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orientations on the screen are shown:apex -up (left) and apexdown (right) views. Ao, aorta; RA, right atrium; RV, right ventricle; RVOT, right ventricular outflow t ract. B: Left and Right, Short-axis view (45–60 degrees) of the aortic valve in two different image displays. *, Left atrial ( LA) appendage. C: Left and Right, Two-chamber view (65–100 degrees with leftward rotation of TEE shaft). Arrow, LA appendage i n two different image displays. D: Left and Right, Long-axis view (125–140 degrees) of the left ventricle ( LV).

Figure 3-3 Primary multiplane transesophageal views (0, 45, 90, and 135 degrees) are obtained by rotating the array indicator from left to right on the icon. The transducer is in midesophagus. At 0 degrees (transverse plane), an oblique view of the basal structures, including the noncoronary ( N) and right coronary ( R) cusps of the aortic valve ( AV), is obtained. At 45 degrees, a short -axis view of the basal structures, including the left coronary cusp ( L) and N and R cusps of the AV, is obtained. At 90 degrees (longitudinal plane), a long -axis view of the basal cardiac structures, including the ascending aorta (Asc Ao), is obtained. At 135 degrees, the array is aligned with the long axis of the left ventricle ( LV). LA, left atrium; LVO, left ventricular outflow; MPA, main pulmonary artery; RA, right atrium; RAA, right atrial appendage; RV, right ventricle; RVO, right ventricular outflow; TV, tricuspid valve;

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VS, ventricular septum. (From Seward et al [17]. Used with permission of Mayo Foundation for Medical Educa tion and Research.)

Figure 3-4 Tomographic anatomy of the heart at midesophagus. The anatomic specimens have been cut to correspond to the echocardiographic images shown in Figure 33. Specimens are presented from the perspective of 0 -degree rotation of the imaging array ( left) to 135-degree rotation (right). In an oblique short -axis cut at the base of the heart (0-degree rotation), the esophagus ( E) is posterior and adjacent to the left atrium ( LA). The image array is in the short axis of the body, an d, consequently, the cusps of the aortic valve (AV) are cut obliquely. Frequently, the LA appendage (LAA) and left upper (superior) ( LUPV) and left lower (inferior) (LLPV) pulmonary veins are visualized in this short -axis view. The right atrium ( RA) is to the viewer's left; the right ventricular outflow ( RVO) is anterior. In a short -axis view of the aortic valve (45 -degree rotation), the AV cusps, left coronary (L), noncoronary ( N), and right coronary ( R), are optimally displayed. The descending thoracic ao rta (Ao) is cut obliquely. The RVO is anterior, and the esophagus is posterior. In a longitudinal scan (90 -degree rotation), the basal structures of the cardiac specimen, including the proximal ascending aorta ( Asc Ao), are in the long axis of the body. Th e

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esophagus is posterior. A membranous atrial septum (arrowheads) and patent foramen ovale ( arrow) are evident in this view. The right pulmonary artery ( RPA) courses posterior to the ascending aorta. In a long -axis view of the LA (135 degree rotation) (ide ntical to the parasternal long -axis view), the esophagus is posterior and adjacent to the LA. The AV, left ventricular outflow ( LVO), and body of the left ventricle are viewed in the long axis. The RVO is anterior. In this tomographic cut, the view of the heart is from the left ventricle toward the ventricular septum ( VS) and right ventricle. AS, atrial septum; B, bronchus; IVC, inferior vena cava; MV, mitral valve; PM, posteromedial papillary muscle; PV, pulmonary valve; RV, right ventricle; TS, transverse sinus (a pericardial space separating LA, RPA, Asc Ao , and RA); TV, tricuspid valve. (From Seward et al [17]. Used with permission of Mayo Foundation for Medical Education and Research.)

Figure 3-5 Series of longitudinal echocardiographic views obtained with the tip of the transducer in midesophagus. Rotation of the shaft of the scope to the patient's left (counterclockwise rotation of the shaft) produces an optimal image of the mitral valve ( MV) and left ventricular ( LV) inflow. A sequence of longitudinal views is obtained by progressive

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rotation of the shaft of the scope to the patient's right. (Note that the array is kept at 90 degrees throughout this maneuver.) The sequence presentation begins at the right in this illustration:1) a two -chamber LV inflow view is obtained with the scope rotated to the left; 2) right ventricular outflow (RVO) is depicted by a slight rightward rotation of the scope; 3) next, further rightward rotation (neutral positio n) results in a long-axis view of the proximal ascending aorta ( Asc Ao); and 4) a long-axis view of the superior ( SVC) and inferior ( IVC) vena cava and atrial septum is obtained by further rightward rotation of the scope. AV, aortic valve; AW, anterior wall; IW, inferior wall; LA, left atrium; LVO, left ventricular outflow; MPA, main pulmonary artery; PV, pulmonary valve; RA, right atrium; RAA, right atrial appendage; TV, tricuspid valve; VS, ventricular septum. (From Seward et al [17]. Used with permission of Mayo Foundation for Medical Education and Research.)

Figure 3-6 Midesophageal longitudinal tomographic anatomic sections cut to correspond to the echocardiographic images in Figure 3-5. Anatomic views are described from the viewer's right to left. In a two-chamber view, the esophagus is posterior to the left atrium ( LA), which is the primary chamber visualized along with the left ventricle ( LV). Mitral valve ( MV) inflow is

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demonstrated best in this view. The LA appendage ( LAA) is seen in the anteri or LA. The view of the specimen is from the LV toward the chambers on the right side of the heart. In a long-axis view of right ventricular outflow ( RVO), the section is oblique to the body of the heart but in the long axis of the RVO, pulmonary valve ( PV), and proximal main pulmonary artery (MPA). The posteriorly located LA is adjacent to the esophagus. In a long -axis view of the proximal ascending aorta (Asc Ao), the LV and aortic valve ( AV) are cut obliquely. This view is best for visualizing the membran ous ventricular septum (VS and arrow). The right pulmonary artery ( RPA) is posterior to the ascending aorta. In a long -axis view of the superior (SVC) and inferior ( IVC) vena cava, the specimen is viewed from the left toward the free wall of the right atri um (RA). The right atrial appendage ( RAA) is anterior in the RA cavity. The right pulmonary artery ( RPA), transected in the short axis, courses posterior to SVC. The posteriorly located LA is adjacent to the esophagus. AS, atrial septum; AW, anterior wall; B, bronchus; Desc Ao, descending thoracic aorta; IW, inferior wall; LCA, left main coronary artery; LPA, left pulmonary artery; LVO, left ventricular outflow; Pul V, left inferior pulmonary vein; TS, transverse sinus; TV, tricuspid valve. (From Seward et al [17]. Used with permission of Mayo Foundation for Medical Education and Research.)

P.34

P.35

P.36

Transgastric Multiplane Views With the transducer tip in the fundus of the stomach (about 40–45 cm from the incisors), the transducer array at 0 degrees produces the short -axis view of the LV and right ventricle (RV) (Figs. 3-7 and 3-8). Anteflexion or slight withdrawal of the tip of

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techom the transducer optimizes the basal short -axis view of the ventricles, whereas retroflexion of the tip produces a more apical short-axis view. Sequential rotation of the multiplane transducer provides the primary transgastric views of the LV:1) 0 degrees, short-axis view of the LV and RV; 2) 70 to 90 degrees, longitudinal two-chamber view of the LV; and 3) 110 to 135 degrees, transgastric view of the LVOT and aortic valve.

Pulmonary Artery Bifurcation To visualize the bifurcation of the pulmonary artery, the tip of the transducer needs to be withdrawn to a level slightly higher than the LA. With the transducer array at 0 degrees, the main pulmonary artery and the proximal bifurcation of the right and left pulmonary arteries are visualized ( Fig. 3-9). By rotating the transducer shaft counterclockwise, only the very proximal portion of the left pulmonar y artery can be visualized. By rotating the transducer shaft clockwise, the long axis of the right pulmonary artery and the short axis of the superior vena cava and the right upper pulmonary vein are viewed adjacent to the ascending aorta. This is the best view for identifying an anomalous connection of the right upper pulmonary vein with the superior vena cava ( 6).

Pulmonary Veins The best methods for consistently visualizing the pulmonary veins are the following two maneuvers:1) For the right pulmonary ve ins, set the transducer array to 45 to 60 degrees (oblique short -axis view of the aortic valve) and rotate the shaft of the transducer to the patient's extreme right (clockwise rotation of the transducer shaft); this allows the right upper and lower pulmon ary veins to be visualized simultaneously, which appear as a “Y† configuration, where they enter the LA ( Fig. 3-10). 2) For the left pulmonary veins, set the transducer array to about 110 degrees and rotate the shaft of the transducer to the patient's P.37

P.38

extreme left (counterclockwise rotation of the shaft of the transducer) to visualize simultaneously the left upper and lower pulmonary veins as a “Y† configuration entering the LA ( Fig. 140

techom 3-10). The connection of the pulmonary veins with th e LA are also visualized from the transverse view (0 degrees) with the transducer behind the LA. The upper pulmonary veins are easier to see, but the lower veins also are seen by slightly advancing the probe from the position used for the upper pulmonary v eins.

Figure 3-7 A series of multiplane transgastric echocardiographic views. With the tip of the transducer anteflexed in a stable transgastric position, the array can be rotated to obtain the following sequence of short- and long-axis views:1) short -axis left ventricula r and right ventricular ( RV) array at 0 degrees (transverse plane); 2) two -chamber left ventricular (LV) array at 70 to 90 degrees (longitudinal plane) with a slight leftward rotation of the scope; 3) long -axis left ventricular outflow ( LVO) array at 110 t o 135 degrees, which best visualizes the LVO and aortic valve ( AV) (a good view to obtain Doppler velocity from LVO and the aortic valve); and 4) mirror-image short-axis view by over -rotation of the array, a mirror-image (right-left reversal) short -axis view results. If the transducer shaft is rotated rightward (clockwise), chambers and structures on the right side of the heart are visualized (not shown). AL, anterolateral papillary muscle; APM, anterior papillary muscle; AW, anterior wall; IW, inferior wal l; LA, left atrium; MV, mitral valve; PM, papillary muscle; PPM, posterior papillary muscle; RVO, right ventricular outflow; VS, ventricular septum. (From Seward et al [17]. Used with

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permission of Mayo Foundation for Medical Education and Research.)

Figure 3-8 Transgastric short - and long-axis tomographic anatomic specimens cut to correspond to the views in Figure 37. In a short-axis midventricular view (0 degrees of rotation), the anatomic specimen is viewed from the apex toward the base. The esophagus (E) is posterior and adjacent to the inferior wall ( IW) of the left ventricle. The left ventricle is to the viewer's right, and the right ventricle is to the viewer's left. The right ventricular outflow ( RVO) and left ventricular anterior wall ( AW) are viewed anteriorly. The thoracic aorta (Ao) is posterior and to the left of the esophagus (viewer's right). In a two -chamber view (70 to 90 degrees of rotation), the left ventricle ( LV) and left atrium ( LA) are in the same long-axis tomographic cut. This view is excellent for assessing the mitral support apparatus and LV wall motion. In an LV outflow view (110 to 135 degrees of rotation), the aortic valve (AV) and LV outflow ( LVO) are cut in the long axis. The esophagus is posterior to the LV inferior wall. In a mirrorimage short-axis view (180 degrees of rotation), the anatomic specimen is viewed from the base toward the apex. It represents the bisected apical half of the cardiac specimen shown at 0 degrees of rotation. AL, anterolateral papillary muscle; Asc Ao, ascending aorta; B, bronchus; CS, coronary

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sinus; LAA, left atrial appendage; LPA, left pulmonary artery; MV, mitral valve; PM, posteromedial papillary muscle; Pul V, pulmonary vein; RAA, right atrial appendage; RPA, right pulmonary artery; RV, right ventricle; T, trachea; TS, transverse sinus; TV, tricuspid valve; VS, ventricular septum. (From Seward et al [17]. Used with permission of Mayo Foundation for Medical Education and Research.)

Figure 3-9 A: Echocardiographic view of the bifurcation of the pulmonary artery. With the array at 0 degrees (transverse plane), the scope is withdrawn to the level of the bifurcation of the pulmonary artery (the image shown is a composite wide field view for optimal i llustration of the anatomy). The transesophageal transducer is posterior to the right pulmonary artery (RPA). Note the excellent visualization of this artery, including its bifurcation into left and right branches. Anteriorly, the ascending aorta ( Asc Ao) and superior vena cava ( SVC) are visualized in the short axis. In this image, only a small portion of the proximal left pulmonary artery ( LPA) is visualized. MPA, Main pulmonary artery. B: The corresponding anatomic section shows the bifurcation of the pul monary artery. The esophagus (E) lies between the right ( RB) and left ( LB) bronchi, adjacent to the thoracic aorta ( Ao), and posterior to the RPA. Frequently, the LB obscures visualization of the LPA. The ascending aorta ( Asc Ao), cut in the short axis, li es between the MPA and SVC. Note the right upper (superior) pulmonary vein (RUPV) medial to the SVC. LUPV, left upper (superior) pulmonary vein. (From Seward et al [17]. Used with permission of Mayo Foundation for Medical Education and Research.)

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Figure 3-10 Right (A) and left (B) pulmonary veins ( arrows) seen on multiplane transesophageal echocardiography (see text for details). LA, left atrium; LLPV, left lower (inferior) pulmonary vein; LUPV, left upper (superior) pulmonary vein; RLPV, right lower (inferior) pulmonary vein; RPA, right pulmonary artery; RUPV, right upper (superior) pulmonary vein.

Left Atrial Appendage With the transducer behind the upper portion of the LA, the basal short-axis view (0 - to 45-degree array position) and the longitudinal view (90 degrees) show the crescent -shaped LA appendage (Fig. 3-2 C). The LA appendage is normally multilobed. The LA is visualized also from the two -chamber view, with the transducer array at 90 degrees and rotated counterclockwise.

Thoracic Aorta The anatomic relation between the thoracic aorta and the esophagus is intimate. The proximity between these two structures allows superb visualization of the aorta with TEE. The proximal part of the aortic arch and the distal portion of the ascending aorta may not be accessible with transverse imaging because of the interposed trachea, but the longitudinal view and multiplane TEE usually allow complete visualization of the entire thoracic aorta. The multiplane TEE examination of the aorta is as follows. With the transducer in the midesophagus, set the array at 0 degrees (transverse plane). The descending thoracic aorta is to the patient's left and posterior to the esophagus; thus, from the probe position for cardiac imaging, rotate the shaft o f the scope to the patient's left until the short axis of the midthoracic aorta is

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Coronary Arteries The proximal portions of the coronary arteries are nor mally seen with TEE. The left coronary artery is visualized best from the transverse basal short -axis view (0 degrees). The left main coronary artery is located immediately below the level of the LA appendage. From the transverse LA appendage view, the probe needs to be withdrawn slightly to demonstrate the left main coronary artery and its bifurcation into the left anterior descending and circumflex coronary arteries ( Fig. 3-12). At 90 degrees of transducer orientation and leftward rotation of the P.39

probe, a short -axis view of the left main coronary artery is obtained. With further leftward rotation, a long -axis view of the left anterior descending and short -axis to long -axis view of the circumflex coronary artery can be obtained. The proximal right coronary artery is visualized best in the longitudinal plane (90 to 135 degrees), arising from the anteriorly located right aortic sinus, about 1 to 2 cm above the aortic valve ( Fig. 3-12 B). Anomalous coronary arteries, coronary aneurysms, and coronary fis tulas can be diagnosed with TEE (see Chapter 10).

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Figure 3-11 Transverse (0 degrees) and longitudinal (90 degrees) images of the normal descending thoracic aorta.

Figure 3-12 A: Transverse view above the aortic valve showing the left main ( large arrow) coronary artery and its bifurcation into the circumflex ( Cx) and left anterior descending (LAD) coronary arteries. B: Long-axis view of the aorta ( Ao) showing the ostium of the right coronary artery ( arrow). (See Chapter 10 for transesophageal imaging of abnormal coronary arteries.) LA, left atrium; RV, right ventricle; SVC, superior vena cava; VS, ventricular septum.

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Figure 3-13 Basal short-axis view showing a bulbous ( arrow) structure (which resembles a cotton swab [Q-tip]), separating the left superior pulmonary vein ( PV) from the left atrial appendage (LAA). It is a normal structure. Ao, aorta; LA, left atrium; RVOT, right ventricular outflow tract.

Caveats TEE has improved the visualization not only of cardiovascular structures previously seen with TTE but structures that were not well appreciated with TTE. Understanding unfamiliar but normal structures helps to minimize misinterpretation of TEE findings. Previously unrecognized normal structures seen with TEE are the most frequent reasons for misinterpretation. The most frequently misinterpreted TEE images are shown in Figures 3-13, 3-14, 3-15 and 3-16. A large hiatal hernia, pneumopericardium, or a mechanical valve prosthesis may interfere with imaging the heart with TEE.

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Figure 3-14 Basal short-axis view showing soft tissue masses (arrow) in a space between the left atrium ( LA) and aorta (Ao). The space is the transverse sinus. The soft tissue masses are either fibrin material in pericardial effusion or the tip of the LA appendage. RVO, right ventricular outflow.

Figure 3-15 A: Longitudinal view (90 degrees) with the probe shaft turned clockwise (rightward), showing a linear density in the right atrium ( RA). It is the eustachian valve ( EV). B: Fourchamber view showing a linear density ( arrow) in the RA. It is another manifestation of the EV, but it was obstructive in this patient. AS, atrial septum; LA, left atrium; SVC, superior vena cava; TV, tricuspid valve.

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Intracardiac Echocardiography TEE has been used to monitor and direct interventional catheterization procedures and generally has been the standard method for echocardiographic imaging. However, it has limitations, specifically the need for general anesthesia and potential problems related to airway management for prolonged TEE in a supine patient (18). Some views of the posterior and inferior atrial septum may not be adequate to exclude important defects or shunts because of the proximity of the probe to that area of the atrial septum. Also, apical portions of the ventricular septum may be relatively inaccessible i n some patients. Although mechanical intracardiac ultrasound systems were introduced in the 1980s, the current intracardiac echocardiography (ICE) system using an 8F or 10F phased array system was developed from single -array TEE prototype probes. The initi al ICE probe was a 10F catheter (AcuNav Diagnostic Ultrasound Catheter, Mountain View, California). This is a 64 -element vector, phased array transducer, which is multifrequency (5.5–10 MHz), mounted on a 3.3 -mm (10F) catheter with a maneuverable four way tip (Fig. 3-17). The probe is capable of high -resolution two dimensional and full Doppler imaging (pulsed, continuous wave, and tissue Doppler). The longitudinal plane provides a 90 -degree sector image, with tissue penetration of 2 to 12 cm. Currently, t he probe is also available as an 8F catheter. This catheter has echo capabilities similar to those of the 10F catheter but is longer. The added length of the 8F catheter may make it more difficult to manipulate. The ICE catheter is advanced to the right at rium (RA) under P.41

fluoroscopic guidance ( 19). Image quality is optimized by adjusting gain, depth, frequency, and focal length controls. Complete ICE evaluation of the left and right sides of the heart is then performed, sometimes with assistance of f luoroscopy to guide orientation and position of the ICE catheter.

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Figure 3-16 A large mass (arrows) in the left atrioventricular groove seen from both the four -chamber (left) and long-axis (right) views. This appearance is typical of excessive calcification of the mitral anulus, a benign transesophageal echocardiographic finding. Ao, aorta; LA, left atrium; LV, left ventricle; RA, right atrium.

Figure 3-17 A: Diagnostic ultrasound catheter (Ac uNav) next to a pediatric transesophageal echocardiography probe showing the relatively small size of the 10F catheter. B: Close-up of the 3.3-mm–diameter catheter tip ( arrows) showing the longitudinally oriented crystal array (palette). C: Overhead view of the four-way maneuverability of the tip of the diagnostic catheter.

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Detailed Description of an Intracardiac Echocardiography Examination The movements described relate to the manipulation of the control mechanisms on the handle of the ICE catheter. Moving the control handle to the left of midline moves the catheter tip to the left, as visualized from the front of the probe handle. However, these movements may not result in the catheter tip moving in the same direction as illustrated outside the body because during an examination the imaging palette is also being rotated in various directions to achieve a particular image plane. The imaging p alette of the probe can be identified by the black stripe on the outside of the catheter and the black side of the probe evident on fluoroscopy. Thus, if the probe has been rotated to visualize a posterior structure (palette directed posteriorly), posterio r or rightward movement of the probe handle controls moves the catheter tip more medially toward the atrial septum. When the catheter is angulated into an unusual position, such as that needed to achieve a short -axis image plane (anterior and leftward cont rol movement), simple rotation of the catheter does not produce the longitudinal scanning effect as in TEE, but P.42

rather, the tip of the probe moves in a large 360 -degree arch. In practice, either the echocardiographic images can be followed and the probe manipulated to obtain the desired image or the position of the probe tip can be monitored with fluoroscopy to obtain a standard probe position.

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Figure 3-18 A: Illustration of catheter course and probe position for view of the right ventricular infl ow. B: Anteroposterior radiograph showing the intracardiac echocardiography catheter tip in the right atrium ( arrow), with the transducer palette pointed toward the tricuspid valve. C: Lateral radiograph showing the corresponding lateral image with the tra nsducer tip (arrow) pointed anteriorly. D: Corresponding intracardiac echocardiographic image of the tricuspid valve and right ventricle ( RV), with mild tricuspid insufficiency shown with color flow imaging. PA, pulmonary artery; RA, right atrium.

By advancing the ICE catheter from the inferior vena cava with the control mechanism in a free or neutral position, the catheter is placed in the mid -RA, and a tricuspid valve inlet view is obtained by rotating the imaging palette of the catheter anteriorly a nd slightly leftward ( Fig. 3-18). The catheter tip is then rotated clockwise to visualize the aorta and LVOT ( Fig. 3-19). The lower atrial septum (cardiac crux) and mitral valve are then visualized by further clockwise rotation of the catheter ( Fig. 3-20). In some cases, the catheter tip is deflected posteriorly with slight posterior

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techom movement of the controls and a classic four -chamber view of the cardiac crux may be obtained ( Fig. 3-20 D and E). Continued clockwise rotation and cranial advancement of the ca theter produces a long -axis view of the atrial septum ( Fig. 3-21). In most cases, slight leftward or anterior movement of the controls, with lateral deflection of the catheter tip, is needed to optimize this long-axis image by moving the transducer P.43

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tip back and away from the atrial septum. With further cranial and caudal positioning of the catheter and slight counterclockwise and clockwise rotation, the entire atrial septum is evaluated with two dimensional and color flow imaging. Usual ly, the lipomatous superior margin of the atrial septum (septum secundum) is clearly recognized, as is the membrane of the fossa ovalis ( Fig. 3-22). From this same position, posterior and leftward imaging beyond the atrial septum allows visualization and e valuation of the LA and the left superior and inferior pulmonary veins as they course in front of the descending thoracic aorta ( Fig. 3-21). The pulmonary veins are evaluated further with color flow imaging and pulsed wave Doppler interrogation. Continued clockwise rotation then allows evaluation of the right inferior pulmonary veins and, subsequently, the right superior pulmonary vein ( Fig. 3-23), which is anterior and inferior to the right pulmonary artery. In some patients, visualization of the right pul monary veins requires not only clockwise rotation but also cranial advancement of the probe. With anterior flexion of the catheter tip and leftward movement of the controls, the superior vena cava can be evaluated ( Fig. 3-24). The crista terminalis is often visible near the superior vena cava.

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Figure 3-19 A: Illustration of catheter course and probe position for view of the left ventricular outflow tract and aortic valve. B: Anteroposterior radiograph showing the intracardiac echocardiography catheter ( arrow) now rotated slightly clockwise to point to the left ventricular outflow tract. C: Lateral image of the same catheter position ( arrow). D: Corresponding intracardiac echocardiographic image of the left ventricular (LV) outflow tract with color flow i maging. Ao, ascending aorta; MPA, main pulmonary artery; RA, right atrium.

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Figure 3-20 A: Illustration of catheter course and probe position for view of the lower atrial septum and crux of the heart. B: Anteroposterior radiograph showing the intracardi ac echocardiography catheter ( arrow) rotated further clockwise to image the cardiac crux portion of the atrial septum above the mitral valve. C: Lateral image of the same catheter position (arrow). D: Corresponding intracardiac echocardiographic image of the cardiac crux ( arrow) just above the mitral valve and coronary sinus ( CS). E: Four-chamber view of the cardiac crux showing a small right -to-left shunt across a patent

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foramen ovale ( arrow). LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

Figure 3-21 A: Illustration of catheter course and probe position for the long -axis view of the atrial septum. B: Anteroposterior radiograph of the intracardiac echocardiography catheter ( arrow) after further clockwise rotation and slight anterior and lateral retroflexion of the catheter shows a long -axis image of the atrial septum. C: Lateral image of the catheter position ( arrow) showing the

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slight anterior flexion of the catheter. D: Corresponding intracardiac echocardiographic image showing the long axis of the atrial septum ( arrow). E: Color flow image of left pulmonary venous return and a small left -to-right atrial shunt (arrow). DAo, descending aorta; LA, left atrium; LLPV, left lower (inferior) pulmonary vein; LPA, left pulmonary artery; LUPV, left upper (superior) pulmonary vein; RA, right atrium.

A short-axis image of the atrial septum and aortic root can be obtained with combined anterior and leftward movement of the controls and with clockwise rotation of the handle. This directs the tip anteriorly and medially P.46

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toward and sometimes across the tricuspid valve anulus ( Fig. 325). Short-axis images are important to access appropriate device positioning near the aortic root and to provide a typical transverse image of the aortic valve and atrial septum. Typically, the right inferior pulm onary veins are visible near the back wall of the LA.

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Figure 3-22 A: Intracardiac echocardiographic long -axis image showing a large (10 mm) patent foramen ovale ( PFO) in a 25year-old patient who had previously had a stroke. B: Corresponding color flow image showing a large right -to-left shunt through the patent foramen ovale ( arrow). C: The same long-axis image of the patent foramen ovale with a large resting right -to-left shunt ( arrow) shown with injection of agitated saline into the inferior vena cava . DAo, descending aorta; LA, left atrium; RA, right atrium.

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Figure 3-23 A: Illustration of catheter course and probe position for viewing the right pulmonary veins. B: Anteroposterior radiograph showing the position of the tip (arrow) of an intracardiac echocardiography catheter after further clockwise rotation of the catheter to the right to image the right pulmonary veins. C: Lateral radiograph showing the same catheter position ( arrow). D: Corresponding intracardiac echocardiograph ic image shows all three right pulmonary veins. Note that the right upper (superior) pulmonary vein ( RUPV) courses anterior and then inferior to the right pulmonary artery (RPA). E: With the catheter tip moved across the atrial defect, the image next shows a long-axis view of the RPA, with the RUPV just inferior to the RPA. LA, left atrium; RLPV, right lower

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(inferior) pulmonary vein; RMPV, right middle pulmonary vein; SVC, superior vena cava.

Figure 3-24 A: Illustration of catheter course and probe position to view the superior vena cava. B: Anteroposterior radiograph showing anterior and lateral flexion of the catheter (arrow) to scan superiorly into the superior vena cava. C: Lateral image of the same catheter position ( arrow) scanning superiorly. D: Corresponding intracardiac echocardiographic image showing flow from the superior vena cava ( SVC) into the right atrium ( RA). The right upper (superior) pulmonary vein (RUPV) is seen as it courses anterior and inferior to the right pulmonary artery ( RPA).

To cross the atrial septum, reposition the catheter tip in the mid RA and, with the imaging palette facing posteriorly toward the atrial septum, manipulate the controls with a po sterior or rightward movement to push the catheter tip toward the atrial septum. With the catheter tip seated adjacent to the atrial septum or, in many cases, across the interatrial defect, the pulmonary veins are evaluated again ( Fig. 3-23). Once across t he septal defect, further

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techom posterior and rightward movement of the controls (catheter flexion) provides an en face view of mitral inflow ( Fig. 3-26). With the catheter across the atrial septum, in a neutral position and rotated anteriorly (counterclockwise), a detailed short -axis view of the aortic valve is obtained, and with slight clockwise rotation of the catheter, the RVOT and pulmonary valve are observed ( Fig. 327). With posterior and rightward movement of the probe controls similar to that for the mit ral valve view, the probe can be advanced into the LV or near the lateral atrioventricular groove, where scans of the ventricular septum and both atrioventricular valves and ventricles can be obtained, similar in appearance to a four -chamber view (Fig. 3-28). This view provides excellent imaging of the inlet and membranous ventricular septum.

Figure 3-25 A: Illustration of catheter course and probe position for the short -axis view of the atrial septum and aorta. B: Anteroposterior radiograph showing retroflexion of the catheter tip by anterior and leftward movement of the probe controls and subsequent rotation of the catheter tip clockwise to place the tip ( arrow) near or through the tricuspid valve. C:

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Lateral image showing the catheter position ( arrow) near the tricuspid valve. D: Corresponding intracardiac echocardiographic image showing a typical short -axis image of the heart at the level of the aortic valve. A small left -to-right shunt (arrow) is observed through the superior margin of the atrial septal defect. The main pulmonary artery ( MPA) is also visible posterior to the aorta. Ao, ascending aorta; LA, left atrium; RA, right atrium; RPV, right pulmonary vein.

Figure 3-26 A: Illustration of catheter course and probe position for en face view of the mitral valve from the left atrium (LA). B: Anteroposterior radiograph showing the intracardiac echocardiography catheter ( arrow) advanced across the atrial septal defect and flexed inferiorly to view the mitral valve orifice. C: Lateral radiograph showing the same catheter position ( arrow). Note the posterior location of the catheter in the left atrium. D: Corresponding intracardiac echocardiographic image of en face view of mitral orifice. LV, left ventricl e.

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Figure 3-27 A: Illustration of catheter course and probe position for view of the aorta and pulmonary artery from the left atrium. B: Anteroposterior radiograph of the intracardiac echocardiography catheter tip ( arrow) placed across the atrial septal defect into the left atrium but rotated counterclockwise to an anterior position immediately behind the aortic valve. C: Lateral image of the same catheter position ( arrow). Note that the transducer is pointing anteriorly. D: Corresponding intracardiac echocardiographic short -axis image showing fine detail of the aortic valve leaflets. E: Additional clockwise

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rotation of the catheter produces a view of the right ventricular outflow tract and main pulmonary artery ( MPA). Arrow, aortic valve; arrowhead, pulmonary valve; Ao, ascending aorta; TV, tricuspid valve.

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From within the RA, with combined anterior and leftward movement of the controls similar to that to obtain a short -axis image, the curved probe can be manipulated across the tricuspid valve to visualize structures within the RV. With advancement of the probe into the RV, scans of the RVOT and pulmonary valve are easily obtained (Fig. 3-29). By releasing the curvature on the probe, it can be rotated to scan inferiorly to obtain short -axis images of the LV and ventricular septum. These same views can be used to scan the membranous and muscular portions of the ventricular septum to visualize ventricular septal defects ( Fig. 3-30).

Applications of Intracardiac Echocardiography The potential applications of ICE to interventional cardiac catheterization continue to expand, not only with respect to catheter-based treatment of congenital and acquired heart disease but to management of cardiac arrhythmias. Patients are more comfortable during ICE than during TEE P.52

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imaging (18, 19, 20, 21, 22, 23,24). ICE bypasses potentially poor acoustic windows that are commonly encountered during TTE and may occur also during TEE. Furthermore, ICE requires only one operator, so another echocardiographer is not needed in the catheterization laboratory providing that the primary operator is also familiar with ICE imaging and interpretation. The primary operator, who is an interventionalist, has control of the ICE images and must be able to provid e the appropriate image planes for diagnosis and catheter intervention. The ability to provide this imaging rapidly and without the need for other echocardiographic support expedites the procedure and shortens interventional procedure time.

Figure 3-28 A: Illustration of catheter course across the atrial septum and probe position just inside the left ventricle near the left atrioventricular groove. Rightward and posterior movement of the control produces angulation of the probe for viewing the ventricula r septum and both ventricles. B: Anteroposterior radiograph of the intracardiac echocardiography catheter tip ( arrow) at the left

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atrioventricular groove. C: Lateral radiograph showing the catheter position ( arrow). D: Corresponding intracardiac echocardiographic image showing a four -chamber–like view of both left ( LV) and right ( RV) ventricles and the ventricular septum ( VS). The membranous inlet portion of VS is well visualized. RA, right atrium.

Figure 3-29 A: Illustration of catheter course and probe position across the tricuspid valve in the right ventricle. Because of the leftward and anterior manipulation of the control, the probe is angulated to visualize the pulmonary outflow tract and valve superiorly. B: Anteroposterior radiograph of the intracardiac echocardiography catheter (arrow) in the right ventricle. C: Lateral radiograph showing the anterior location of the catheter ( arrow). D: Corresponding intracardiac echocardiographic image of the pulmonary o utflow and color flow through the pulmonary valve. Ao, aorta; PA, pulmonary artery.

Superior image quality and visualization of intracardiac structures allow accurate guidance of interventional procedures, thereby reducing both fluoroscopic and total proc edure times. Procedures

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techom for which ICE imaging has been reported to be of benefit include, but are not limited to, guidance of transseptal puncture to gain access to the LA, transcatheter closure device placement, radiofrequency ablation, cardiac biopsy, mi tral valvuloplasty, and occlusion of the LA appendage ( 18).

Electrophysiology Procedures The first reports of intracardiac ultrasonography during electrophysiology procedures were for use of a mechanical, single element intracardiac echocardiography probe (25,26). Anatomic definition was thought to be of great benefit for ablation procedures because fluoroscopic guidance did not provide adequate definition of the tissue. Intracardiac imaging with the newer phased array ICE catheter has P.53

been incorpora ted to guide electrophysiology procedures. Proper location of the transseptal puncture as guided by ICE has been useful in conjunction with electrophysiology. Anatomic landmarks that are important for a successful ablation are visualized best with ICE and are not easily seen fluoroscopically.

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Figure 3-30 A: Illustration of catheter course and probe position across the tricuspid valve and with the probe directed posterior to the ventricular septum to visualize the left ventricle in the short axis. B: Corresponding echocardiographic images showing the right ventricle ( RV) anteriorly and the left ventricle (LV) in the short axis. C: Color flow imaging showing flow in the LV. A small jet ( arrow) near the ventricular septum (VS) represents flow from a mus cular ventricular septal defect.

One of the most common uses of ICE imaging in electrophysiologic procedures has been during pulmonary vein isolation for ablation of atrial flutter ( 27). ICE imaging provides exact determination of the pulmonary vein anatomy (number and position), including the presence or absence of an antrum that may receive the left superior and inferior pulmonary veins before joining the LA ( 28). Visualization of pulmonary vein ostia with ICE facilitates guiding the position of the catheter to ensure that the contact between the catheter tip and the tissue is adequate for delivery of radiofrequency energy, thereby improving the success of the

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Device Closure Procedures Another primary application of ICE that has been rapidly adopted in clinical practice is for guidance of de vice closure of atrial septal defects, such as secundum atrial septal defect or patent foramen ovale. Transcatheter placement of closure devices for either of these defects is facilitated by ICE guidance in the cardiac catheterization laboratory. Intracard iac images provide superior imaging of the atrial septum ( 18, 19, 20, 21, 22, 23,24). Assessment of the defect or defects and the relation to the surrounding cardiac structures is critical for a successful procedure and is facilitated by the proximity of the ICE catheter to the atrial appendages and walls, eustachian valve, limbus of the fossa ovalis, and pulmonary veins. Documentation of normal pulmonary venous return to the LA ( Figs. 3-21 and 3-23) is an important aspect of closure of an atrial septal de fect and is easily accomplished with ICE (2). Compared with fluoroscopy, long -axis and short -axis ICE views (Fig. 3-31) are helpful in analyzing the dimensions of a septal defect and allow very accurate measurement of both the static diameter and, more imp ortantly, the balloon -stretched diameter (typically used to select the appropriate device size) ( 19). The spatial relations between devices and surrounding cardiac structures are visualized better with ICE than with TEE. During deployment and subsequent de livery of an occlusion device, there is no shadowing of the RA disk of the device by the LA disk when ICE guidance is used. Therefore, ICE imaging provides superior visualization of septal rims in relation to the position of the device before final deploym ent is accomplished, reducing the risk of device embolization. In contrast, when TEE is used to evaluate

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the atrial septum, increasing the time needed for imaging before the device can be delivered to its optimal position.

Figure 3-31 A: Intracardiac echocardiographic image showing the long axis of the atrial septum, with a moderate left -to-right shunt (arrow) through a secundum atrial septal defect. B: Similar image showing an occluder device in place ( arrows), with a small residual central shunt. C: A short-axis image showing a device in place behind the aortic root. Ao, aortic root; LA, left atrium; RA, right atrium.

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Figure 3-32 A: Intracardiac echocardiographic image obtained from within a right -sided morphologic left ventricle ( LV) in a young man with congenitally corrected transposition of the great arteries. An iatrogenic ventricular septal defect is observed (arrow) near the inlet ventricular septum ( VS). B: Color flow imaging shows a large left -to-right shunt originating in the morphologic right ventricle ( RV). A prosthetic atrioventricular valve is observed near the left atrium ( LA).

Transcatheter closure of a muscular ventricular septal defect (congenital or after myocardial infarction) is now possible ( 29). For a ventricular septal defect that develops after myocardial infarction, TEE imaging may not be tolerated by patients with a clinically com promised condition. ICE is an additional imaging modality that can be used to visualize cardiac structures during sizing of the defect and delivery and deployment of the septal closure device. Monitoring of tricuspid valve regurgitation is facilitated by I CE during such procedures. To visualize the ventricular septal defect properly, the ICE catheter may need to be manipulated through the right atrioventricular valve orifice into the right-sided ventricle, as described above ( Fig. 3-32).

Perivalvular Leak Perivalvular leak can occur in patients with acquired heart disease (such as rheumatic valvular disease) or congenital heart disease who have undergone mechanical valve replacement. Often, acoustic shadowing by the mechanical valve precludes adequate echocardiographic imaging from one side of the valve. Depending on the intracardiac anatomy, both ICE and TEE may be needed to facilitate evaluation of such defects for their location and proximity to the mechanical valve and for their size ( 29). Also, during

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techom deployment of closure devices, assurance of valve function during and after device placement is critical. Evaluation of leaflet mobility is important, and the device must not interfere with normal valve function. Continuous monitoring during deployment, pos itioning, and delivery of the device is easily accomplished with ICE ( Fig. 333). Judicious use of TEE may be needed to fully evaluate some patients during closure of a perivalvular leak, but it can be minimized to facilitate patient comfort during supine imaging with the additional use of ICE.

Other Applications Device closure of the LA appendage has been under investigation as a treatment to decrease embolic risk with chronic atrial fibrillation. ICE imaging of the LA appendage before device closure facilitates evaluation of thrombus in the appendage. Continuous monitoring during the interventional procedure is typically performed from the RA, with proximity to the LA structures allowing adequate visualization of the device during deployment and final deli very. Intracardiac thrombus related to the procedure can be evaluated with ICE. During mitral valvuloplasty, ICE may help in monitoring the location of the initial transseptal puncture, particularly in situations in which the atrial septum is excessively t hickened. Also, ICE may be used to assess valve morphology, measure the anulus, and monitor the results of balloon valvuloplasty. Instantaneous monitoring for catheter -related complications is also possible with ICE. Detection of left -sided thrombus or spo ntaneous contrast in a cardiac chamber as a precursor to thrombus is facilitated with the use of ICE, with its high -frequency imaging and superb image quality. Pericardial effusion can be visualized easily with ICE and then promptly treated to prevent comp lications (22).

Extracardiac Use of the Intracardiac Echocardiography Probe The intracardiac echocardiography probe has been used also for TEE imaging in small infants during surgical repair P.56

of a congenital cardiac defect ( 30, 31, 32). The small siz e of this probe facilitates its placement in children who weigh less than 3.0

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techom kg. To date, our center has performed approximately 100 studies with this probe in children weighing less than 3 kg. Initial reports about the TEE use of the ICE probe in animal models and small children have been encouraging ( 31, 32). In 2002, Bruce and colleagues (32) demonstrated successful use of the probe in a group of 17 infants who weighed between 2.1 and 5.6 kg. No major complications were reported. In 13 of 22 studies per formed by these authors, the standard biplane pediatric TEE probe could not be advanced into the esophagus because of the patient's small size. Therefore, TEE imaging would not have been performed if the ICE probe had not been available. High -quality two-dimensional and Doppler images of the descending thoracic aorta ( Fig. 3-34), both ventricles ( Fig. 3-35), and apical and outlet ventricular septa are obtained with the ICE probe. Also, the systemic and pulmonary venous connections to the atria and atrial se ptum are visualized adequately with this probe.

Figure 3-33 A: Intracardiac echocardiographic image obtained from the right atrium ( RA) in a patient with a left ventricular to-right atrial shunt following mitral valve ( MV) replacement. This view of the crux of the heart shows the entrance ( arrow) of the fistula in the RA. B: Color flow imaging showing a moderate shunt from the left ventricle (LV) to RA. LA, left atrium.

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Figure 3-34 A: Transesophageal echocardiographic image obtained with an intracardiac echocardiography catheter in a small infant with critical discrete coarctation ( arrow) of the aorta (Ao). B: Color flow imaging ( top) shows aliased flow through the obstruction, with a 4 m/s velocity recorded with continuous wave Doppler echocardiography ( bottom).

The major disadvantage of the ICE probe is that it is monoplane. Longitudinal imaging is effective; however, the crux of the heart and the inlet ventricular septum are not vis ualized adequately. This probe has not been suitable P.57

during repair of atrioventricular septal defects. However, these defects are rarely repaired in the newborn period. Transgastric imaging is also suboptimal with this probe because the orientation of the phased array pallet does not permit articulation near the probe tip. To avoid thermal injury, it is recommended that imaging time be short and that the probe be powered only when in use. Although performing TEE with this probe has technical limitati ons, it does provide reliable and adequate imaging in patients in whom TEE could not otherwise be performed during cardiac surgery.

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Figure 3-35 A: Transesophageal echocardiographic image obtained with an intracardiac echocardiography catheter in an infant after repair of truncus arteriosus. The patch closure (*) is observed to close the ventricular septal defect between the right ventricle ( RV) and left ventricle ( LV). B: Color flow imaging shows that the patch is intact. Ao, aorta; LA, left atrium.

References 1. Seward JB, Khandheria BK, Oh JK, et al. Transesophageal echocardiography:Technique, anatomic correlations, implementation, and clinical applications. Mayo Clinic Proceedings, 1988;63:649–680. 2. Erbel R, Engberding R, Daniel W, et al. Echocardiography in diagnosis of aortic dissection. Lancet, 1989;1:457–461. 3. Freeman WK, Schaff HV, Khandheria BK, et al. Intraoperative evaluation of mitral valve regurgitation and repair by transesophageal echocardiography:Incidence and significance of systolic anterior motion. Journal of the American College of Cardiology, 1992;20:599–609. 4. Randolph GR, Hagler DJ, Connolly HM, et al. Intraoperative transesophageal echocardiography during surgery for congenital heart defects. Journal of Thoracic a nd Cardiovascular Surgery, 2002;124:1176–1182. 5. Klein AL, Grimm RA, Murray RD, et al, Assessment of Cardioversion Using Transesophageal Echocardiography Investigators. Use of transesophageal echocardiography to guide cardioversion in patients with atri al fibrillation. New England Journal of Medicine, 2001;344:1411–1420.

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techom 6. Pascoe RD, Oh JK, Warnes CA, et al. Diagnosis of sinus venosus atrial septal defect with transesophageal echocardiography. Circulation, 1996;94:1049–1055. 7. Karalis DG, Bansal RC , Hauck AJ, et al. Transesophageal echocardiographic recognition of subaortic complications in aortic valve endocarditis:Clinical and surgical implications. Circulation, 1992;86:353–362. 8. Agmon Y, Khandheria BK, Meissner I, et al. Relation of coronary artery disease and cerebrovascular disease with atherosclerosis of the thoracic aorta in the general population. American Journal of Cardiology, 2002;89:262–267. 9. Klein AL, Murray RD, Becker ER, et al, ACUTE Investigators. Economic analysis of a transe sophageal echocardiography -guided approach to cardioversion of patients with atrial fibrillation:The ACUTE economic data at eight weeks. Journal of the American College of Cardiology, 2004;43:1217–1224. 10. Mas JL, Arquizan C, Lamy C, et al, Patient Fora men Ovale and Atrial Septal Aneurysm Study Group. Recurrent cerebrovascular events associated with patent foramen ovale, atrial septal aneurysm, or both. New England Journal of Medicine, 2001;345:1740–1746. 11. Sohn DW, Shin GJ, Oh JK, et al. Role of tra nsesophageal echocardiography in hemodynamically unstable patients. Mayo Clinic Proceedings, 1995;70:925–931. 12. Min JK, Spencer KT, Furlong KT, et al. Clinical features of complications from transesophageal echocardiography:A single center case series of 10,000 consecutive examinations. Journal of the American Society of Echocardiography, 2005;18:925–929. 13. Novaro GM, Aronow HD, Militello MA, et al. Benzocaine -induced methemoglobinemia:Experience from a high -volume transesophageal echocardiography l aboratory. Journal of the American Society of Echocardiography, 2003;16:170–175. 14. Brinkman WT, Shanewise JS, Clements SD, et al. Transesophageal echocardiography:Not an innocuous procedure. Annals of Thoracic Surgery, 2001; 72:1725–1726. 15. Sharma SC, Rama PR, Miller GL, et al. Systemic absorption and toxicity from topically administered lidocaine during transesophageal echocardiography. Journal of the American Society of Echocardiography, 1996;9:710–711.

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techom 16. Steckelberg JM, Khandheria BK, Anhalt JP, et al. Prospective evaluation of the risk of bacteremia associated with transesophageal echocardiography. Circulation, 1991;84:177–180. 17. Seward JB, Khandheria BK, Freeman WK, et al. Multiplane transesophageal echocardiography:Image orientation, ex amination technique, anatomic correlations, and clinical applications. Mayo Clinic Proceedings, 1993; 68:523–551. 18. Bartel T, Konorza T, Arjumand J, et al. Intracardiac echocardiography is superior to conventional monitoring for guiding device closure of intratrial communications. Circulation, 2003;107:795–797. 19. Earing MG, Cabalka AK, Seward JB, et al. Intracardiac echocardiographic guidance during transcatheter device closure of atrial septal defect and patent foramen ovale. Mayo Clinic Proceedings, 2004;79:24–34. 20. Khositseth A, Cabalka AK, Sweeney JP, et al. Transcatheter Amplatzer device closure of atrial septal defect and patent foramen ovale in patients with presumed paradoxical embolism. Mayo Clinic Proceedings, 2004;79:35–41. 21. Hijazi Z, Wang Z, Cao Q, et al. Transcatheter closure of atrial septal defects and patent foramen ovale under intracardiac echocardiographic guidance:Feasibility and comparison with transesophageal echocardiography. Catheterization and Cardiovascular Interventi ons:Official Journal of the Society for Cardiac Angiography & Interventions, 2001;52:194–199. 22. Jongbloed MR, Schalij MJ, Zeppenfeld K, et al. Clinical applications of intracardiac echocardiography in interventional procedures. Heart, 2005; 91:981–99 0. 23. Mullen MJ, Dias BF, Walker F, et al. Intracardiac echocardiography guided device closure of atrial septal defects. Journal of the American College of Cardiology, 2003;41:285–292. P.58

24. Bruce CJ, Nishimura RA, Rihal CS, et al. Intracardiac echocardiography in the interventional catheterization laboratory:Preliminary experience with a novel, phased -array transducer. American Journal of Cardiology, 2002;89:635–640.

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techom 25. Chu E, Fitzpatrick AP, Chin MC, et al. Radiofrequency catheter ablation guid ed by intracardiac echocardiography. Circulation, 1994;89:1301–1305. 26. Tardif JC, Cao QL, Schwartz SL, et al. Intracardiac echocardiography with a steerable low -frequency linear -array probe for left-sided heart imaging from the right side:Experimental studies. Journal of the American Society of Echocardiography, 1995;8:132–138. 27. Packer DL, Stevens CL, Curley MG, et al. Intracardiac phased array imaging:Methods and initial clinical experience with high resolution, under blood visualization:Initial e xperience with intracardiac phased -array ultrasound. Journal of the American College of Cardiology, 2002;39:509–516. 28. Packer D. Intracardiac echocardiography and cardiac electrophysiology. Journal of the American Society of Echocardiography. In press. 29. Holzer R, Balzer D, Amin Z, et al. Transcatheter closure of postinfarction ventricular septal defects using the new Amplatzer muscular VSD occluder:Results of a U.S. Registry. Catheterization and Cardiovascular Interventions:Official Journal of the So ciety for Cardiac Angiography & Interventions, 2004;61:196–201. 30. Cabalka AK, Hagler DJ, Mookadam F, et al. Percutaneous closure of left ventricular -to-right atrial fistula after prosthetic mitral valve rereplacement using the Amplatzer duct occluder. Catheterization and Cardiovascular Interventions:Official Journal of the Society for Cardiac Angiography & Interventions, 2005;64:522–527. 31. Bruce CJ, Packer DL, O'Leary PW, et al. Feasibility study:Transesophageal echocardiography with a 10F (3.2 -mm), multifrequency (5.5 - to 10-MHz) ultrasound catheter in a small rabbit model. Journal of the American Society of Echocardiography, 1999;12:596–600. 32. Bruce CJ, O'Leary P, Hagler DJ, et al. Miniaturized transesophageal echocardiography in newborn infant s. Journal of the American Society of Echocardiography, 2002;15:791–797.

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7. 4 - Doppler Echocardiography and Color Flow Imaging > Table of Contents > 4 - Doppler Echocardiography and Color Flow Imaging: Comprehensive Noninvasive Hemodynamic Assessment

4 Doppler Echocardiography and Color Flow Imaging: Comprehensive Noninvasive Hemodynamic Assessment Hemodynamic assessment is a major part of a routine echocardiography examination. Stroke volume, cardiac output, intracardiac pressures, pressure gradients, a nd vascular resistance are reliably determined with two -dimensional (2D), Doppler, and color flow imaging echocardiography. This noninvasive measurement of hemodynamic variables not only has replaced many invasive hemodynamic procedures but it also can be superior to them under certain circumstances. Because many therapeutic decisions, including surgical intervention, are based on echocardiography, it is critical that everyone involved in the care of cardiac patients as well as everyone involved in performi ng echocardiography understand how a hemodynamic assessment is performed by echocardiography and know its advantages and potential limitations.

Doppler Echocardiography Doppler in the heart and great vessels and is based on the Doppler effect, which was de scribed by the Austrian physicist Christian Doppler in 1842 ( 1). The Doppler effect is the increase in sound frequency as a sound source moves toward the observer and the decrease in sound frequency as the source moves away from the observer. In the circul atory system, the moving target is the red blood cell. When an ultrasound beam with known frequency ( fo) is transmitted to the heart or great vessels, it is reflected by the red blood cells. The frequency of the reflected ultrasound waves ( fr) increases when the red blood cells are moving toward the source of ultrasound. Conversely, the frequency of reflected ultrasound waves decreases when the red blood cells are moving away from the source. The change in frequency between the transmitted

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techom sound and the ref lected sound is termed the frequency shift (Δ f) or Doppler shift ( fr-fo). The Doppler shift depends on the transmitted frequency ( fo), the velocity of the moving target ( v), and the angle (θ) between the ultrasound beam and the direction of the moving target as expressed in the Doppler equation ( Fig. 41):

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where c is the speed of sound in blood (1,540 m/s). If the angle θ is 0 degree (i.e., the ultrasound beam is parallel with the direction of blood flow), the maximal frequency shift is measur ed because the cosine of 0 degree is 1. Note that as angle θ increases, the corresponding cosine becomes progressively less than 1, and this will result in underestimation of the Doppler shift (Δ f) and, hence, peak velocity, because peak flow velocity is derived from Δ f by rearranging the Doppler equation:

Blood flow velocities determined by Doppler echocardiography are used, in turn, to derive various hemodynamic data (see below).

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Figure 4-1 Diagram of the Doppler effect (see text for explanation). RBCs, red blood cells.

Figure 4-2 Drawing of pulsed wave and continuous wave Doppler echocardiography from the apical view (see text for explanation). Ao, aorta; LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

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Figure 4-3 Representative pulsed wave and continuous wave Doppler spectra from a 60 -year-old patient who has aortic stenosis (AS) and aortic regurgitation ( AR). The pulsed wave Doppler sample volume is placed at the left ventricular outflow tract (LVOT), and the Doppler spectrum shows systolic LVOT velocity and turbulent diastolic signal of aortic regurgitation recorded on both sides of the baseline. Although AR flow is toward the transducer, aliasing (velocity wraparound) occurs because of high velocity (4–5 m/s). Continuous wave Doppler detects flow velocities all along its beam (LVOT and aortic valve) and is able to record high velocity. Systolic flow away from the transducer (spectrum below the base line) represents flow across the stenotic aortic valve ( AS) and diastolic flow is from AR. Peak AS velocity across the stenotic valve varies (5.0–5.5 m/s) because of atrial fibrillation.

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Figure 4-4 A: Continuous wave Doppler recording from the apex. There is an unusual velocity recording ( upward arrows) away from the apex with a velocity close to 4 m/s, which occurs about 100 ms before mitral inflow ( downward arrows). S indicates systolic flow velocity away from the apex; it has a dagger configuration. B: Color M-mode from the same patient shows that the unusual flow comes from the apical area (blue) to the mid-cavity, starting before mitral inflow, typical of mid cavitary obstruction. During isovolumic relaxation period, there is a dyssynchrony of myocardial relaxation that results in a pressure gradient from the apex to the basal segment across the obstructed mid -cavity.

The most common uses of Doppler echocardiography are the pulsed wave and continuo us wave forms (Fig. 4-2). Both modalities are essential parts of a Doppler echocardiography examination and provide complementary information. In the pulsed wave mode, a single ultrasound crystal sends and receives sound beams. The crystal emits a short bu rst of ultrasound at a certain frequency (pulse repetition frequency). The ultrasound is reflected from moving red blood cells and is received by the same crystal. Therefore, the maximal frequency shift that can be determined by pulsed wave Doppler is one -half the pulse repetition frequency; this is called the Nyquist frequency. If the frequency shift is higher than the Nyquist frequency, aliasing occurs; that is, the Doppler spectrum is cut off at the Nyquist frequency, and the remaining frequency shift is recorded on the top or bottom of the opposite side of baseline ( Fig. 4-3). P.61

Pulsed wave Doppler measures flow velocities at a specific location

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techom within a “sample volume.† The pulse repetition frequency varies inversely with the depth of the sampl e volume: the shallower the location of the sample volume, the higher the pulse repetition frequency and Nyquist frequency. In other words, higher velocities can be recorded without aliasing by pulsed wave Doppler the closer the sample volume is to the tra nsducer. In the continuous wave mode, the transducer has two crystals: one to send and the other to receive the reflected ultrasound waves continuously. Therefore, the maximal frequency shift that can be recorded by continuous wave Doppler is not limited by the pulse repetition frequency or Nyquist phenomenon. Unlike pulsed wave Doppler, continuous wave Doppler measures all the frequency shifts (i.e., velocities) present along its beam path; hence, it is used to detect and to record the highest flow veloci ty available. Occasionally, recording of a high -velocity flow is the first clue to an unsuspected lesion within the path of a continuous wave Doppler beam ( Fig. 4-4). Continuous wave Doppler usually is performed with either an image -guided or nonimaging tr ansducer. A small nonimaging transducer (pencil probe) is more suitable for interrogation of a high -velocity jet from multiple windows, including areas between the ribs. An image -guided continuous wave examination is more helpful when the direction of bloo d flow is eccentric or the amount of desired blood flow is trivial. The characteristics and clinical applications of these Doppler modalities are summarized in Table 4-1. Table 4-2 lists the mean and range of maximal velocities recorded from normal subject s by Doppler echocardiography. Echocardiographers should be familiar with the characteristic configuration and timing of normal and abnormal Doppler signals ( Figs. 4-4 and 4-5).

Color Flow Imaging Color flow imaging, based on pulsed wave Doppler principles, displays intracavitary blood flow in three colors (red, blue, and green) or their combinations, depending on the velocity, direction, and extent of turbulence ( 2). It uses multiple sampling sites along multiple ultrasound beams (multigated). At each sampling site (or gate), the frequency shift is measured, converted to a digital format, automatically correlated (autocorrelation) with a preset color scheme, and displayed as color flow superimposed on 2D imaging (Fig. 4-6A). Blood flow directed to ward the transducer has a positive frequency shift (i.e., reflected ultrasound frequency is higher than the transmitted frequency) and is color -coded in

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techom shades of red. Blood flow directed away from the transducer has a negative frequency shift and is color -coded in shades of blue. Each color has multiple shades, and the lighter shades within each primary color are assigned to higher velocities within the Nyquist limit. When flow velocity is higher than the Nyquist frequency limit, color aliasing occurs and is depicted as a color reversal ( Fig. 46B). With each multiple of the Nyquist limit, the color repeatedly reverts to the opposite color. Turbulence (i.e., blood moving in multiple directions with multiple velocities) is characterized by the presence of va riance. The degree of the variance from the mean velocity can be coded as a variance color, usually a shade of green. Therefore, abnormal blood flow is easily recognized by combinations of multiple colors according to the direction, velocity, and degree of turbulence (Fig. 4-6). The width and size of abnormal intracavitary flows are P.62

used to semiquantify the degree of valvular regurgitation or cardiac shunt.

Table 4-1 Comparison of pulsed wave and continuous wave Doppler

Pulsed Wave

Continuous Wave

Measures specific blood flow

Measures blood flow

velocity by placing the

velocities along the axis

“sample volume† at the

of the entire ultrasound

region of interest

beam (range ambiguity)

Maximal measurable velocity

Able to measure high

without aliasing is usually 15 cm/s) than that from the medial anulus (normally >10 cm/s) ( Fig. 5-1). In our laboratory, mitral anulus velocities are usually, but not always, obtained from the septal anulus. Regional myocardi al dysfunction or valvular surgery involving the mitral anulus may affect mitral anulus velocities. A localized disease process, such as lateral myocardial infarction, can result in mitral anulus velocities being lower at the lateral anulus than at the sep tal anulus.

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Figure 5-1 Tissue Doppler imaging of the septal (A) and lateral (B) mitral anulus in a normal subject. In tissue Doppler imaging of the anulus, there are three major velocities: systolic velocity (S′ or Sa), E′ (or Ea), and A′ (or Aa). S′ reflects the systolic function of the left ventricle ( LV), and E′ and A′ are related to diastolic function of the LV. E′ reflects the status of myocardial relaxation, and the normal value from the medial mitral anulus is more than 10 cm/s and from the lateral anulus, more than 15 cm/s. Arrow, middiastolic velocity, which is seen in young normal subjects. IVC, isovolumic contraction; IVR, isovolumic relaxation; LA, left atrium.

Table 5-1 Comparison of twodimensional (2D) gray scale and tissue doppler imaging (TDI)

TDI

Variable

2D Gray

Color

Pulsed

Scale

Doppler

Doppler

Temporal

30–50

20–90

>250

resolution

frames/s

frames/s

frames/s

(but 400

>150

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frames/s

frames/s

possible)

possible)

Spatial

1 × 1 mm

Typically 2

1 × 1

resolution

(may be

× 2 mm

mm

No

Yes

Yes

++

+++

+++

No

Yes

No

++++

++

+

less)

Angle dependency

Applicability to all myocardium

Intramural function

Attenuation dependency

From Sutherland G. Doppler myocardial imaging: Rationale, principles and instrumentation. In: GarcÃa-FerÅ„andez MA, Declan JL, eds. Proceedings of the International Summit in Doppler Tissue Imaging , 1997; 17–24. Used with permission.

Late diastolic velocity (Aa or A′) of the mitral anulus at the time of atrial contraction increases during early diastolic dysfunction, as is the case for the mitral inflow A wave, but decreases as atrial function deteriorates. A′ has been correlated with left atrial (LA) function (6).

Estimation of Left Ventricular Filling Pressure LV diastolic filling pressures can be estimated reliably with 2D and Doppler echocardiography. The deceleration time

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(DT) of mitral inflow early diastolic velocity (E) has a good inverse correlation with the pulmonary capillary wedge pressure (PC WP) of less than 130 milliseconds usually indicates a PCWP greater than 20 mm Hg. However, mitral inflow DT alone is not highly accurate in patients who have a relatively normal LVEF or atrial fibrillation. Because Ea is reduced in patients with impaired r elaxation and is affected less by preload than mitral inflow E, the ratio (E/Ea) between mitral inflow early diastolic velocity and mitral anulus early diastolic velocity increases as PCWP increases (see Chapter 8). Investigations at Baylor College and in our laboratory have demonstrated that PCWP is higher than 20 mm Hg when E/Ea is more than 10 (using the lateral anulus Ea) or 15 (using the medial anulus Ea) (7,8). This ratio works well even in patients who have fused mitral inflow signals, preserved LVEF , and atrial fibrillation (9,10). The only exception is patients with constrictive pericarditis, in whom Ea, especially from the medial anulus, is increased (≥8 cm/s) and E/Ea is reduced with high filling pressures (see Chapter 17). Because PCWP can be e stimated reliably with E/Ea, estimation of PCWP with exercise is feasible ( 5, which is helpful is assessing patients who have exertional dyspnea (see diastolic stress test in Chapter 8).

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Figure 5-2 Tissue Doppler imaging can be color coded, with red indicating movement of myocardial tissue toward the transducer and blue indicating movement away from the transducer. A: The sample volume was placed in the mid septum, and myocardial tissue velocities o f systolic (Sm), early diastolic (Em), and late diastolic ( Am) velocities were recorded. Similar velocity patterns can be obtained automatically in a digitized form ( B and C). Still image of color -coded tissue Doppler imaging was obtained from the cardiac cycle indicated by the vertical red line during systole (B) and early diastole (C). AVC, aortic valve closure; AVO, aortic valve opening.

Evaluation of Regional and Global Systolic Function The extent of systolic movement of the mitral anulus correlates with LV systolic function and stroke volume. Normally, the systolic velocity (Sa or S′) of the mitral anulus is more than 6 cm/s. Although TDI of the mitral anulus reflects the global systolic and diastolic function of the LV, segmental or regional functi on can be assessed by performing TDI of various LV segments by placing the sample volume (2–5 mm) in the region of interest. The size of the sample volume depends on the location and intensity of the signal and is usually between 2 and 5 mm. Further clin ical experience with this variable will determine if Sa (or S′) can replace other more commonly used systolic variables.

Tissue Velocity Gradient TDI can measure the difference in velocities of adjacent myocardial tissues (velocity gradient), and this can be P.83

used to assess the viability and deformation (strain) of the myocardium (11). The velocity of the endocardium is normally higher than that of the epicardium, thus producing a tissue velocity gradient. In akinetic but viable or nontransmurally infarcted myocardium, the myocardial velocity gradient persists, but there is no velocity gradient in scarred or transmurally infarcted myocardium. Because days to weeks are needed for myocardial contractility to recover after successful reperfusion of an occluded

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techom coronary artery, measurement of the tissue velocity gradient can be useful in patients with an acute myocardial infarction. To record or display the myocardial velocity gradient, the direction of myocardial contractility needs to be aligned in parallel with the direction of the ultrasound beam. Therefore, imaging views are limited to the parasternal windows to image anterior or posterior walls.

Figure 5-3 Tissue Doppler imaging, strain rate, and strain imaging from a normal subject. A: The sample volume was placed at the basal portion of the inferior septum. Peak systolic velocity (Sm) was slightly more than 6 cm/s, early diastolic velocity (Em) was 10 cm/s, and late diastolic velocity ( Am) was 6 cm/s. B: Recording of strain rate, which represents the rate of deformation; the peak negative strain rate ( arrow) was 1.3/s. C: Strain recording, which is the integration of the strain rates; the negative peak strain ( arrow) occurred slightly after aortic valve closure ( AVC). The normal strain value is usually more than -15%. AVO, aortic valve opening.

Cardiac Time Intervals Cardiac time intervals are regulated precisely by the mechanics and functions of the myocytes; hence, these intervals are a good measure of cardiac function. TDI is well suited for determining the timing of myocardial events. The precise timing of these events is helpful in understanding the mechanism of myocardial relaxat ion 229

techom and myocardial suction during early diastolic filling ( 12,13,14). In healthy hearts, in which efficient myocardial relaxation is used effectively to suck blood from the LA into the LV during early diastole, the time of onset of mitral inflow (E) coinci des with that of myocardial early diastolic motion (relaxation) of the mitral anulus (Ea). However, in hearts with delayed myocardial relaxation and increased filling pressure, diastolic filling (onset of the E wave) depends more on the increased LA pressu re and occurs earlier than the onset of the early diastolic motion of the mitral anulus (Ea). Therefore, the time interval between the onset of mitral E velocity and that of the mitral anulus diastolic motion (Ea) increases, and this increased interval has been proposed as a new variable to assess LV filling pressures (see Chapter 8). A limitation of measuring cardiac time intervals by pulsed wave Doppler echocardiography is nonsimultaneity because different cardiac cycles are usually needed to measure vari ous intervals which in turn are used together. One solution is to have the capability of obtaining multiple P.84

pulsed wave Doppler recordings simultaneously. Another creative means to measure cardiac intervals from a single cardiac cycle is to use tissue Doppler anatomic color M -mode from the anterior mitral leaflet ( 15) (Fig. 5-4). From this technique, isovolumic contraction time, isovolumic relaxation time, and LV ejection time can be measured reliably from a single cardiac cycle.

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Figure 5-4 Tissue Doppler anatomic M -mode of the anterior mitral leaflet was obtained from color tissue Doppler imaging. Mitral motion recorded the timing of mitral valve closure (MVC), aortic valve opening ( AVO), aortic valve closure ( AVC), and mitral valve opening (MVO).

Mechanical dyssynchrony is measured by time intervals between peak ejection systolic velocities or peak strain of multiple myocardial segments, as discussed below.

Evaluation of Thick Walls The ventricular walls become thick for several reasons in cluding LV hypertrophy, hypertrophic cardiomyopathy, infiltrative cardiomyopathy, restrictive cardiomyopathy, and the athletic heart. These entities can usually be differentiated on the basis of clinical and laboratory findings, but differentiating them ca n occasionally be difficult. The evaluation of myocardial relaxation with TDI is able to distinguish between a thick athletic normal heart and other disease conditions ( 16). Mitral anulus motion is well preserved in the athletic heart because myocardial re laxation is preserved, but it is reduced in all other conditions that have impaired myocardial relaxation.

Prognostication

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techom Because E/Ea can estimate LV filling pressures and patients with increased filling pressures have higher rates of morbidity and mortality, it is expected that a high E/Ea predicts a poor outcome. E/Ea more than 15 was found to be associated with increased mortality of patients with acute myocardial infarction ( 17). By itself, Ea is also a good predictor for clinical outcome. In var ious clinical conditions, patients who have an Ea less than 5 cm/s are more likely to have a much higher mortality than those with an Ea more than 5 cm/s ( 18).

Strain and Strain Rate Imaging Myocardial velocities measured with TDI may be overestimated or underestimated by translational motion or tethering of the myocardium, respectively. This limitation can be overcome by measuring the actual extent of myocardial deformation (stretching or contraction) by strain (ε) and strain rate imaging ( Fig. 5-3). Strain rate is the rate of change in length calculated as the difference between two velocities normalized to the distance between them; it is expressed as seconds - 1 (19,20,21,22) (Fig. 55). By convention, shortening is represented by negative values and lengthening by positive values for both strain and strain rate: Strain rate = (V a - V b )/d where V a - V b is the instantaneous velocity difference at points a and b, and d is the distance between the two points. Strain (ε) is the percentage change in length du ring myocardial contraction and relaxation and is expressed as a percentage:

where L 0 is the original length, L 1 is the final length, and Δ L is the change in length. Strain can be derived echocardiographically by the following:

where strain (ε) is the sum of the instantaneous strain rate (SR) values from starting time (t 0 ) to ending time (t).

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Figure 5-5 Diagram of the concept of strain imaging. A narrow sector width was used to attempt to align the direction of myocardial movement in parallel wit h the direction of the ultrasound beam. (See text for details about how to obtain strain and strain rate.)

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Tissue tracking, also known as displacement, is similar to strain, except it is the integral of the tissue velocity over a given time. It represents the distance a region of interest moves relative to its original location ( Fig. 5-6).

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Figure 5-6 Tissue tracking imaging. The displacement of the tissue was color coded. The sample volume was placed at the mid portion of the septum, and tissue tracking demonstrated green and purple colors in the region of interest, corresponding to 6 to 8 mm of displ acement since the starting time demarcated by the first red bracket on the ECG tracing. AVC, aortic valve closure; AVO, aortic valve opening; Sm, peak systolic velocity.

In the normal heart, longitudinal strain rate values are similar from the base to the apex, unlike tissue velocity, which is higher at the base than at the apex ( 23). Every effort is made to ensure that the direction of tissue movement is less than 30 degrees from the direction of the beam ( Fig. 5-7), but this is technically challenging in the apical segments as the angle becomes wider ( 21,22). The narrow-sector angle approach on an individual wall obviates some of the above problems, which precludes concurrent comparison of contralateral segments. Strain imaging is similar to measuring the myocardial velocity gradient, which is limited to analyzing the myocardium that contracts in the direction that is parallel with the ultrasound beam. However, better spatial resolution and a higher frame rate (up to 200 frames/s) in strain rate imaging al low simultaneous calculation of the strain rate of the myocardium within a selected sector, which can be color coded ( Fig. 5-3). A curved cursor can be placed

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techom along the entire circumference of the LV to analyze regional strain rate. However, accurate measu rements of strain rate depend on properly aligning the ultrasound beam so it is parallel with the direction of myocardial motion.

Detection of Myocardial Ischemia Regional strain and strain rate are disturbed during the early stage of myocardial ischemia. Some studies have suggested that strain imaging is more sensitive for detecting acute ischemia than regional wall motion analysis ( 23,24). It has been shown that the longitudinal peak regional strain and strain rate decrease as wall motin worsens in patien ts with an acute myocardial infarction. During balloon inflation, systolic strain imaging has been shown to be more sensitive for detecting myocardial ischemia than TDI. This better sensitivity of strain rate imaging has also been shown during dobutamine stress echocardiography ( 25). An interesting observation during ischemia is regional delay in the onset of myocardial motion, which is difficult to identify visually ( 24). In acute ischemia, the transition from regional systole to early diastolic lengthenin g is delayed. When a time delay of more than 20% was used, it identified ischemic myocardium during dobutamine stress echocardiography with a sensitivity of 92% and a specificity of 75% ( 26). However, its main limitations are additional time in analysis, g ain dependency, and variability. Whether this quantitative assessment provides incremental diagnostic value is not certain, especially when the physician who is interpreting stress echocardiograms is experienced in regional wall motion analysis.

Assessment of Myocardial Viability The myocardial velocity gradient can be used to differentiate viable from nonviable myocardium in patients with an acute myocardial infarction treated with acute reperfusion ( 11). It has been observed that myocardial contraction oc curs even after closure of the aortic valve, called postsystolic shortening ( 27,28). This can be an indication of asynchronous motion during the isovolumic relaxation period. TDI and strain imaging are able to demonstrate this unusual cardiac motion ( Fig. 5-8). Postsystolic shortening of stunned myocardium may disappear with gradual infusion of dobutamine ( 29). The presence of postsystolic shortening during acute myocardial ischemia also predicts functional recovery after reperfusion therapy ( 27, 29).

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Evaluation of Cardiomyopathy By measuring regional myocardial function, TDI and strain imaging have potential incremental value for the evaluation of cardiomyopathy and diastolic heart failure. Thick walls due to athletic training would have normal TDI and stra in values, whereas thick walls due to infiltration or primary myopathy would have reduced values. In addition, the pattern of regional dysfunction may be different for various cardiomyopathies. TDI of myocardium provides different information from that of strain imaging because TDI is affected by translation as well as by actual movement of the tissue (Fig. 5-9). A report from France demonstrated that all components of strain were significantly reduced in hypertrophic cardiomyopathy despite an apparently no rmal LVEF. Average longitudinal, transverse, circumferential, and radial strain in patients with hypertrophic cardiomyopathy and control were -15% vs. -20%, -23% vs. -27%, -17% vs. -20%, and -25% vs. -37%, respectively ( 30). In patients with asymmetrical h ypertrophic cardiomyopathy, longitudinal septal strain was significantly lower than for other LV segments combined: -9% vs. -13% (P = .001).

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Figure 5-7 Diagram showing how to obtain strain imaging of basal to mid anterolateral (A), interventricular (B), inferolateral (C), anteroseptal (D), inferior (E), and anterior (F) left ventricular ( LV) wall segments; mid right ventricular free wall segments (G); interatrial septum (H); and midventricular short -axis LV segments (radial strain) (I). (From Gilman et al. [22]. Used with permission.)

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Speckle Tracking Echocardiography Speckle tracking is a method for quantifying myocardial motion in various planes using 2D images. Reflection, scattering, and

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techom interference of the ultrasound beam in the myocardial tissue produce a speckle formation. Myocardial regions with unique speckle patterns in the gray scale 2D image can be tracked from frame to frame throughout the cardiac cycle ( 30). This allows assessment of LV rotational motion, often referred to as torsio n or twist (Fig. 5-10). The spiral shape of the LV myocardial fibers results in a complex three -dimensional (3D) torsion mechanism for systolic contraction and untwisting for diastolic relaxation ( 31). The LV myocardium consists of P.87

two layers. The s ubendocardial layer wraps around the LV cavity in the direction of a right -handed helix, and the subepicardial layer wraps around in the direction of a left -handed helix. When viewed from the LV apex, apical rotation is counterclockwise and basal rotation is clockwise during systole. An analogy for LV contraction is the motion of wringing out a wet towel with your hands. As the two hands twist the ends of the towel in opposite directions the portion of the towel between the hands thickens and shortens longi tudinally.

Figure 5-8 Strain rate (A) and strain imaging (B) of a patient with postsystolic shortening ( arrow). Postsystolic shortening was present in the mid septum (aqua color). AVC, aortic valve closure; AVO, aortic valve opening.

Speckle tracking is an alternative method for quantification of LV systolic, and potentially diastolic, function. It also is another method for measuring strain using 2D images instead of the TDI method described above. Speckle tracking does not have the

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techom limitation of angl e dependence that TDI -derived strain measurements have.

Figure 5-9 A: Tissue Doppler imaging from basal ( yellow), mid (blue), and apical (red) segments of the ventricular septum in a patient with hypertrophic cardiomyopathy. Systolic velocities (Ss) from all three segments are decreased equally to 4 cm/s. B: Strain recordings from the same three segments are markedly different. Strain ( arrows) was normal at the apex (red, -30%) and decreased at the base ( yellow, -10%) and lengthened (blue, + 5%).

Dyssynchrony Assessment Biventricular pacemaker therapy, or cardiac resynchronization therapy (CRT), is a rapidly developing device therapy for heart failure. This therapy is unique in that cardiologists from at least three major subspecialties (heart fail ure, device, and echocardiography groups) are involved in the management of patients. In fact, echocardiography serves a vital role throughout the management from preimplant assessment to device optimization, evaluation of treatment efficacy, and, finally, to the prediction of a favorable response. Multiple echocardiographic techniques, especially new echocardiographic technologies, are used to assess systolic asynchrony (or dyssynchrony) of the ventricle or ventricles. Key aspects of the practical use of echocardiography in the CRT era are summarized below.

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Figure 5-10 Speckle tracking A: Top, Viewed from the apex, the apical rotation is counterclockwise ( top thick arrow ) and basal rotation is clockwise ( bottom thick arrow ). Bottom, Speckle tracking regi ons of interest are denoted by white boxes in the echocardiographic image of the animal model. Rotational changes are noted by the dotted white arrows during enddiastole and end-systole frames. B: Apical and basal rotation and torsion at Baseline, with Dobutamine, and with Ischemia. Dashed lines, rotation measured by implanted sonomicrometry crystals; solid lines, speckle tracking echo. LVP, left ventricular pressure; dP/dt, change in pressure/change in time. (From Helle-Valle et al. [30]. Used with perm ission.)

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Systolic Dyssynchrony of the Ventricle or Ventricles and Its Implication for Worsening of Heart Failure Systolic mechanical dyssynchrony can be defined as the uncoordinated timing of contraction in different regions of the heart. That is, myocardial segmental contractions do not occur

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techom simultaneously. Systolic dyssynchrony is commonly manifested as prolongation of the QRS duration on surface electrocardiography (ECG). This prolongation of the QRS duration is a relatively simple marker that i ndicates the presence of electromechanical coupling delay in the ventricle or ventricles. Morphologically, the prolonged QRS can be manifested in the form of a bundle branch block (left or right) or intraventricular conduction delay. QRS prolongation (>120 milliseconds) has been described in one -fourth to one-half of patients who have heart failure ( 32). Systolic dyssynchrony can be divided into intraventricular (within the LV) and interventricular (between the LV and right ventricle [RV]) dyssynchrony. Intraventricular dyssynchrony results in a fragmented profile of ineffective contraction, with prolongation of the isovolumic contraction and relaxation times. The regional “shifting† rather than ejection of blood from the LV worsens regional wall stress and aggravates mitral regurgitation. These factors, in combination with activation of neurohormonal and proinflammatory cytokine pathways, accelerate cardiac dilatation, resulting in progressive LV dilatation and cardiac remodeling. Interventricular dyssynchrony, especially in the presence of paradoxical septal motion in systole, may adversely affect RV function, further impeding venous return to the LV.

Cardiac Resynchronization Therapy for Heart Failure CRT is designed to pace different regions of the ventricles simultaneously. Two ventricular pacing leads are implanted: one is implanted by the coronary sinus or epicardial approach at the LV free wall region, and the other is implanted by the conventional RV approach at the septum. Currently, P.89

CRT is recommended for patients who have advanced heart failure with New York Heart Association functional class III or IV, QRS duration longer than 130 milliseconds, systolic dysfunction, and LV dilatation, an d heart failure refractory to optimal medical therapy (33). The proven benefits of CRT include improvement in heart failure symptoms, exercise capacity (e.g., 6 -minute walk distance), quality of life, heart failure rehospitalization, and mortality (34,35,36). Other important and objective indicators of structural and functional benefits with CRT include echocardiographic

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techom evidence of LV reverse remodeling and improvement of systolic function (37).

Patient Selection for Implantation of CRT Echocardiography is the first step for confirming and assessing the severity of LV systolic dysfunction, in particular, identifying patients who have a low LVEF (typically AV s h o r t + QA s h o r t (AV l o n g + QA l o n g ) - (AV s h o r t + QA s h o r t ) = Δ t = the degree of “A† wave truncation Optimum AV delay + AV short + Δ t If the patient has pronounced mitral regurgitation, the Ishikawa method can be attempted. A long AV delay is chosen that results in either diastolic mitral regurgitation or diastasis until isovolumic contraction, when systolic mitral regurgitation commences. The duration of diastolic mitral regurgitation or diastasis is subtracted from the long AV interval, yielding an optimum AV interval that places the end of the atrial filling wave at the onset of isovolumic contraction.

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techom A recent investigation ha s suggested that the optimum AV delay as defined by the Ritter formula does not work as well as a maximized mitral inflow time velocity integral or duration when compared with invasive indices of systolic function ( 40). This observation may result from the diminutive “A† wave in patients with restrictive filling and associated modest differences in “A† wave duration at long and short AV delays. The atrial contribution to filling may also attenuate at the higher LV pressure of late diastole. Thus, it is appropriate to consider an “iterative† P.90

approach to optimization of diastolic filling, in which an AV interval is chosen that yields the most robust appearing atrial contribution to filling. Optimization of forward cardiac output can also be examined. In this approach, the time velocity integral of forward flow at the LV outflow tract (LVOT) is measured at multiple AV intervals, typically 20 milliseconds apart, and selected to maintain biventricular stimulation. The largest time velocity integ ral corresponds to the highest stroke volume and, presumably, the optimum AV delay.

Figure 5-11 Ritter method for atrioventricular ( AV) optimization with cardiac resynchronization therapy. A: Pulsed wave mitral inflow assessment of QA l o n g interval (56

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milliseconds) in the setting of a long pacemaker AV delay of 150 milliseconds. T 1 and T 2 , two time measurements. B: QA s h o r t interval (146 milliseconds) in the setting of a short pacemaker AV delay of 50 milliseconds. C: Optimal AV delay was calculated to be 150 milliseconds - (146 milliseconds - 56 milliseconds) = 60 milliseconds. This AV delay allowed for a complete A wave without truncation, while minimizing E and A wave fusion.

Centers vary in inclination to formally optimize the AV delay after implantation of a biventricular device. Some institutions, including our own, select an empiric AV interval of 100 milliseconds after sensed P wave and perhaps a 50 -millisecond larger AV interval after paced P wave, recognizing that these values are comparable to the values typically derived by echocardiographic AV optimization in randomized trials. Formal AV optimization is generally reserved for nonresponders to CRT. If formal AV optimization is to be performed routinely, it should be repeated in long-term follow-up because changes in the optimum AV delay over time have been described in a substantial number of patients.

Optimization of Interventricular Interval After CRT It has been proposed that sequential biventricular stimulation, in which LV or RV stimulation precedes the other by 20 to 60 milliseconds, may compensate for regional delays in LV activation or suboptimal coronary sinus lead placement during CRT and thereby provide greater LV synchrony than simultaneous biventricular stimulation, in which LV and RV stimulation occur at the same time. Small studies using CRT patients as their own controls have demonstrated improved indices of systolic function or dyssynchrony (or both) with sequential compared to simultaneous biventricular stimulation. As with AV optimization, centers must decide whether to optimize the VV interval in all CRT recipients or reserve this optimization for nonresponders. The most common approach to VV optimization involves stroke volume assessment at the LVOT P.91

at various VV offsets typically separated by approximately 20 milliseconds. Although trials of VV optimization have generally 245

techom optimized the AV interval first, there is some logic to optimizing the VV interval first because of the potential influence of improv ed LV synchrony on the diastolic filling period. In either approach, it must be remembered that current devices define the AV interval as the time delay from atrial channel to first ventricular channel. Therefore, when RV first VV offsets are tested, the A V delay must be shortened by a time equal to the VV offset to maintain an unchanged mechanical interval from LA to LV contraction.

The Role of Echocardiography in Identifying Nonresponders of CRT Despite compelling evidence for the benefit of CRT, about on e-third of patients do not have a response to this treatment ( 35,38). This is because ECG is not a sensitive marker for predicting the presence or absence of electrical activation delay in the LV or electromechanical coupling delay. The other contributing factor for the lack of a favorable response to CRT is placement of the LV lead at a suboptimal site where the efficacy of resynchronization therapy is greatly reduced. Several methods have been used to characterize nonresponders to CRT, including hemodynam ic, clinical, and echocardiographic variables. It is important to appreciate that the prevalence of nonresponders is higher (54%) among patients with a borderline prolonged QRS duration of 120 to 150 milliseconds than among those (32%) with a severely prol onged QRS duration of more than 150 milliseconds ( 41).

Echocardiographic Tools for the Assessment of Systolic Asynchrony A few echocardiographic tools have been described for the assessment of mechanical dyssynchrony in systole. These include the M-mode measurement of septal -to-posterior wall delay, Doppler echocardiography for interventricular mechanical delay, TDI for assessment of regional delay and calculation of indices of systolic asynchrony based on different models of 2 to 12 LV segments, 3D echocar diography, and postprocessing of TDI such as strain, strain rate, displacement mapping, and tissue synchronization imaging.

M-Mode Measurement

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techom Parasternal long -axis or short-axis views of the LV can be used for the M-mode assessment of dyssynchrony ( Fig. 5-12 A). The septal to-posterior wall motion delay can be calculated by the difference in the time to peak inward movement of the ventricular septum and posterolateral walls ( 42). A septal -to-posterior wall motion delay of 130 milliseconds or more predicts those who are more likely to have improvement with CRT. One potential limitation of this method is that it assesses only the mechanical timing delay between two segments of the ventricle. Another limitation is that if patients have an akinetic septum there is no peak to measure for septal inward motion. M -mode recording color TDI of the septum and the posterior wall may make it easier to measure wall motion delay (Fig. 5-2 B).

Pulsed Wave Doppler Measurement Pulsed wave Doppler measurements at the LVOT and RV outflow tract can provide information about both intraventricular and interventricular dyssynchrony. The aortic preejection time is measured with pulsed wave Doppler echocardiography from the onset of the QRS complex on ECG to the onset of LVOT flow ( Fig. 5-13). Whether the onset of the QRS complex or the peak of the R wave is used as a reference point for timing measurements is not important for measurements comparing the difference in time to peak velocity between two or more ventricular segments. Howe ver, it is important to use the onset of the QRS complex as the reference point for measuring aortic preejection time because it represents the time from electrical activation to the onset of flow through the LVOT. The aortic preejection time is prolonged in patients who have LV dyssynchrony.

Tissue Doppler Imaging TDI allows measurement of peak systolic velocity in the ejection phase of different regions of the myocardium. Moreover, systolic dyssynchrony can be assessed by measuring the precise timing of peak systolic velocity in the ejection phase (Ts) with reference to the beginning of the QRS complex ( Fig. 5-14). Integration of this information allows an accurate assessment of electromechanical coupling and evaluation of interventricular and intraventric ular dyssynchrony. Septal -to-lateral wall delay can be assessed with pulsed wave tissue Doppler measurement of the difference in the Ts for the basal septal and basal lateral walls ( Fig. 5-15). A timing

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techom delay of more than 60 milliseconds has been reported to have some predictive value for CRT responders ( 43). The assessment of multiple segments with TDI has the theoretic advantage of having the capability of examining different patterns of systolic asynchrony, such as those with delay other than septal to-lateral wall delay. In this regard, the use of 2D color -coded TDI is advantageous, in which cine loops of multiple views are collected and analyzed objectively off -line. In the six-basal, six-mid segmental model, the dyssynchrony index is derived by calcula ting the standard deviation of Ts of the 12 LV segments (or Ts -SD). From the apical four -chamber, two-chamber, and five-chamber (or apical long -axis) views, six basal, and six mid segments are obtained in the LV, namely the septal, lateral, anterior, infer ior, anteroseptal, and posterior segments at both basal and mid levels ( 38,42). The systolic myocardial velocities consist of an isovolumic contraction phase and ejection phase, both of which are positively directed, that P.92

is, apically directed. During diastole, it consists of the isovolumic relaxation phase (negative or biphasic profiles), early diastolic relaxation, and late diastolic relaxation, which is negatively directed. To calculate the dyssynchrony index, the peak myocardial systolic velocity is identified from 12 segments. To measure the time to peak systolic velocity in the ejection phase (Ts) of individual segments, use the following rules of thumb: 

Use aortic valve opening and closure markers that superimpose on TDI tracings to guide t he identification of the ejection phase (from a Doppler recording of the LVOT or aortic valve in the apical long -axis view).



Measure the time from the onset of the QRS complex to the highest systolic peak during the ejection phase (between aortic valve opening and closure).



If there are multiple peaks in the ejection phase, use the highest peak.



If two or more peaks in the ejection phase have the same amplitude in velocity, then choose the earliest peak among those with the same highest velocity.



If the segment has only a negative peak in the ejection phase or the velocity is so noisy with very low and inconsistent

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techom velocities, neglect those particular segments and proceed with the rest of the measurable segments. 

Do not measure Ts on the isovolumic contracti on phase or isovolumic relaxation phase or during postsystolic shortening.

Figure 5-12 A: Intraventricular dyssynchrony measurement by M-mode echocardiography. Left, The M-mode echocardiogram of the left ventricle shows synchronous motion ( arrows) of the interventricular septum and posterior wall, with simultaneous peak systolic ejection. Right, The M-mode of the left ventricle shows dyssynchronous or asynchronous peak contraction (arrows) of the septum and posterior wall. B: Left, When wall motion is reduced (the ventricular septum [ VS] in this patient with reduced left ventricular ejection fraction and left bundle branch block), it is difficult to identify the peak of systolic ejection (right). Right, Color M-mode of tissue Doppler imaging clearly identifies the peak of systolic contraction simply by change in color—from blue to red in VS and from red to blue in the posterior wall ( PW). The space between the two dotted lines indicates the time between two systolic peaks. LV, left ventricle.

The Ts-SD is calculated as the standard deviation of Ts among six basal, six mid LV segments ( Fig. 5-16)—the larger the value of Ts-SD, the more severe the systolic asynchrony.

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Figure 5-13 Determination of interventricular dyssynchrony. Left, Left ventricular outflow tract velocity was obtained from the apical long -axis view, and the interval ( arrows) from the onset of the QRS to the onset of the left ventricular outflow tract velocity was measured. This is the preejection interval of the left ventr icle. Right, Pulsed wave Doppler examination from the right ventricular outflow tract from the parasternal short axis view. The interval ( arrows) from the onset of the QRS to the onset of the right ventricular outflow tract velocity was measured. This is t he preejection time for the right ventricular outflow tract. The difference between these two intervals is the interventricular dyssynchrony timing. The normal value is less than 40 milliseconds.

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To apply an echocardiographic index of systolic dyss ynchrony in clinical practice, it is mandated that a cutoff value be identified objectively to determine clinically relevant systolic asynchrony. Furthermore, a variable needs to predict a favorable response with high sensitivity to be incorporated as a sc reening test or high specificity as a “rule in† test to ascertain the presence of systolic dyssynchrony. The key studies that examined intraventricular or interventricular asynchrony by TDI and its postprocessing technologies which also derived a cutof f value for predicting a favorable response to CRT are summarized in Table 52 (38,43,44,45,46,47,48,49,50). These studies ranged from the assessment of 2 to 12 LV segments with TDI.

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Figure 5-14 Tissue velocity (A) and strain imaging (B) in a normal subject. Time to peak tissue velocity is measured from QRS onset to the systolic peak ( red arrowheads in A) during the ejection period. Maximum strain ( red arrowheads in B) often occurs shortly after aortic valve closure ( AVC) in a normal popu lation. AVO, aortic valve opening.

It should be noted, however, that there is a large overlap between the Ts-SD of normal subjects and that of patients with poor LVEF and left bundle branch block. In the Mayo Clinic experience, standard deviation of time intervals obtained by strain imaging is more specific for patients with poor LVEF and left bundle branch block. As a CRT Working Group at Mayo Clinic, we are performing a P.94

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prospective study of 200 patients undergoing CRT to assess various aspects of this impressive device therapy for those with systolic heart failure. The aim is to provide the most reliable and practical approach for identifying the patients who will benefit from CRT.

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Figure 5-15 Tissue velocity assessment of septal -to-lateral delay (95 milliseconds). Time is measured from the onset of the QRS complex to the peak tissue velocity (between arrows) during the ejection period. The isovolumic contraction peak that occurs during or imme diately after the QRS complex is not used for this measurement of dyssynchrony. TDI, tissue Doppler imaging.

Table 5-2 Published criteria of systolic asynchrony by tissue Doppler imaging that predict a favorable echocardiographic response to cardiac resynchronization therapy

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onset of myocardial systolic velocity; Ts -SD, standard deviation of time to peak myocardial systolic velocity.

Figure 5-16 A and B: Tissue Doppler velocity recordings from four segments of the left ventricle in the apical four -chamber view. There is a marked difference in the timing of basal lateral (red) and other segments at baseline before cardiac resynchronization therapy (CRT) (A). Post-CRT timing of the four segments was much better coordinated, with improved

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synchrony (B). C and D: Pre- and post-CRT timing measurements from the apical two -chamber view. There was a significant difference between the peak velocity from the basal inferior wall (yellow) and other segments (C). Post-CRT measurements showed improvement in dyssynchrony, although there is still some difference in the timing of peak systolic velocities (D). E and F: Pre- and post-CRT timing measurements from the apical lo ng-axis view showing improved synchrony of the four segments (F) compared with baseline (E). AVC, aortic valve closure; AVO, aortic valve opening.

Pacing therapy for inappropriately selected patients could actually result in worsening of mechanical asynch rony.

Mechanical Dyssynchrony in Patients with Heart Failure and a Narrow QRS LV mechanical dyssynchrony in fact is present in patients with heart failure who have normal QRS duration. This phenomenon was first described with TDI, in which a Ts -SD value of more than 32.6 milliseconds (a cutoff value derived from the normal population) was identified in 43% of patients with heart failure who had narrow QRS complexes ( 51). Two subsequent studies have also reported the presence of intraventricular dyssynchrony in a similar population ( 52). The use of TDI or strain to identify systolic dyssynchrony in a population with a narrow QRS complex may potentially help more patients with heart failure to benefit from CRT. In a recent pilot study, improvement in clinical status, cardiac function, and LV reverse remodeling was observed after CRT in such a population ( 53).

Assessment of the Mechanism of Benefit of CRT by Echocardiography In patients with heart failure who have a prolonged QRS duration, widespread LV delay has been observed among various LV segments, with a large variation in regional Ts. CRT achieved systolic synchronicity by homogeneously delaying the time of early contracting segments to a time similar to that of the delayed segments. Therefore, not only was septal -to-lateral delay abolished, but other patterns of delay were corrected. Furthermore, improvement in regional displacement, strain, and

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techom strain rate has been reported ( 54). When interventricular dyssynchrony was examined, the septal -to-RV free wall delay also improved after CRT ( 37). The improvement of intraventricular dyssynchrony is probably the main mechanism for mediating the echocardiographic benefits of CRT, which include LV reverse remodeling, improvement in systolic function, reduction of m itral regurgitation, and gain in LV diastolic filling time. Of interest, all the echocardiographic benefits are pacing -dependent, and withholding pacing results in progressive worsening of these indices (37). In fact, LV reverse remodeling not only represe nts a structural benefit of the heart but is also a strong predictor of favorable long -term outcome, such as all -cause mortality or hospitalization for heart failure (or both) ( 39). Apart from the predictive outcome, the degree of LV reverse remodeling is related closely to the amount of systolic dyssynchrony before pacing.

Figure 5-17 Pre–cardiac resynchronization therapy (CRT) (A) and post-CRT (B) dyssynchrony measurement with 3D echocardiography. The volumetric changes of 16 left ventricular segments are recorded, and the smallest volume of the 16 segments occurs more closely together post -CRT (B) than at baseline (A). Ant, anterior; Inf, inferior; Lat, lateral; Post, posterior; Sept, septal.

Future Perspectives in the Echocardiographic Assessment of CRT There is a continuous quest for identifying responders to CRT more accurately in order to decrease the number of nonresponders and to improve the cost -effectiveness of the treatment. In this regard, echocardiography holds promise because it is nonin vasive and readily available and serial assessment is harmless to patients with 258

techom implanted devices. Therefore, echocardiography potentially could be used as an adjunctive measure in patient selection, regardless of QRS duration. It is important that present knowledge be integrated into clinical practice so that prospective clinical trials can be conducted to examine the efficacy of CRT based on the use of established indices of systolic asynchrony in patients who have a wide range of QRS durations. Echocardi ographic technology for assessing systolic asynchrony is also evolving, and those that are potentially useful include 3D echocardiography and tissue synchronization imaging. With 3D echocardiography, complete 3D volume-rendered data can be captured within a few beats (Fig. 517). The time to minimum volume can be determined for each of the 16 segments of the LV. A standard deviation index of these variables can be calculated to assess the degree of intraventricular asynchrony. With the continuous improvemen t in image quality, P.97

acquisition capability, and the speed and accuracy of off -line analysis of systolic asynchrony in multiple segments, 3D echocardiography has a good potential to be applied as a screening tool (55).

Figure 5-18 Tissue synchronization imaging (TSI) ( top left) and regular two -dimensional imaging ( bottom left). Green

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areas, segments with an early time to peak tissue velocity. Red area, the segment with the greatest delay in time to peak tissue velocity. Visualizing the tissue velocity curves allows confirmation of the correct position of the TSI brackets on the ECG (red brackets ). Note they were positioned to coincide with the ejection period (time from aortic valve opening [ AVO] to aortic valve closure [ AVC]).

Tissue synchronization imaging allows rapid visual and semiquantitative identification of regional delay in the LV, and automated calculation of the indices of systolic dyssynchrony is possible (46,47). This offers the advantage of a color -coded display that highlights the areas of the ventricle that have the greatest delay (Fig. 5-18). A potential limitation is that the peak velocity needed for automated calculations can be measured incorrectly from the TDI curves. This can be detected by examining the raw TDI curves and ensuring that the tissue synchronization imaging starting and ending brackets on the ECG are correctly located close to the time of aortic valve opening and closure, respectively. The role of other postprocessing imaging of TDI, such as dis placement and strain mapping, remains to be determined ( 50). To be widely accepted clinically, the optimal method for assessing ventricular dyssynchrony should be accurate, not exceedingly time consuming, and widely available, with technology that is or so on will be available in most echocardiography laboratories. Work continues in this field to determine which method of asynchrony assessment will be accepted routinely for selecting patients for CRT.

References 1. Isaaz K, Thompson A, Ethevenot G, et al. Doppler echocardiographic measurement of low velocity motion of the left ventricular posterior wall. American Journal of Cardiology, 1989;64:66–75. 2. McDicken WN, Sutherland GR, Moran CM, et al. Colour Doppler velocity imaging of the myocardium. Ultraso und in Medicine & Biology, 1992;18:651–654. 3. Sohn DW, Chai IH, Lee DJ, et al. Assessment of mitral annulus velocity by Doppler tissue imaging in the evaluation of left ventricular diastolic function. Journal of the American College of Cardiology, 1997; 30:474–480. 260

techom 4. Nagueh SF, Sun H, Kopelen HA, et al. Hemodynamic determinants of the mitral annulus diastolic velocities by tissue Doppler. Journal of the American College of Cardiology, 2001;37:278–285. 5. Ha JW, Oh JK, Pellikka PA, et al. Diastolic st ress echocardiography: A novel noninvasive diagnostic test for diastolic dysfunction using supine bicycle exercise Doppler echocardiography. Journal of the American Society of Echocardiography, 2005;18:63–68. 6. Khankirawatana B, Khankirawatana S, Peters on B, et al. Peak atrial systolic mitral annular velocity by Doppler tissue reliably predicts left atrial systolic function. Journal of the American Society of Echocardiography, 2004;17:353–360. 7. Nagueh SF, Middleton KJ, Kopelen HA, et al. Doppler tiss ue imaging: A noninvasive technique for evaluation of left ventricular relaxation and estimation of filling pressures. Journal of the American College of Cardiology, 1997;30:1527–1533. 8. Ommen SR, Nishimura RA, Appleton CP, et al. Clinical utility of Doppler echocardiography and tissue Doppler imaging in the estimation of left ventricular filling pressures: A comparative simultaneous Doppler -catheterization study. Circulation, 2000;102:1788–1794. 9. Nagueh SF, Mikati I, Kopelen HA, et al. Doppler estim ation of left ventricular filling pressure in sinus tachycardia: A new application of tissue Doppler imaging. Circulation, 1998;98:1644–1650. 10. Sohn DW, Song JM, Zo JH, et al. Mitral annulus velocity in the evaluation of left ventricular diastolic func tion in atrial fibrillation. Journal of the American Society of Echocardiography, 1999;12:927–931. 11. Derumeaux G, Ovize M, Loufoua J, et al. Assessment of nonuniformity of transmural myocardial velocities by color -coded tissue Doppler imaging: Characte rization of normal, ischemic, and stunned myocardium. Circulation, 2000;101:1390–1395. 12. Oh JK, Tajik AJ. The return of cardiac time intervals: The phoenix is rising. Journal of the American College of Cardiology, 2003;42:1471–1474.

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techom 13. Hasegawa H, Little WC, Ohno M, et al. Diastolic mitral annular velocity during the development of heart failure. Journal of the American College of Cardiology, 2003;41:1590–1597. 14. Diwan A, McCulloch M, Lawrie GM, et al. Doppler estimation of left ventricular filli ng pressures in patients with mitral valve disease. Circulation, 2005 Jun 21;111:3281–3289. Epub 2005 Jun 13. 15. Kjaergaard J, Hassager C, Oh JK, et al. Measurement of cardiac time intervals by Doppler tissue M -mode imaging of the anterior mitral leaflet. Journal of the American Society of Echocardiography, 2005;18:1058–1065. 16. Derumeaux G, Mulder P, Richard V, et al. Tissue Doppler imaging differentiates physiological from pathological pressure overload left ventricular hypertrophy in rats. Ci rculation, 2002;105:1602–1608. 17. Hillis GS, Møller JE, Pellikka PA, et al. Noninvasive estimation of left ventricular filling pressure by E/e′: A powerful predictor of survival following acute myocardial infarction [abstract]. Journal of the America n College of Cardiology, 2003;41:452A. 18. Wang M, Yip GW, Wang AY, et al. Peak early diastolic mitral annulus velocity by tissue Doppler imaging adds independent and incremental prognostic value. Journal of the American College of Cardiology, 2003;41:820â €“826. 19. Heimdal A, Stoylen A, Torp H, et al. Real -time strain rate imaging of the left ventricle by ultrasound. Journal of the American Society of Echocardiography, 1998;11:1013–1019. 20. Sutherland GR, Di Salvo G, Claus P, et al. Strain and strain rate imaging: A new clinical approach to quantifying regional myocardial function. Journal of the American Society of Echocardiography, 2004;17:788–802. 21. Yip G, Abraham T, Belohlavek M, et al. Clinical applications of strain rate imaging. Journal of the American Society of Echocardiography, 2003;16:1334–1342. 22. Gilman G, Khandheria BK, Hagen ME, et al. Strain rate and strain: A step -by-step approach to image and data acquisition. Journal of the American Society of Echocardiography, 2004;17:1011–102 0. 23. Kowalski M, Kukulski T, Jamal F, et al. Can natural strain and strain rate quantify regional myocardial deformation? A study in

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28. Jamal F, Szilard M, Kukulski T, et al. Changes in systolic and postsystolic wall thickening during acute coronary occlusi on and reperfusion in closed -chest pigs: Implications for the assessment of regional myocardial function. Journal of the American Society of Echocardiography, 2001;14:691–697. 29. Rambaldi R, Bax JJ, Rizzello V, et al. Post -systolic shortening during dobutamine stress echocardiography predicts cardiac survival in patients with severe left ventricular dysfunction. Coronary Artery Disease, 2005;16:141–145. 30. Helle-Valle T, Crosby J, Edvardsen T, et al. New noninvasive method for assessment of left ventr icular rotation: Speckle tracking echocardiography. Circulation, 2005;112:3149–3156. 31. Sengupta PP, Khandheria BK, Korinek J, et al. Apex -to-base dispersion in regional timing of left ventricular shortening and lengthening. Journal of the American Coll ege of Cardiology, 2006 Jan 3;47:163–172. Epub 2005 Dec 1.

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techom 32. Baldasseroni S, Opasich C, Gorini M, et al., Italian Network on Congestive Heart Failure Investigators. Left bundle -branch block is associated with increased 1 -year sudden and total mortality rate in 5517 outpatients with congestive heart failure: A report from the Italian Network on Congestive Heart Failure. American Heart Journal, 2002;143:398–405. 33. Gregoratos G, Abrams J, Epstein AE, et al., American College of Cardiology/American Heart Association Task Force on Practice Guidelines/North American Society for Pacing and Electrophysiology Committee to Update the 1998 Pacemaker Guidelines. ACC/AHA/NASPE 2002 guideline update for implantation of cardiac pacemakers and antiarrhythmia dev ices: Summary article: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/NASPE Committee to Update the 1998 Pacemaker Guidelines). Circulation, 2002;106:2145–2161. 34. Cazeau S, Leclercq C, Lavergne T, et al., Multisite Stimulation in Cardiomyopathies (MUSTIC) Study Investigators. Effects of multisite biventricular pacing in patients with heart failure and intraventricular conduction delay. New England Journal of Medicine, 2001;344:873–8 80. 35. Abraham WT, Fisher WG, Smith AL, et al., MIRACLE Study Group, Multicenter InSync Randomized Clinical Evaluation. Cardiac resynchronization in chronic heart failure. New England Journal of Medicine, 2002;346:1845–1853. 36. Bristow MR, Saxon LA, Bo ehmer J, et al., Comparison of Medical Therapy, Pacing, and Defibrillation in Heart Failure (COMPANION) Investigators. Cardiac -resynchronization therapy with or without an implantable defibrillator in advanced chronic heart failure. New England Journal of Medicine, 2004;350:2140–2150. 37. Yu CM, Chau E, Sanderson JE, et al. Tissue Doppler echocardiographic evidence of reverse remodeling and improved synchronicity by simultaneously delaying regional contraction after biventricular pacing therapy in heart f ailure. Circulation, 2002;105:438–445. 38. Yu CM, Fung JW, Zhang Q, et al. Tissue Doppler imaging is superior to strain rate imaging and postsystolic shortening on the prediction of reverse remodeling in both ischemic and nonischemic heart failure after cardiac resynchronization therapy. Circulation, 2004 Jul 6;110:66–73. Epub 2004 Jun 14. 264

techom 39. Yu CM, Bleeker GB, Fung JW, et al. Left ventricular reverse remodeling but not clinical improvement predicts long -term survival after cardiac resynchronization th erapy. Circulation, 2005 Sep 13;112:1580–1586. Epub 2005 Sep 6. 40. Jansen AH, Bracke FA, van Dantzig JM, et al. Correlation of echo-Doppler optimization of atrioventricular delay in cardiac resynchronization therapy with invasive hemodynamics in patient s with heart failure secondary to ischemic or idiopathic dilated cardiomyopathy. American Journal of Cardiology, 2006 Feb 15;97:552–557. Epub 2006 Jan 4. 41. Yu CM, Fung JW, Chan CK, et al. Comparison of efficacy of reverse remodeling and clinical improvement for relatively narrow and wide QRS complexes after cardiac resynchronization therapy for heart failure. Journal of Cardiovascular Electrophysiology, 2004;15:1058–1065. 42. Yu CM, Fung WH, Lin H, et al. Predictors of left ventricular reverse r emodeling after cardiac resynchronization therapy for heart failure secondary to idiopathic dilated or ischemic cardiomyopathy. American Journal of Cardiology, 2003;91:684–688. 43. Bax JJ, Marwick TH, Molhoek SG, et al. Left ventricular dyssynchrony pred icts benefit of cardiac resynchronization therapy in patients with end -stage heart failure before pacemaker implantation. American Journal of Cardiology, 2003;92:1238–1240. 44. Penicka M, Bartunek J, De Bruyne B, et al. Improvement of left ventricular fu nction after cardiac resynchronization therapy is predicted by tissue Doppler imaging echocardiography. Circulation, 2004 Mar 2;109:978–983. Epub 2004 Feb 9. 45. Notabartolo D, Merlino JD, Smith AL, et al. Usefulness of the peak velocity difference by ti ssue Doppler imaging technique as an effective predictor of response to cardiac resynchronization therapy. American Journal of Cardiology, 2004;94:817–820. 46. Gorcsan J III, Kanzaki H, Bazaz R, et al. Usefulness of echocardiographic tissue synchronizati on imaging to predict acute response to cardiac resynchronization therapy. American Journal of Cardiology, 2004;93:1178–1181. 47. Yu CM, Zhang Q, Fung JW, et al. A novel tool to assess systolic asynchrony and identify responders of cardiac resynchronizat ion

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techom therapy by tissue synchronization imaging. Journal of the American College of Cardiology, 2005;45:677–684. 48. Mele D, Pasanisi G, Capasso F, et al. Left intraventricular myocardial deformation dyssynchrony identifies responders to cardiac resynchron ization therapy in patients with heart failure. European Heart Journal, 2006 May;27:1070–1078. Epub 2006 Mar 30. 49. Suffoletto MS, Dohi K, Cannesson M, et al. Novel speckle tracking radial strain from routine black -and-white echocardiographic images to quantify dyssynchrony and predict response to cardiac resynchonization therapy. Circulation, 2006 Feb 21;113:960–968. Epub 2006 Feb 13. 50. Miyazaki C, Lin G, Powell BD, et al. Prediction of the effect of cardiac resynchronization therapy by cardiac timi ng intervals and mechanical dyssynchrony by strain imaging. Journal of the American Society of Echocardiography, 2006;19:666. 51. Yu CM, Lin H, Zhang Q, et al. High prevalence of left ventricular systolic and diastolic asynchrony in patients with congestive heart failure and normal QRS duration. Heart, 2003;89:54–60. 52. Bleeker GB, Schalij MJ, Molhoek SG, et al. Relationship between QRS duration and left ventricular dyssynchrony in patients with end-stage heart failure. Journal of Cardiovascular Electrophysiology, 2004;15:544–549. 53. Achilli A, Sassara M, Ficili S, et al. Long -term effectiveness of cardiac resynchronization therapy in patients with refractory heart failure and “narrow† QRS. Journal of the American College of Cardiology, 2003;42:211 7–2124. 54. Sun JP, Chinchoy E, Donal E, et al. Evaluation of ventricular synchrony using novel Doppler echocardiographic indices in patients with heart failure receiving cardiac resynchronization therapy. Journal of the American Society of Echocardiogra phy, 2004;17:845–850. 55. Zhang Q, Yu CM, Fung JW, et al. Assessment of the effect of cardiac resynchronization therapy on intraventricular mechanical synchronicity by regional volumetric changes. American Journal of Cardiology, 2005;95:126–129.

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9. 6 - Contrast Echocardiography 6 Contrast Echocardiography Contrast echocardiography has been available since the early stage of echocardiography, when indocyanine green and agitated saline were used to identify cardiac structures seen on M -mode and twodimensional (2D) echocardiography ( 1,2). The clinical applications of contrast echocardiography have been expanded, and it is now used to identify intracardiac and intrapulmonary shunts, to augment Doppler velocity signals, to enhance the endocardial border, and, most recently, to assess myocardial perfusion. In an echocardiography practice, agitated saline or a contrast agent is used daily in 10% to 15% of all studies and in 30% to 40% of stress tests. This chapter discusses the routine clinical use an d potential future applications of contrast echocardiography.

Evaluation of Shunts The most frequent shunt lesion evaluated in an echocardiography laboratory is an atrial shunt through a patent foramen ovale, which is a common finding even in a normal popu lation. The evaluation can be made with either transthoracic or transesophageal echocardiography ( Fig. 6-1 and 6-2). With transthoracic echocardiography, either the apical four -chamber view or subcostal view is used. With transesophageal echocardiography, the 0-degree transverse or 90 -degree atrial septal view (with the transducer rotated clockwise) is optimal for imaging. An intravenous catheter is required (usually in an arm vein), with a three -way stopcock and two 12-mL syringes to agitate the saline imm ediately before it is injected. Bubbles created by agitated saline do not appear in the left side of the heart unless there is a communication between the right and left chambers. With a three -way stopcock, 10 mL of saline can be squirted back and forth (i .e., agitated) between two syringes at least five times before the saline is injected into the venous circulation. To facilitate the saline injection, the upper arm is massaged with two hands soon after the injection is made. The injection should be coordi nated with the person who performs echocardiography so that the most optimal imaging view for identifying a suspected shunt lesion is shown on the screen when the saline is injected. If an atrial shunt is present, bubbles from the agitated saline will appe ar immediately in the left atrium after

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techom being seen in the right atrium. In case of a left -to-right shunt, a negative contrast effect is seen. If the patient has an intrapulmonary shunt, more than three cardiac cycles may be needed for the bubbles to go thr ough the pulmonary circulation before they appear in the left atrium. An intrapulmonary shunt can be located by visualizing the pulmonary veins with transesophageal echocardiography ( Fig. 6-3). Another indication for agitated saline is the evaluation of a persistent left superior vena cava that drains into the coronary sinus. In this case, agitated saline should be injected into a left arm vein. The enlarged coronary sinus in the left atrioventricular groove will be opacified ( Fig. 6-4), although both the l eft and right superior vena cava can drain into the coronary sinus.

Augmentation of the Doppler Velocity Signal Bubbles created by agitated saline strengthen Doppler velocity signals from the right heart chambers. To estimate right ventricular (RV) and pul monary artery systolic pressure, it is necessary to record tricuspid regurgitation velocity, which may not be detectable in 30% of patients. In some patients, the tricuspid regurgitation signal is faint and a stronger signal is needed to provide a reliable estimate P.100

of RV systolic pressure. Agitated saline (prepared as described above) improves the chance of obtaining tricuspid regurgitation signals (see Chapter 9). However, if tricuspid regurgitation is not detected with color flow imaging, its sign al is not likely to appear even with the injection of agitated saline.

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Figure 6-1 Left and right, Transthoracic echocardiograms demonstrating, with agitated saline, a right -to-left shunt. Because of a shunt through a patent foramen ovale, the contrast microbubbles ( arrows) appear immediately in the left atrium (LA) after appearing in the right atrium ( RA). In contrast, if the patient has a pulmonary atrial ventricular shunt, the microbubbles appear in the LA several cardiac cycles after they appear in t he RA. The apical four -chamber view is best for evaluating an atrial shunt, but a subcostal view may be used. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

Augmentation of the Doppler velocity signal from the left heart chambers requires gas-filled microbubbles. A good example is augmentation of the Doppler signal from aortic stenosis or a coronary artery ( 3,4,5).

Gas-Filled Microbubbles Currently, the most frequent indication for the use of a contrast agent with gas -filled microbubbles is to enhance the definition of the endocardial border ( 6,7). Microbubbles generally are 4 - to 5µm spheres able to pass through the microcirculation. They undergo volumetric oscillations upon exposure to ultrasound waves. These oscillations create the acoustic signals that opacify cardiac chambers or other areas of blood flow ( 8). Microbubbles need to be packaged within a stable shell.

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Figure 6-2 With agitated saline, transesophageal echocardiography can demonstrate a patent foramen ovale and right-to-left shunt. A: No shunt through the atrial septum (arrows); B: large right-to-left shunt ( arrows). The echocardiography probe is set at a 60 -90–degree angle to obtain the atrial septal–superior vena cava ( SVC) view. The connection of the S VC with the right atrium ( RA) is well visualized, as is the patent foramen ovale and atrial septum. Agitated saline is injected instead of contrast agent. After the agitated saline is injected into an arm vein, it appears in the SVC and then the RA. Becaus e of a patent foramen ovale, agitated saline microbubbles appear immediately in the left atrium (LA). Some patients may have a right -to-left shunt only when they perform a Valsalva maneuver or cough. Therefore, imaging should be done with agitated saline a nd with the patient's cough or upon release of the Valsalva maneuver.

Modifications of the microbubble shell and gas properties have improved their stability through the pulmonary circulation and have provided good imaging of microbubbles in the left hear t chambers and myocardium. The microbubble shell consists of lipid, polymer, galactose, surfactant, albumin, or a combination of these ( 7). The gas contents are usually perfluorocarbons and sulfur hexafluoride. Ultrasound generates positive and negative (s inusoidal) pressures, and microbubbles are compressed and expanded by the ultrasound acoustic energy in a nonlinear fashion if the acoustic pressure is sufficiently high at the resonant frequency of the microbubbles. This nonlinear property of microbubbles generates harmonic signals when the microbubbles are contacted by ultrasound waves P.101

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(Fig. 6-5). When ultrasound waves are transmitted at high frequency (fundamental frequency) to the microbubbles, returning signals have not only the fundamental frequency, fo, but also a second harmonic frequency, 2 fo (frequency twice that of the fundamental frequ ency) (Fig. 6-6). Myocardial tissue also generates signals with a second harmonic frequency but a much smaller amount than the nonlinearly behaving microbubbles. Therefore, modifying the imaging device to receive the signals with the second harmonic freque ncy (second harmonic imaging) enhances the detection of microbubbles. Even without microbubbles in the cardiac chambers, second harmonic imaging of tissue also improves the image quality of myocardial structures. Although the second harmonic imaging signal s increase with higher ultrasound power, the microbubbles are deformed by higher positive and negative pressures to the point of being destroyed. The ultrasound acoustic power is expressed as the mechanical index, which is proportional to the acoustic pressure and inversely proportional to the square root of the ultrasound frequency. A mechanical index higher than 0.7 is likely to destroy the microbubbles:

Figure 6-3 Visualization of left pulmonary vein. Left, Left upper pulmonary vein ( arrow). Right, Contrast (arrows) demonstrates the location of an intrapulmonary shunt. PA, pulmonary artery.

Several techniques have been developed by the ultrasound industry to enhance second harmonic signals from microbubbles ( Fig. 6-7). The pulse-inversion method sends out two ultrasound pulses of inverted (or out of) phase (analogous to sine and cosine curves) to 271

techom the myocardial tissue and microbubbles. Myocardial tissue with linear properties produces two ultrasound signals of inverted phase at the fundamental fre quency which are canceled by each other, but the microbubbles, with nonlinear properties, produce residual signals from two nonlinearly reflected signals. Another method is pulse-modulation, which sends out two successive pulses, one signal with half the a mplitude of the other signal. The returning signal of the half -amplitude signal is doubled and subtracted from the full signal. In linearly behaving tissue signals, both signals are canceled, but in nonlinearly behaving microbubbles, some signals remain and are imaged.

Figure 6-4 Left, Parasternal long -axis view showing a large coronary sinus ( arrow). *, Descending thoracic aorta; Ao, aorta; LA, left atrium; LV, left ventricle; RV, right ventricle. Right, Agitated saline injected into the left arm opacif ies the coronary sinus, indicating a persistent left superior vena cava. Arrows, Opacification of the coronary sinus.

Blood flow velocity and volume can be measured with contrast echocardiography by using the unique interaction between microbubbles and ultrasound. Microbubbles are destroyed by high energy ultrasound (high mechanical index), and the rate of the reappearance of the microbubbles reflects the velocity of blood flow. Full replenishment of microbubbles after destruction represents blood volume in the myocardium. Therefore, the lack of or decreased replenishment of microbubbles several cardiac cycles after their destruction indicates a perfusion defect in the myocardium (5,6,7).

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techom Myocardial contrast echocardiography to enhance the interface between the blood pool and adjacent tissue or even a mass is performed with low mechanical index (0.4–0.5) harmonic imaging (Fig. 6-8). A high mechanical index may destroy the microbubbles, especially at the apex of the heart. It is also important to use a sufficient amount of contrast agent to opacify the entire cavity. The administration of different contrast agents varies, as follows: P.102

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Administer an intravenous bolus of 0.3 mL of the diluted solution, followed by 3 mL of normal saline over 10 seconds

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If images are not optimal, repeat step 3 as needed up to a total of 2 vials or 21 mL

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Figure 6-5 Diagram demonstrating second harmonic imaging. A: Ultrasound beam with fundamental frequency fo is aimed at a blood cavity containing microbubbles. B: When the fundamental frequency ultrasound beam is reflected by the microbubbles, not only the fundamental frequency but also the resonating harmonic frequency ultrasound beam returns because of the oscillation of the microbubbles and their nonlinear behav ior. Depending on the power of the ultrasound beam, the size of microbubbles changes nonlinearly, which is important for development of second harmonic imaging.

Figure 6-6 A: Acoustic signal returning from contrast gas -filled microbubbles. Imaging was at a fundamental frequency of 3.75 MHz; returning signals contain both fundamental fo and second harmonic (2fo) signals. B: Improved microbubble signal relative to tissue and received as second harmonic (2 fo) rather than as fundamental frequency fo. Signal amplitude is greater from microbubbles than from tissue at the second harmonic frequency. ( A From Burns PN, Powers JE, Simpson DH, et al. Harmonic Imaging: Principles and preliminary results. Clinical

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Radiology, 1996;51 Suppl:50–55. Used with permission . B From Lindner JR, Wei K. Contrast echocardiography. Current Problems in Cardiology , 2002;27:454–519 . Used with permission.)

Figure 6-7 A: Drawing showing how pulse inversion imaging works. (See text for details.) B: Drawing showing how power modulation imaging works. (See text for details.) (From Lindner JR, Wei K. Contrast echocardiography. Current Problems in Cardiology , 2002;27:454–519 . Used with permission.)

Figure 6-8 Harmonic imaging from the apical view without (left) and with (right) intravenous myocardial contrast agent. The mechanical index was set at 0.4 to minimize destruction of microbubbles. The definition of the left ventricular ( LV)

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endocardial border ( dotted line on right) is much clearer with injection of contrast. RV, right ventricle.

Left ventricular (LV) opacification with imaging microbubbles improves the definition of the LV border. This provides better quantitation of LV volume and assessment of LV wall motion analysis. LV volume measured with LV opacification correlates much better with LV volume measured with magnetic resonance imaging than that measured without opacification ( 6,9). Also, analysis of regional wall motion is better with LV opacification, and this is especially helpful during stress echocardiography. In our stress echocardiography laboratory, a contrast agent is used in 45% of dobutamine stress studies and 25% of exercise echocardiography studies. In critically ill patients i n the intensive care unit, LV opacification is frequently needed to assist echocardiographic evaluation of LV contractility and ejection fraction. LV opacification is also helpful in the evaluation of an intracardiac thrombus or mass and a pseudoaneurysm ( Fig. 6-9 and 6-10). The presence and absence of vascularity in an intracardiac or paracardiac mass demonstrated with contrast echocardiography pixel intensity measurements are useful in distinguishing between thrombus and tumor ( 10). Another indication for LV opacification is the assessment of apical or mid -cavity hypertrophic cardiomyopathy, which is often overlooked or mistaken for a dyskinetic apical segment because the epicardial motion of the hypertrophic apex appears to bulge outward unless the apical endocardium is visualized clearly with the use of a contrast agent (Fig. 6-11). Contrast imaging is also helpful in the assessment of other apical abnormalities such as noncompaction or hypereosinophilic syndrome ( Fig. 6-11).

Myocardial Perfusion Imaging Because myocardial ischemia and infarction affect both myocardial perfusion and contractility, it would be ideal to assess both these features simultaneously ( 7). Myocardial contrast perfusion echocardiography provides that capability. If the amount of microbubbles in the myocardium is sufficient, they can be destroyed with a high mechanical index (>1.5) of ultrasound. If the myocardium is normal, the microbubbles are replenished within five to seven cardiac cycles (or 5 seconds) ( Fig. 6-12). However, if th e myocardium has no or decreased perfusion, the microbubbles are not replenished as normally and the areas of myocardium affected

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techom appear dark or patchy ( Fig. 6-13). The destruction and replenishment of microbubbles can be imaged in real time, which also allows a visual assessment of myocardial contractility. A myocardial perfusion defect is more sensitive for detecting myocardial ischemia than regional wall motion analysis in patients who have chest pain syndrome ( 11). If well -trained personnel are availabl e in the emergency department, myocardial contrast perfusion echocardiography can be a very helpful diagnostic tool to screen the large population of patients who have chest pain syndrome.

Figure 6-9 Two-dimensional echocardiographic imaging suggested the presence of an apical mass ( arrows), but the imaging study was not diagnostic. Contrast harmonic imaging showed a large mass attached to the apical segment of the left ventricle (LV) in gray scale ( left) and in angiographic color display (right). LA, left atrium; RV, right ventricle; VS, ventricular septum.

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Figure 6-10 A: Top, An apical mass ( yellow arrows) at the apex of the left ventricle. The mass appears dark, with no evidence of vascularity. Bottom, The pixel intensity of the mass was low compared with that of the myocardium. This is a typical characteristic of thrombus in the heart. B: Top, Contrast echocardiography showed another intracardiac mass ( yellow arrows). Bottom, The pixel intensity of th e mass was higher than that of the myocardium. This mass was a vascular tumor (bottom left). (From Kirkpatrick JN, Wong T, Bednarz JE, et al. Differential diagnosis of cardiac masses using contrast echocardiographic perfusion imaging. Journal of the Ameri can College of Cardiology , 2004;43:1412–1419 . Used with permission.)

Figure 6-11 Contrast echocardiography. A: Apical view showing a mid -cavity obstruction ( arrows) that was not visualized clearly with two -dimensional echocardiography without contrast injection. An apical pouch ( A) is clearly seen. B: Apical four-chamber view ( left) showing apical abnormalities in the left ( LV) and right ( RV) ventricles. Contrast echocardiography ( right) showed that the apical mass ( arrows) is a thrombus, with normal perfusion of the underlying myocardium typical of hypereosinophilic syndrome. LA, left atrium; RA, right atrium.

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Figure 6-12 The process of performing real -time myocardial perfusion imaging. A: A high mechanical index of 1.7 is applied to the heart, destroying all the microbubbles in the myocardium. B: Immediately after the destruction, no microbubbles are present (black areas indicated by arrows). C: Myocardium with normal perfusion is replenished with the microbubbles within 5 to 10 cardiac cycles. LV, left ventricle.

Figure 6-13 Contrast myocardial perfusion. A: Imaging shows patchy defect in the lateral wall of the left ventricle ( LV) (arrows). B: Apical long-axis view shows a dark endocardial area between the two arrows consistent with myocardial

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infarction of the apical septum. RV, right ventricle; VS, ventricular septum. ( A Courtesy of N. Chung, MD.)

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Myocardial contrast perfusion imaging can be combined with pharmacologic stress testing with either dobutamine or a vasodilator such as dipyridamole or adenosine ( Fig. 6-14). A perfusion defect demonstrated with myocardial contrast perfusion echocardiography with a v asodilator correlates well with a perfusion defect detected with nuclear imaging. Theoretically, myocardial risk area, final infarct size, and the amount of myocardial salvage by reperfusion therapy can be measured with serial contrast perfusion echocardio graphy if the study is performed acutely before reperfusion is attempted or several days after reperfusion therapy. This practice is not clinically feasible and does not add much to the care of patients who have acute myocardial infarction, especially when they present with a typical ST -segment elevation myocardial infarction. One exception may be that apical ballooning syndrome is suspected. For patients who have acute myocardial infarction, a more clinically pertinent application of myocardial perfusion e chocardiography is the evaluation of myocardial viability soon after acute reperfusion therapy ( 12,13,14,15,16,17,18). When a patient has an acute myocardial infarction, the affected myocardial segments become akinetic. In our current practice of managing patients who have acute coronary syndromes, thrombolytic therapy is administered or percutaneous coronary intervention is performed unless contraindicated or the duration of ischemia is too long (>12 hours). However, even after establishing TIMI (Thromboly sis in Myocardial Infarction) III coronary flow with acute reperfusion therapy, almost one -third of the patients may

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techom not recover myocardial function because of the no -reflow phenomenon ( 12,13). Although TIMI III flow indicates patency of the epicardial cor onary artery, it does not always indicate the intactness of the microvascular circulation. Myocardial perfusion imaging is a better method for assessing the coronary microcirculation. We performed contrast echocardiography with intravenous Optison and Defi nity in patients who underwent revascularization (thrombolysis, percutaneous coronary intervention, or both) after acute myocardial infarction and identified three different patterns of myocardial perfusion imaging: 1) normal, 2) patchy, and 3) absent myoc ardial perfusion ( 14). Myocardial perfusion contrast echocardiography was performed using real -time perfusion imaging. After the microbubbles were destroyed with a high mechanical index (1.7), their reappearance in the myocardium was assessed after five to seven cardiac cycles. Six to 8 weeks after the patients had myocardial infarction, 2D echocardiography was repeated to assess the functional recovery of the akinetic myocardium. Normal perfusion predicted functional recovery, with a positive predictive va lue of 66% and a negative predictive value of 81% ( Fig. 6-12). The accuracy of the technique was superior for myocardial segments supplied by the left anterior descending coronary artery, with positive and negative predictive values of 70% and 90%, respect ively, and the sensitivity and specificity for detecting functional recovery in these segments were 80% and 88%, respectively. Therefore, our experience indicates that real-time intravenous myocardial contrast echocardiography is a helpful predictor of fun ctional recovery of akinetic myocardium after myocardial infarction.

Figure 6-14 Apical four-chamber view of a patient with coronary artery disease undergoing adenosine myocardial

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contrast echocardiography. The resting study ( left) shows a patchy subendocardial rim of decreased perfusion ( arrows), but the study was not diagnostic. However, with adenosine infusion (right), the subendocardial patchy rim became thicker ( arrows) at the apical and lateral wall of the left ventricle ( LV). This is diagnostic of coronary artery disease, and subsequent coronary angiography confirmed stenosis in the left anterior descending and circumflex coronary arteries. RV, right ventricle; VS, ventricular septum. (Courtesy of N. Chung, MD.)

Many technical and clinical i ssues still need to be resolved before myocardial contrast perfusion echocardiography becomes routine clinical practice. This technique has not been standardized regarding the amount of myocardial contrast used, the mode of intravenous administration (bolu s or continuous infusion), and other technical aspects. Also, contrast imaging depends on the concentration of microbubbles in the myocardium, and the drop -out area P.107

in the lateral wall or artifactually darkened areas decrease the specificity of myo cardial contrast imaging. However, considering the steady progress that has been made with this important technique, its use will soon be routine and newer contrast agents will be available. Another important feature of myocardial contrast echocardiography is to display readily interpretable images on the screen using parametric data ( 19) (Fig. 6-15). Several attempts have been made to display myocardial perfusion defects more clearly. Contrast echocardiography also has been used in combination with color k inesis to demonstrate the degree of myocardial thickening ( 20) (Fig. 6-16). This technique P.108

undoubtedly will be combined with three -dimensional echocardiography to provide a more robust quantitative method for measuring LV volume and assessing wall motion with stress echocardiography.

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Figure 6-15 Parametric display of myocardial perfusion imaging. Left, Apical four-chamber view shows reduced contrast from distal septum to apex. Right, Color-coded map of calibrated contrast intensity (CI). Cool (blue) colors indicate a CI ≤ - 18 dB. (From Yano A, Ito H, Iwakura K, et al. Myocardial contrast echocardiography with a new calibration method can estimate myocardial viability in patients w ith myocardial infarction. Journal of the American College of Cardiology, 2004;43:1799–1806. Used with permission.)

Figure 6-16 A and B: Combination of color kinesis and myocardial contrast imaging for border definition. With the combination of these two techniques, the degree of thickening of the coronary artery can be demonstrated at baseline and during occlusion and reperfusion. That ca n be quantified according to left ventricular segments. A: Blue arrow indicates (top) decreased perfusion and ( bottom) systolic contraction. B: a, apical; b, basal; lt, lateral; m, medial; REDA, regional end -

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diastolic area; RFCA, regional fractional area c hange; sp, septal. (From Mor-Avi V, Korcarz CE, Collins KA, et al. Simultaneous real time echocardiographic imaging of myocardial perfusion and regional function using color -encoded, contrast -enhanced power modulation. Journal of the American Society of Echocardiography , 2003;16:1258–1266 . Used with permission.)

Myocardial contrast perfusion echocardiography has been an essential tool for performing alcohol ablation of the septal coronary artery in patients with obstructive hypertrophic cardiomyopathy (21). Because the myocardial distribution of the septal perforator artery varies, it is critical to know during the procedure the amount of myocardium that would be damaged by the injection of alcohol into a septal perforator.

References 1. Gramiak R, Shah P. Echocardiography of the aortic root. Investigative Radiology, 1968;3:356–366. 2. Seward J, Tajik A, Spangler J, et al. Echocardiographic contrast studies: Initial experience. Mayo Clinic Proceedings, 1975;50:163–192. 3. Nakatani S, Imanishi T, Ter asawa A, et al. Clinical application of transpulmonary contrast -enhanced Doppler technique in the assessment of severity of aortic stenosis. Journal of the American College of Cardiology, 1992;20:973–978. 4. Lepper W, Sieswerda G, Franke A, et al. Repeat ed assessment of coronary flow velocity pattern in patients with first acute myocardial infarction. Journal of the American College of Cardiology, 2002;39:1283–1289. 5. Youn H, Foster E. Demonstration of coronary artery flow using transthoracic Doppler e chocardiography. Journal of the American Society of Echocardiography, 2004;17:178–185. 6. Hundley WG, Kizilbash A, Afridi I, et al. Administration of an intravenous perfluorocarbon contrast agent improves echocardiographic determination of left ventricul ar volumes and ejection fraction: Comparison with cine magnetic resonance

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techom imaging. Journal of the American College of Cardiology, 1998;32:1426–1432. 7. Lepper W, Belcik T, Wei K, et al. Myocardial contrast echocardiography. Circulation, 2004;109:3132–3 135. 8. Burns P, Powers J, Simpson D, et al. Harmonic power mode Doppler using microbubble contrast agents: An improved method for small vessel flow imaging. Ultrasonic Symposium, 1994:1547–1550. 9. Porter T, D'sa A, Turner C, et al. Myocardial contrast echocardiography for the assessment of coronary blood flow reserve: Validation in humans. Journal of the American College of Cardiology, 1993;21:349–355. 10. Schrope B, Newhouse V. Second harmonic ultrasonic blood perfusion measurement. Ultrasound in Med icine and Biology, 1993;19:567–579. 11. Kaul S, Senior R, Firschke C, et al. Incremental value of cardiac imaging in patients presenting to the emergency department with chest pain and without ST-segment elevation: A multicenter study. American Heart Jou rnal, 2004;148:129–136. 12. Ito H, Tomooka T, Sakai N, et al. Lack of myocardial perfusion immediately after successful thrombolysis: A predictor of poor recovery of left ventricular function in anterior myocardial infarction. Circulation, 1992;85:1699†“1705. 13. Kaul S, Ito H. Microvasculature in acute myocardial ischemia: Part II: Evolving concepts in pathophysiology, diagnosis, and treatment. Circulation, 2004;109:310–315. 14. Hillis G, Mulvagh S, Gunda M, et al. Contrast echocardiography using intravenous octafluoropropane and real -time perfusion imaging predicts functional recovery after acute myocardial infarction. Journal of the American Society of Echocardiography, 2003;16:638–645. 15. Main M, Magalski A, Morris B, et al. Combined assessment of microvascular integrity and contractile reserve improves differentiation of stunning and necrosis after acute anterior wall myocardial infarction. Journal of the American College of Cardiology, 2002;40:1079–1084. 16. Lepper W, Hoffmann R, Kamp O, et a l. Assessment of myocardial reperfusion by intravenous myocardial contrast echocardiography and coronary flow reserve after primary

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techom percutaneous transluminal coronary angiography in patients with acute myocardial infarction. Circulation, 2000;101:2368–23 74. 17. Swinburn J, Lahiri A, Senior R. Intravenous myocardial contrast echocardiography predicts recovery of dysynergic myocardium early after acute myocardial infarction. Journal of the American College of Cardiology, 2001;38:19–25. 18. Shimoni S, Fran gogiannis N, Aggeli C, et al. Microvascular structural correlates of myocardial contrast echocardiography in patients with coronary artery disease and left ventricular dysfunction: Implications for the assessment of myocardial hibernation. Circulation, 200 2;106:950–956. 19. Yu E, Skyba D, Leong -Poi H, et al. Incremental value of parametric quantitative assessment of myocardial perfusion by triggered low -power myocardial contrast echocardiography. Journal of the American College of Cardiology, 2004;43:1807 –1813. 20. Spencer K, Bednarz J, Mor -Avi V, et al. Automated endocardial border detection and evaluation of left ventricular function from contrast-enhanced images using modified acoustic quantification. Journal of the American Society of Echocardiograph y, 2002;15:777–781. 21. Nagueh S, Lakkis N, He Z, et al. Role of myocardial contrast echocardiography during nonsurgical septal reduction therapy for hypertrophic obstructive cardiomyopathy. Journal of the American College of Cardiology, 1998;32:225–22 9.

10. 7 - Assessment of Systolic Function and Quantification of Cardiac Chambers 7 Assessment of Systolic Function and Quantification of Cardiac Chambers Quantification of cardiac chambers and assessment of ventricular systolic function are essential part s of all echocardiography examinations. New ultrasound technologies such as tissue Doppler imaging, strain imaging, and three -dimensional (3D) echocardiography have been introduced to make echocardiographic evaluation of cardiac function more quantitative and precise, but

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techom two-dimensional (2D) echocardiography is still the primary tool for chamber quantification and evaluation of left ventricular (LV) systolic function. Also, 2D echocardiography allows visualization of the endocardial border and thickening o f the ventricular walls, by which global and regional ventricular systolic functions are assessed. A quantitative assessment of global systolic function is usually based on changes in ventricular size and volume. Regional (or segmental) wall motion analysi s is fundamental in evaluating coronary artery disease and in performing stress echocardiography. Mechanical synchrony of regional myocardial contraction has an important role in maintaining optimal systolic function, and this can be assessed with tissue D oppler and strain imaging. Both systolic function and diastolic function change as a disease process progresses or regresses (by natural history or treatment). The treatment strategy (medications, device therapy, and surgery) for a patient's condition is f requently guided by systolic function. Therefore, the evaluation of systolic function is a basic echocardiographic assessment in all patients because it provides the initial clues or information necessary for diagnosis, treatment, and prognosis of almost a ll cardiac conditions. The quantification of cardiac chambers and determination of LV volumes are essential components in clinical trials of heart failure and LV remodeling ( 1). This chapter discusses the traditional and newer echocardiographic approaches to the quantification of cardiac dimensions, area, volume, mass, and systolic function. A report on recommendations for chamber quantification has been published recently by the American Society of Echocardiography ( 2). Normal values from the report are li sted in the Appendix.

Left Ventricular and Right Ventricular Dimensions In our laboratory, LV dimensions usually are measured from 2D guided M-mode echocardiograms of the LV at the papillary muscle level (Fig. 7-1), using the parasternal short -axis view (from the trailing edge of the septum to the leading edge of the posterior wall). When there are no regional wall motion abnormalities, the LV dimensions measured from the level of the papillary muscle of the LV can be used to calculate the LV ejection fraction P.110

(LVEF) (Fig. 7-1). The thickness of the ventricular posterior wall

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techom and that of the ventricular septum are measured from the same M mode echocardiogram. These values are used to calculate LV mass. The l ong-axis and short-axis dimensions of the ventricle can also be obtained directly from the systolic and diastolic frames of 2D parasternal long -axis and apical views ( Fig. 7-2), as recommended by the American Society of Echocardiography ( 2). The LV end diastolic and end -systolic dimensions are measured at the level of the mitral leaflet tips as the largest and smallest LV dimension, respectively ( Fig. 7-3). Satisfactory delineation of the endocardial border is critical for reliable chamber quantification, a nd it can be enhanced with the administration of a perfluorocarbon contrast agent. The normal values are listed in the Appendix. These values were obtained with fundamental imaging. Harmonic imaging generally produces higher values for wall thickness (henc e mass) and smaller values for dimensions and volumes.

Figure 7-1 Two-dimensional–guided M -mode echocardiogram of the left ventricle ( LV) at the papillary muscle level. The LV end-diastolic internal dimension ( EDd) measured at the onset of QRS is 60 mm, and the LV end -systolic internal dimension (ESd) is 38 mm. Therefore,

If apical contractility is normal,

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LV mass is also calculated from LV dimensions, posterior wall (PW) thickness, and ventricular septal ( VS) thickness. RV, right ventricle.

Measurements of LV dimensions are used to calculate the LVEF and are clinically useful for detecting LV dilatation and for following up patients who have valvular regurgitation, cardiomyopathy, or acute myocardial infarction. The detection of right ventric ular (RV) dilatation may be the first clue to RV pressure or volume overload (Fig. 7-4) and 7-5). Chronic RV pressure overload is also accompanied by an increase in RV wall thickness in addition to dilatation, whereas RV dysplasia is associated with a thin RV wall. The thickness of the RV wall is normally less than 5 mm and is best measured from the subcostal view at the peak of the R wave ( Fig. 7-4). The RV wall needs to be distinguished carefully from the trabeculations and epicardial fat. The size of the RV is best measured from the apical four -chamber view. An example of measuring the RV short axis and long axis is shown in Figures 7-2 and 7-4. The dimension of the LV outflow tract (LVOT) is measured from the parasternal long -axis view and that of the RV outflow tract is measured from the parasternal short -axis view (Fig. 7-5).

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Figure 7-2 Measurement of ventricular dimensions. A: The major long axis is measured in the apical four -chamber view from the apical endocardium to the plane of the mitral valve. The minor short axis is measured from one -third the length of the long axis from the base and orthogonal to it. B: With the use of these same criteria, the long and short axes can be measured from the parasternal long -axis view, but this view rarely shows the true apex of the left ventricle ( LV). C: The short axis is measured in the parasternal short -axis view at the level of the ti p of the papillary muscle. Ao, aorta; LA, left atrium; RA, right atrium; RV, right ventricle. (From Schiller et al [20]. Used with permission.)

Atrial Size and Volume By convention, the size of the left atrium (LA) is determined from the parasternal long-axis view at end -systole (Fig. 7-3). The convention for M -mode measurements is to measure from the leading edge of the posterior aortic wall to the leading edge of the posterior LA wall (see Figure 2-17 D). However, to avoid the variable extent of spa ce between the LA and aortic root, the trailing edge of the posterior aortic wall is recommended. The size of the LA may be P.111

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underestimated from the parasternal view because this chamber may enlarge longitudinally. Therefore, the size of the LA should also be measured from apical views (from the tip of the mitral valve to the posterior wall of the LA). The area and volume of the LA are best measured from two apical orthogonal views ( 2,3) (Fig. 7-6). Four different methods are used to determin e LA volume: 1) prolate ellipse method, 2) biplane area -length method, 3) biplane Simpson method, and 4) 3D echocardiography.

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Figure 7-3 Left ventricular ( LV) end-diastolic dimension ( EDd) (A) and end-systolic dimension ( ESd) (B) are measured at the level of the mitral leaflet tips (at one -third the distance along the length of the long axis) from the parasternal long -axis view. The left atrial dimension ( LA-d) is measured at end systole, when it is largest. LA, left atrium; RV, right ventricle.

Figure 7-4 A: Measurement of the right ventricular ( RV) longaxis (long arrow) and short -axis (short arrows) dimensions. The RV is smaller than the left ventricle ( LV) when it is normal size (left) and is at least moderately enlarged when it is larger than LV (right). RV enlargement in this case ( right) was due to

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an atrial septal defect. B: The subcostal view is used to measure RV wall thickness ( arrows), which needs to be differentiated from the trabeculations. This image is from a patient who has cardiac amyloidosis, with thick walls and enlarged atria, and a small pericardial effusion ( PE). Ao, aorta; LA, left atrium; RA, right atrium; SVC, superior vena cava.

Figure 7-5 Parasternal long-axis (A) and short-axis (B) views showing measurement of the left ventricular outflow tract (LVOT) and right ventricular outflow tract ( RVOT), respectively, in a 67-year-old asymptomatic woman with cardiomegaly due to an atrial septal defect. The right ventricle ( RV) is dilated in both views. Ao, aorta; AV, aortic valve; LA, left atrium; LV, left ventricle; RA, right atrium.

The prolate ellipse method requires measuring LA dimensions from the parasternal long -axis view (D 1 ) and apical four -chamber view (D 2 and D 3 ), from which LA volume is calculated as D 1 × D 2 × D 3 × 0.523 (Fig. 7-6). The biplane area -length method requires measuring LA area from two orthogonal apical views (A1 and A2) and LA length (L), from which LA volume is calculated as (0.85 à — A1 × A2)/L (Fig. 7-6 and 7-7). When LA length is measured from two apical views, the shorter value is used to calculate LA volume. LA volume measured with the prolate ellipse method is usually 5 to 10 mL smaller than that obtained with the area -length method. Although LA volume can be measured with the biplane Simpson or 3D volumetric method, the area -length method is the method that our laboratory uses and the American Society of Echocardiography recommends. The influence of body surface area on LA volume is corrected with the use of an indexed value by dividing LA vo lume by body surface area. The normal value for the LA volume index is

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prognosis (4,5). The size of the RA is quantified most commonly from the apical four -chamber view. The normal RA minor dimension ranges from 2.9 to 4.5 cm.

Figure 7-6 Diagrams showing left atrial ( LA) volume calculations by the prolate ellipse ( A) and biplane area -length (B) methods.

Figure 7-7 Still frames of apical four -chamber (A) and twochamber (B) views (two orthogonal views) showing the measurement of left atrial (LA) area ( dotted circle) and longaxis length ( dotted vertical line ) for calculating LA volume with the biplane area -length method:

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LA volume is indexed by dividing it by body surface area. LV, left ventricle; RA, right atrium; RV, right ventricle.

Left Ventricular Mass The two methods for calculating LV mass from 2D echocardiography are the area-length method and the truncated ellipsoid method (6,7). Both methods require the short -axis view of the LV at the papillary muscle level and the apical four -chamber view at end diastole (Fig. 7-8). Also, LV wall volume can be derived by subtracting the intracavitary (endoca rdial) LV volume from the entire (epicardial) LV volume, including the LV walls and ventricular septum, measured with the biplane Simpson method. Myocardial mass is equal to the product of the volume and the specific gravity of the myocardium, 1.04 or 1.05 g/mL. Built-in software in the ultrasonographic unit can make both methods available so that the mass is calculated automatically after all the variables have been entered. The LV mass also can be estimated from measurements of LV dimension and wall thick nesses made with 2D or M-mode echocardiograms, as described above. Without measuring the major axis of the LV, the LV mass is obtained from the LV short-axis dimension and a simple geometric cube formula. According to Devereux and associates ( 6, the following equation provides a reasonable determination of LV mass in grams: 1.04 [(LVID + PWT + IVST) 3 - LVID 3 ] × 0.8 + 0.6 where LVID is the internal dimension, PWT is the posterior wall thickness, IVST is the interventricular septal thickness, 1.04 is the specific gravity of the myocardium, and 0.8 is the correction factor. All measurements are made at end -diastole (at the onset of the R wave) in centimeters. Values for the LV mass determined with the above formula are given in the Appendix. Harmonic real -time 3D imaging is the most accurate echocardiographic way to measure LV volume and mass. P.114

From a pyramidal volume data set, 3D echocardiography allows off line selection of anatomically correct apical views without foreshortening. Tracing of endocardia l and epicardial boundaries of

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techom anatomically correct, nonforeshortened apical views provides a more accurate quantification of LV volume and mass ( 8,9). Mor-Avi and colleagues ( 8) showed that, compared with magnetic resonance imaging (MRI), intraobserver va riability was 37% ± 19% of the measured LV mass with 2D echocardiography and 7% ± 10% with real -time 3D echocardiography. Intraobserver variability was 19% ± 10% and 8% ± 5%, respectively. Increased LV mass is an important risk factor for the developme nt of decreased LVEF and heart failure. Also, LV mass is an important end point of treatment trials for hypertension and heart failure. With increasing experience with real -time 3D echocardiography, it will become the standard way to measure LV volume and mass.

Figure 7-8 Top, Diagram of the left ventricular ( LV) short axis at the level of the papillary muscle tip showing epicardial and endocardial perimeters that are traced to calculate myocardial thickness (t), short-axis radius (b), and areas (A 1 and A 2 ). Note that the papillary muscles ( dashed circles) are excluded when measuring these perimeters. Two methods of computing LV mass use the short axis in this manner. Am, area of muscle mass. Bottom, LV mass by area length ( AL) and truncated ellipsoid (TE), where a is the long or semimajor axis from widest minor axis radius to apex, b is the short-axis radius and is back-calculated from the short -axis cavity area, t is the myocardial thickness back -calculated from the short -axis

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epicardial and cavity areas , and d is the truncated semimajor axis from the widest short -axis diameter to the mitral anulus plane.

Volume The volume of the LV is calculated from the dimension and area obtained from orthogonal apical views (four -chamber and two chamber views or four-chamber and five -chamber views). The LV volume then is calculated with the modified Simpson method or disk summation method ( Fig. 7-9). If only one apical view is available, a single-plane area length method is used. The endocardial borders of the LV can be traced manually ( Fig. 7-10) or detected automatically using acoustic quantification or integrated backscatter information. Reliable visualization of the LV endocardial blood -tissue border is the Achille's heel of accurate LV volume measurements by e chocardiography. Because two apical views are used for LV volume measurements, it is important to have nonforeshortened apical views with similar long -axis dimensions. Contrast echocardiography and harmonic imaging have improved the definition of the endoc ardial border. The trabeculations and papillary muscles need to be included in the measurement of LV volume. However, 2D echocardiographic measurements of LV volume usually underestimate the actual volume. Real -time 3D echocardiography has the promise of b eing more reliable. However, the LVEF obtained with MRI was similar to that obtained with 2D and real -time 3D echocardiography. With 3D echocardiography, a real-time LV cast can be created ( Fig. 7-11) and regional volume changes can be displayed, which is useful for quantifying LV dyssynchrony.

Automated Border Detection and Color Kinesis Acoustic quantification is based on the automated detection of the blood-tissue border by using integrated backscatter analysis (10,11). Because the difference between the amplitude of integrated backscatter from the myocardium and the blood is substantial, large changes in the amplitude of the integrated backscatter signal represent the blood -tissue border. Therefore, the blood-tissue border is recognized by a “threshold ”

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techom change in amplitude, and these borders are marked with colored dots. The colored dots superimposed on 2D echocardiographic images represent the LV endocardial border ( Fig. 7-12A and B).

Figure 7-9 Diagram of two orthogonal apical views to illustrate the modified Simpson method in calculating left ventricular (LV) volume. In this method, the LV is divided into a number (n) of cylinders or disks of equal height. The height of each cylinder is determi ned by the number of cylinders; height = L/n. The volume ( V) of each cylinder is calculated from the two diameters of the cylinder ( ai and bi) as shown. L, length of the long axis of LV; LA, left atrium; RA, right atrium; RV, right ventricle. (Modified fro m Schiller et al [20]. Used with permission.)

The area of blood -containing cavity within a region of interest is determined continuously during the cardiac cycle in real time. If the LV cavity is selected as the region of interest, the change in LV cavity area or volume with systolic contraction is calculated instantaneously, conveniently providing the LVEF ( Fig. 7-12C and D). Thus, acoustic quantification is an attractive concept for determining the area, volume, and ejection fraction of the LV. The accuracy of this system has been validated against other established methods. The main limitation of the acoustic quantification system is its dependency on echocardiographic gain and image quality. An increased echo density or artifact in the cardiac cavity is interpreted as “tissue,† and this affects the accuracy of the method. The definition of the lateral wall is less

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techom adequate than it is for other segments of the LV, and it needs to be adjusted by lateral gain. Automated border detection has been combined with an infusion of a perfluorocarbon contrast agent to improve the automatic tracking of the blood -tissue interface ( 12). Spencer and colleagues ( 12) demonstrated that it was feasible to automatically track the contrast-enhanced endocardial border and generate signal -averaged LV volume waveforms (see Chapter 6). Color kinesis is an extension of automated border detection, which compares tissue backscatter values between successive acoustic frames as a means of automatically tracking and displaying endocardial motion in real time ( 10) (Fig. 7-13). This displays the timing and magnitude of endocardial wall motion in real time. This innovative P.115

technique can be used to assess regional fractional area change, timing of cardiac events, and diastolic excursion of the myocardium. Use of contrast, myocardial perfusion imaging, and color kinesis allows simultaneous real -time imaging and quantitative analysis of myocardial perfusion and regional LV function (13) (see Chapter 8).

Figure 7-10 Still frames of two orthogonal views (apical four chamber [top] and apical two -chamber [bottom] views) to calculate the left ventricular ( LV) volume and ejection fraction

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using a modified Simpson method. End -diastolic (EDV) and end-systolic (ESV) frames illustrate 20 cylinders (disks) of equal height. When the endocardial border and long axis (vertical line to the short -axis lines) are identified, a fixed number of cylinders are created, and the volumes of the cylinders are summed to estimate ventricular volume ( Vol). EF, ejection fraction.

Systolic Function Variables There are numerous variables that echocardiography can measure as an expression of systolic function of the heart. These include fractional shortening, ejection fraction, stroke volume and cardiac index, systolic tissue velocity of the mitral anulus and myocardium, tissue tracking, and regional wall motion analysis.

Fractional Shortening Fractional shortening (FS) is the percentage change in LV dimensions with each LV contraction:

where LVED is the LV en d-diastolic dimension and LVES is the LV end-systolic dimension.

Ejection Fraction The most popular expression of global LV function is the LVEF. LVEF is a simple measure of how much of the end -diastolic volume is ejected or pumped out of the LV with each contraction. Although readily influenced by loading conditions, this simple measure has been found to be a strong predictor of clinical outcome in almost all major cardiac conditions and is used to select the optimal management strategy, including the impl antation of an intracardiac defibrillator or biventricular pacing ( 14,15,16. Most frequently, LVEF is determined visually by “eyeballing† 2D echocardiographic images of the LV. This visual assessment is reasonably reliable when performed by an experien ced echocardiographer but has considerable interobserver variation (14). Therefore, whenever possible, the LVEF should be measured more objectively by using volumetric measurements. Quantitatively, LVEF can be calculated from M -mode, 2D, and 3D echocardiograms.

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Figure 7-11 The left ventricular volume cast ( middle right) was created from 3D echocardiography imaging. Regional left ventricular volume changes are shown in the plot at the bottom. The color of each line corresponds to the segment of the same color in the LV cast.

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M-mode recording of 2D measurements of LV dimensions from the mid ventricular papillary muscle level ( Fig. 7-1) is used to calculate the LVEF as follows ( 17:

where %ΔD 2 is the percentage fractional shortening of the square of the minor axis, and %ΔL is the percentage fractional shortening of the long axis, mainly related to apical contraction: 15% for normal, 5% for hypokinetic apex, 0% for akinetic apex, -5% for dyskinetic apex, and -10% for apical aneurysm. There are two components in the equation. The first component is actually a percentage change in the LV area or fractional shortening of the square of the LV short axis. If it is assumed that the apical long -axis dimension remains the same during systolic contraction, the percentage area change or fractional area change 300

techom is equal to the percentage volume change. Because the apical long axis shortens 10% to 15% with systole, an apical correction factor, the second comp onent, is added. This factor varies with the contractility of the apex. LVEF is perferrably calculated from 2D or 3D volume measurements. Although there are several different methods for measuring LV volume and LVEF from 2D echocardiographic images of the LV, the disk summation or biplane Simpson method is used most often (Fig. 7-10). The LV endocardial border is traced from one apical or two orthogonal apical views to create multiple (usually 20) cylinders whose volume is summated to provide LV volume. It is most critical to trace the actual endocardial border, not the trabeculations. Trabeculations and papillary muscles should be included as a part of the LV cavity, not as part of the LV wall. If the definition of the endocardial border is not clear, the intravenous administration of a perfluorocarbon contrast agent will help delineate this border. LV volume is usually larger when measured with the contrast agent. Another crucial technical point for reliably measuring LV volume is avoiding foreshortening of apical views ( Fig. 7-10). The apical long axis is divided by the number of cylinders created within the LV, and the resulting distance (long -axis dimension ÷ number of cylinders) becomes the height of each cylinder. Therefore, the long-axis dimensions fr om two apical views should be similar. In subjects with uniform contractility, LV volume measured with a single plane is very close to the LV volume obtained with the biplane Simpson method. The biplane Simpson method is preferred for measuring the L volum e of an LV with regional wall motion abnormalities. Early experience indicates that real-time 3D echocardiography is more reliable and accurate for measuring LV volume (9, and this may well become the standard mode of measuring LV volume and LVEF in the fu ture.

Stroke Volume Stroke volume is not a true indicator of systolic function because it is determined by multiple factors. However, it provides the amount of blood volume ejected with each cardiac cycle as a final product of the interaction among the mul tiple factors and is an important measure for diagnosis and management of various cardiac conditions. Stroke volume can be measured as the difference between the LV end -diastolic volume and LV end -systolic volume obtained with the biplane Simpson method, a s described above.

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techom The difference should be equal to the stroke volume across the LVOT if there is no valvular regurgitation. If there is mitral regurgitation, regurgitant volume needs to be subtracted to obtain stroke volume across the LVOT. The LVOT stro ke volume can be obtained also from the product of the LVOT area and LVOT TVI (time velocity integral) (see Chapter 4). Cardiac output (CO) is calculated as stroke volume (SV) multiplied by heart rate (HR) and cardiac index (CI) by dividing CO by body surf ace area (BSA):

The LVOT velocity recording is used for calculating stroke volume, and its systolic acceleration (LVOTacc) has been correlated with the LV contractility index, independently of loading conditions ( 18). The LVOTacc is calculated as peak LV OT velocity (PV) divided by the time to PV (t -PV). Under various cardiac conditions, LVOTacc was found to be related linearly to LV maximal elastance and to be correlated with dp/dt.

Figure 7-12 A and B: Ultrasound backscatter differs markedly between the myocardium and intracavitary blood pool. Therefore, the endocardial border is defined where a greater than- preestablished threshold difference in backscatter is identified. The borders are identified a nd dotted. Connecting the endocardial dots creates an endocardial border in real time throughout the cardiac cycle. LV, left ventricle. C: An area of interest is identified by selecting the region. Because we are interested in the volumetric change of the LV, the LV cavity

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was chosen as the region of interest ( ROI). D: From the real time automatic border detection of the LV endocardium, LV volume changes are instantaneously determined to provide end-diastolic volume ( EDV), end-systolic volume ( ESV), and ejection fraction ( EF).

Figure 7-13 A–C: Sequential frames during systole illustrating a progressive color -encoded display of the timing of inward movement of the endocardium by color kinesis. LV, left ventricle; VS, ventricular septum. (From Lau YS, Puryear JV, Gan SC, et al. Assessment of left ventricular wall motion abnormalities with the use of color kinesis: A valuable visual and training aid. Journal of the American Society of Echocardiography , 1997;10:665–672 . Used with permission.)

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Systolic Velocity of Myocardial Tissue or Mitral Anulus (Tissue Doppler and Strain Imaging)

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techom Tissue Doppler imaging records the velocity of myocardial tissue (see Chapter 5). The systolic component (S′) of the mitral anulus correlates well with the LVEF. It has been shown that S′ is a good predictor of clinical outcome. How this can be used in clinical practice with other measures of systolic function requires more experience.

Ventricular Mechanical Synchrony Systolic contraction of the v entricles is performed optimally when regional contractions are coordinated. To be most efficient, all walls should contract within 20 to 30 milliseconds of each other. When this contractile synchrony is disrupted by conduction delay, atrial fibrillation, or a pacemaker, cardiac function and efficiency decrease. The ventricular mechanical synchrony is assessed best with tissue Doppler imaging or strain imaging, which can reliably provide a timing of cardiac events or myocardial movement (see Chapter 5). By resynchronization of cardiac contractility, biventricular pacing improves cardiac function and the functional class of patients with mechanical dyssynchrony. Studies have shown that patients with increased dyssynchrony benefit most from resynchronization t herapy. The degree of ventricular dyssynchrony may not correlate with the duration of the QRS on the electrocardiogram. Tissue tracking and tissue strain imaging, which are modifications of tissue color imaging, are ingenious ways to determine the degree o f dyssynchronization and to identify the myocardial segments with late activation, which is probably the best location for a LV pacing lead. Applications of echocardiography in this area will continue to evolve (see Chapter 5).

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Figure 7-14 Sixteen-segment model for regional wall motion analysis proposed by the American Society of Echocardiography. The left ventricle ( LV) is divided into three levels (basal, mid or papillary muscle, and apical). The basal (segments 1–6) and mid (segments 7 –12) levels are each subdivided into six segments, and the apical level is subdivided into four segments (segments 13–16). All 16 segments can be visualized from multiple tomographic planes. According to contractility, each segment is given a wall moti on score. Segment 13 (apical septum) should be used only once, depending on coronary artery anatomy. Also, it should be noted that there is no apical segment of the posterolateral wall. The apical cap segment can be used especially for a perfusion study. I f the apical cap is added, it becomes the seventeenth segment. Ant, anterior; Ao, aorta; Inf, inferior; IS, interventricular septum; LA, left atrium; Lat, lateral; LV, outflow tract; MVO, mitral valve orifice; Post, posterior; RA, right atrium; RV, right ventricle.

Tissue Tracking With tissue tracking, a byproduct of tissue Doppler imaging, basoapical views of each ventricular segment are displayed as seven color bands, with each color representing a particular

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motion (19). The integral (or summation) of tissue velocity during systole equals the distance of motion along the Doppler axis. Mitral anulus displacement can be determined instantaneously with tissue tracking. A systolic mitral anulus displacement of less than 5 mm determined by tissue tracking correlates well with a severe decrease in the LVEF (15 mm Hg, but Vp can be falsely high in hypertrophic and restrictive cardiomyopathy when LV cavity size is small.

Figure 8-9 Mitral anulus velocities are recorded with tissue Doppler imaging, which is a modification of pulsed wave Doppler. A: A sample volume is placed over the lateral ( left) or medial (right) anulus position. Lateral anulus velocity is usually higher than the v elocity from the medial anulus. Normal mitral anulus velocities are shown. A′, late diastolic anulus velocity; E′, early diastolic anulus velocity; LV, left ventricle; RV, right ventricle; S′, systolic anulus velocity. B: Patterns of mitral inflow an d mitral anulus velocity from normal to restrictive physiology. The mitral anulus velocity was obtained from the septal side of the mitral anulus using Doppler tissue imaging. Each calibration mark in the recording of mitral anulus velocity represents 5 cm /s. E′ is greater than A′ in a normal pattern. In all other patterns, E′ is not greater than A′. In relaxation abnormality, E′ and A′ parallel E and A velocities of mitral inflow. However, when filling pressure is increased (pseudonormalization and

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restrictive physiology), E′ remains decreased (i.e., persistent underlying relaxation abnormality), while mitral inflow E velocity increases. Hence, E/E′ may be useful in estimating LV filling pressure. ( B From Sohn et al. [18]. Used with permissi on.)

Pulmonary Vein Flow Velocities Pulmonary vein Doppler recordings show four distinct velocity components (Fig. 8-13): two systolic velocities (PVS1 and PVS2), diastolic velocity (PVd), and atrial flow reversal velocity (PVa). The first systolic forward flow, PVS1, occurs early in systole and is related to atrial relaxation, which decreases LA pressure and fosters pulmonary venous flow into the LA. The second systolic forward flow, PVS2, occurs in mid to late systole and is produced by the increas e in pulmonary venous pressure. At normal LA pressure, the late systolic increase in pulmonary venous pressure is larger and more rapid than LA pressure. However, at elevated filling pressures, the late systolic pressure increase in the LA is equal to or m ore rapid than that in the pulmonary vein, resulting in earlier peak velocity of PVS2. The remaining pulmonary vein flow velocity components (PVd, PVa, PVS1) follow phasic changes in LA pressure (37). With normal atrioventricular conduction, the systolic c omponents are closely connected, and a distinct PVS1 peak velocity may not be identified in 70% of patients. During diastole, forward flow velocity (PVd) occurs after opening of the mitral valve and in conjunction with the decrease in LA pressure. With atr ial contraction, the increase in LA pressure may result in flow reversal into the pulmonary vein. The extent and duration of the flow reversal are related to LV diastolic pressure, LA compliance, and heart rate. The diastolic phase of pulmonary venous flow resembles early mitral flow (E). The peak velocity and DT correlate well with those of mitral E velocity because the LA functions P.127

mainly as a passive conduit for flow during early diastole. The DT of pulmonary vein diastolic forward flow velocity (PVd) becomes shorter as PCWP increases ( 38) (Fig. 8-14). Both peak velocity (PVa) and duration of pulmonary vein atrial flow reversal (PVa dur)

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techom are important measurements that increase with higher LVEDP (21,22).

Figure 8-10 A plot of early diastolic an ulus velocity E′ against transmitral pressure gradient. In subjects with normal myocardial relaxation ( gray circles), E′ increases as transmitral pressure gradient increases. However, in subjects with abnormal relaxation ( black circles), E′ remains reduced or does not change with increasing transmitral pressure gradient. Tau, relaxation parameter. (From Nagueh et al. [17]. Used with permission.)

The analysis of pulmonary vein flow velocities complements the assessment of the mitral flow velocity pattern. This is especially true if the mitral E and A waves fuse. In this situation, the ratio between pulmonary vein systolic and diastolic flow velocities can be helpful in characterizing diastolic filling in patients with sinus rhythm (PVS2 >> PVd in impaired relaxation, and PVS2 30 mm Hg with exercise) ( 1). It is frequently a manifestation of various systemic and cardiac diseases. If there is no underlying reason for pulmonary hypertension, it is called “primary pulmonary hypertension.† Various causes of pulmonary hypertension are listed, according to the pathophysiologic mechanism, in Table 9-1. However, increased PASP can be due to increased pulmonary flow, as in atrial septal defect. A more complete definition of pulmonary hypertensio n should include

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techom increased pulmonary vascular resistance (PVR), which can be derived from recordings of tricuspid regurgitation and right ventricular outflow tract (RVOT) flow velocities ( 2,3). The determination of pulmonary artery pressure is a routine pa rt of an echocardiography examination. Although certain two dimensional (2D) echocardiographic features suggest pulmonary hypertension, Doppler echocardiography is the primary method for determining actual pulmonary pressures. Systolic and diastolic pulmonary artery pressures are determined from the tricuspid and pulmonary regurgitation velocities, respectively. Transesophageal echocardiography (TEE) provides superb visualization of the main pulmonary trunk, right pulmonary artery, proximal portion of the left pulmonary artery, and all four pulmonary veins and, hence, is useful in detecting pulmonary artery thromboembolism and pulmonary vein stenosis. After pulmonary hypertension has been diagnosed, echocardiography may be helpful in identifying a cardiovascular cause.

Two-Dimensional Echocardiography Pulmonary hypertension is easily recognized when the following M mode and 2D echocardiographic features are present (see Figs. 2-4 and 2-19 I and 9-1) (4,5): 

Diminished or absent “a† (atrial) wave of the pulmonary valve

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Midsystolic closure or notching of the pulmonary valve

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Enlarged chambers on the right side of the heart

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D-shaped left ventricular (LV) cavity caused by a flattened ventricular septum

The ventricular septum is flattened during both systole and diastole in pulmonary hypertension but only during diastole in right ventricular (RV) volume overload. However, these features are not sensitive for pulmonary hypertension. They are qualitative and do not provide actual hemodynamic data.

Doppler Echocardiography Doppler echocardiography allows estimation of pulmonary artery pressures and PVR by measuring tricuspid P.144

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regurgitation velocity, pulmonary regurgitation velocity, and RVOT flow velocity.

Table 9-1 Etiologic classification of pulmonary hypertension

Pulmonary venous hypertension Thoracic aorta Coarctation of the aorta Supravalvular aortic stensis Left ventricle Aortic stenosis or insufficiency Congenital subaortic stenosis Hypertrophic cardiomyopathy Constrictive pericarditis Myocardial disease of various causes Left atrium Ball-valve thrombus Myxoma Cor triatriatum Pulmonary veins Congenital pulmonary vein stenosis Mediastinitis or mediastinal fibrosis Mediastinal neoplasm Chronic hypoxia Residence at high altitude Inadequate respiratory excursion Extreme obesity (pickwickian syndrome) Severe kyphoscoliosis Neuromuscular disorders Extreme pleural fibrosis or lung resecti on Chronic upper airway obstruction Congenital webs Enlarged tonsils Chronic lower airway obstruction Chronic bronchitis Asthmatic bronchitis Bronchiectasis

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Cystic fibrosis Emphysema Chronic diffuse pulmonary parenchymal disease Interstitial fibrosis (idiopathic, chronic pneumonitic, toxic, etc.) Pneumoconioses (silicosis, asbestosis, etc.) Granulomatous diseases (sarcoidosis, tuberculosis, etc.) Alveolar filling disorders (alveolar pro teinosis, etc.) Connective tissue disorders (rheumatoid lung, systemic sclerosis, etc.) Vascular disorders of the lung Primary vascular disease Plexogenic pulmonary arteriography (diet pills, AIDS) Connective tissue disorders (lupus, s ystemic sclerosis, or scleroderma) Thrombotic disease Sickle cell disease Pulmonary veno-occlusive disease Embolic disease Persistent large pulmonary emboli Recurrent pulmonary emboli Tumor emboli (e.g., breast carcinoma ) Schistosomiasis Left-to-right shunts Extracardiac shunts Patent ductus arteriosus Aortopulmonary window Rupture of aortic sinus Intracardiac shunts Ventricular septal defect Atrial septal defect

AIDS, acquired i mmunodeficiency syndrome. From McGoon MD, Fuster V, Freeman WK, et al. Pulmonary hypertension. In: Giuliani ER, Gersh BJ, McGoon MD, et al., eds. Mayo Clinic Practice of Cardiology , 3rd ed. St. Louis: Mosby, 1996;1815–1836. Used with permission of Mayo Foundation for Medical Education and Research.

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Tricuspid Regurgitation Velocity Tricuspid regurgitation velocity usually is obtained with continuous wave Doppler (using either an imaging duplex transducer or a nonimaging transducer) from the RV inflow or the apical four chamber view position. From the apical position, the transducer needs to be angled more medially and inferiorly from the mitral valve signal. Tricuspid regurgitation velocity reflects the pressure difference during systole between the RV a nd the right atrium (RA) (6,7,8,9) (Fig. 9-2). Therefore, systolic RV pressure can be estimated by adding RA pressure to the transtricuspid gradient derived from tricuspid regurgitation velocity, that is, Transtricuspid pressure gradient = 4 Ã — Tricuspid regurgitation velocity 2 The RA pressure can be estimated clinically by measuring jugular venous pressure or from the respiratory motion of the inferior vena cava seen on 2D echocardiograms. When the diameter of the inferior vena cava decreases by 50% or mo re with inspiration ( Fig. 9-2 C), RA pressure is P.145

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usually less than 10 mm Hg, and those with less than 50% inspiratory collapse tend to have an RA pressure more than 10 mm Hg (9). In the absence of pulmonic stenosis or RVOT obstruction, RV systolic pressure is equal to PASP ( Fig. 9-3). The normal tricuspid regurgitation velocity is 1.7 to 2.3 m/s at rest. A higher velocity indicates pulmonary hypertension, RVOT obstruction, or pulmonic stenosis. Four different tricuspid regurgitation velocit y recordings are shown in Figure 9-4. Tricuspid regurgitation velocity may be less than 2.0 m/s when RA pressure is markedly increased because of RV infarct, RV failure, or severe tricuspid regurgitation (Fig. 9-5). Therefore, increased tricuspid regurgita tion velocity represents increased RV systolic pressure, not the severity of tricuspid regurgitation.

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Figure 9-1 A: Parasternal short-axis view demonstrating the D-shaped left ventricular ( LV) cavity and enlarged right ventricular (RV) cavity in pulmonary hypertension. A similar appearance is seen in RV volume overload; however, flattening of the ventricular septum ( VS) persists during the entire cardiac cycle in RV and pulmonary artery pressure overload, but it disappears during systole in RV vol ume overload. B: Corresponding pathology specimen.

Figure 9-2 A: Diagram of the chambers on the right side of the heart demonstrating how to measure systolic right ventricular (RV) pressure from tricuspid regurgitation ( TR) velocity. The peak systolic transtricuspid pressure gradient

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from the RV to the right atrium ( RA) is represented by 4 Ã — (peak TR velocity) 2 . Therefore, systolic RV pressure is estimated by adding RA pressure to the pressure gradient derived from TR velocity. LA, left atrium; LV, left ventricle; RAP, RA pressure; RVP, RV pressure. B: Simultaneous RV and RA pressure tracings and TR velocity recording by continuous wave Doppler echocardiography. Pressure gradients (36, 31, and 29 mm Hg) derived from the peak Doppler velocities of the second, third, and fourth beats (3.0, 2.8, and 2.7 m/s, respectively) are close to the catheter -derived RV and RA gradients (arrows, 33, 28, and 26 mm Hg). C: Subcostal view of the inferior vena cava ( IVC), hepatic vein ( HV), and RA during expiration ( left) and inspiration ( right) in a patient with normal RA pressure. The IVC collapses more than 50% with inspiration.

Figure 9-3 Transesophageal echocardiographic view of the right ventricular outflow tract, which is obstructed by a large tumor (T). Tricuspid regurgitation velocity was increased because of the obstruction, not by pulmonary hypertension. AV, aortic valve; RA, right atrium.

Tricuspid regurgitation is present in more than 75% of the normal adult population. When the tricuspid regurgi tation jet is trivial and its continuous wave Doppler spectrum is suboptimal, injection of agitated saline solution into an arm vein enhances the tricuspid regurgitation velocity signal ( Fig. 9-6).

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Figure 9-4 Representative tricuspid regurgitation velocities (2.5, 2.9, 4.3, 5.3). The numbers in parentheses are pressure gradients derived from peak velocities using the simplified Bernoulli equation.

Figure 9-5 Continuous wave Doppler recording of severe tricuspid regurgitation. Tricuspid regurgitation velocity is very low (1.2 m/s) because severe regurgitation decreases the transtricuspid gradient.

Tricuspid Regurgitation Velocity with Exercise Pulmonary pressure increases mildly with exercise, and it will be helpful to know the range of its increase in normal subjects. Bossone and colleagues ( 10) demonstrated that athletes have higher tricuspid regurgitation velocities than healthy control subjects at rest (2.25 vs. 1.72 m/s) and during supine bike exercise (3.11 vs. 2.46 m/s at 160 W) because of higher stroke

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techom volume and cardiac output in athletes. It appears that well conditioned athletes are capable of reaching a PASP of 60 mm Hg with exercise.

Technical Caveat Tricuspid regurgitation velocity usually varies with respiration, being lower with inspiration, which increases the volume of tricuspid regurgitation and decreases the transtricuspid gradient. To avoid respiratory variation, tricuspid regurgitation velocity usually is obtained with a patient in held -expiration. Doppler velocity recordings from patients with aortic stenosis or mitral regurgitation can mimic the tricuspid regurgitant jet. All three Doppler jets move away from the apex, but they can be differentiated by angulation of the transducer, Doppler peak velocity, flow duration, and the accompanying diastolic signal (see Chapter 4). Tricuspid regurgitation is directed most medially and tricuspid inflow (diastole) velocity is usually less than 0. 5 m/s unless tricuspid regurgitation is severe or the tricuspid valve is P.147

stenotic. Flow duration is shortest in aortic stenosis. The peak velocity of the mitral regurgitant jet is usually, but not always (in patients with hypotension and/or a marke d increase in left atrial [LA] pressure), greater than 4 m/s and always greater than that of aortic stenosis in the same patient.

Figure 9-6 Continuous wave Doppler recording of tricuspid regurgitation velocity without ( left) and with (right) injection of agitated saline.

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techom As tricuspid regurgitation velocity increases, there is a greater potential to miscalculate PASP by making a slight error in tricuspid regurgitation velocity measurements. If the Doppler gain is too high, the peak velocity measurement is often overestimate d (see Fig. 4-12).

Pulmonary Regurgitation Velocity The end-diastolic velocity of pulmonary regurgitation reflects the end-diastolic pressure gradient between the pulmonary artery and the RV (Fig. 9-7). At end-diastole, RV pressure should be equal to RA pressure (RAP). Therefore, PAEDP = 4 × PREDV 2 + RAP where PAEDP is pulmonary artery end -diastolic pressure, and PREDV is pulmonary regurgitation end -diastolic velocity. The peak early diastolic pulmonary regurgitation (PR) velocity is useful in estimating m ean pulmonary artery pressure (MPAP). According to Masuyama and colleagues ( 11, the peak diastolic pressure gradient between the pulmonary artery and the RV approximates MPAP. Therefore, MPAP = 4 × Peak PR velocity 2 MPAP can also be obtained as PAEDP + 1/3 (PASP - PAEDP).

Figure 9-7 A: Continuous wave Doppler spectrum of pulmonary regurgitation velocity in a patient with normal pulmonary artery pressure. Because the pressure difference between the pulmonary artery and right ventricle is small during diastole, contraction of the right at rium (hence, increase in right atrial and ventricular pressures) decreases the pulmonary artery–right ventricular pressure gradient, resulting in a dip

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in pulmonary regurgitation velocity. When pulmonary pressure is high, right atrial contraction usually does not make a notable change in the pulmonary artery–right ventricular pressure gradient; hence, there is no dip in the continuous wave Doppler signal of pulmonary regurgitation. B: Diagram of continuous wave Doppler interrogation of pulmonary regurgi tation (PR) from the left parasternal window and the pulmonary regurgitation Doppler spectrum. If end -diastolic pulmonary regurgitation velocity is 3 m/s, end -diastolic pulmonary artery (PA) pressure = 4 à — 3 2 + 20 = 56 mm Hg, assuming a right atrial (RA) pressure (RAP) of 20 mm Hg. LA, left atrium; RV, right ventricle.

Because pulmonary regurgitation velocity usually reflects small pressure differences between the pulmonary artery and the RV, atrial contraction with increased RV pressure creates a unique “dip” in the velocity curve ( Fig. 9-7). Normally, the pulmonary regurgitation end -diastolic pressure gradient is less than 5 mm Hg. An increase in this pressure gradient (>5 mm Hg) has been found to correlate with systolic dysfunction, diastolic dysfunction, increased brain natriuretic peptide, and decreased functional status ( 12).

Right Ventricular Outflow Tract Flow Acceleration Time The RVOT flow velocity has a characteristic pattern as pulmonary artery pressure increases ( Fig. 9-8). The acceleration phase becomes shorter with increased pulmonary artery pressure. Several investigators have derived regression equations to estimate MPAP from the RVOT acceleration time (AcT) ( 13). Mahan's equation is simplest and preferred for estimating MPAP: MPAP = 79 - 0.45 (AcT) It should be noted that acceleration time is dependent on cardiac output and heart rate ( 14). With increased output through the cardiac chambers on the right side (as in atrial septal defect), acceleration time may be normal even when pu lmonary artery pressure is increased. If the heart rate is slower than 60 beats per minute or more than 100 beats per minute, acceleration time needs to be corrected for heart rate. This method is rarely used in our practice.

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Figure 9-8 A: Right ventricular outflow tract ( RVOT) flow velocity recordings by pulsed wave Doppler echocardiography. The sample volume is placed in the region of the pulmonary valve anulus. Left, Normal flow pattern. Acceleration time ( AcT) is the time interval between the beginning of the flow and its peak velocity (between the two vertical arrows). It is 130 ms (normal, ≥120 ms). Right, Flow velocity in pulmonary hypertension. The arrow indicates peak RVOT velocity with a short AcT. AcT is shortened to 40 ms. Mean pulmonary artery pressure = 79 - (0.45 × 40) = 61 mm Hg, using Mahan's regression equation (9). PW, pulsed wave Doppler. B: M-mode (left) and pulsed wave Doppler ( right) recordings from the pulmonary valve ( PV) characteristic of pulmonary hypertension with “W” shape. Arrow indicates mid -systolic interruption producing a “W† shape in the Doppler recording.

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Using the aforementioned Doppler variables, the systolic, diastolic, and mean pulmonary artery pressures can be estimated ( Fig. 9-9). Tricuspid regurgitation and pulmonary regurgitation are present in more than 85% of normal subjects ( 15). The incidence is higher in those with pulmonary hypertension. The tricuspid regurgitation velocity signal is enhanced wit h the injection of agitated saline or a contrast agent into the RA through an arm vein ( Fig. 9-6). After echocardiography has established that pulmonary artery pressure is increased, the potential causes of this increase should be 375

techom evaluated thoroughly with 2D Doppler and color flow imaging to examine for a left -sided abnormality (e.g., LV failure, mitral stenosis, or mitral regurgitation), left -to-right shunt, atrial septal defect, ventricular septal defect, cor pulmonale, or pulmonary embolism.

Pulmonary Vascular Resistance Pulmonary vascular resistance (PVR) is an important hemodynamic variable in the management of patients with severe heart failure or congenital heart disease and in the evaluation of candidates for cardiac transplantation. Traditionally, PVR is obtained by cardiac catheterization, with the use of the following formula: PVR = (MPAP - PCWP)/CO where PCWP is pulmonary capillary wedge pressure and CO is cardiac output. A few attempts have been made to estimate PVR with Doppler ( 2,3) and color M-mode (16) echocardiography. The simplest Doppler method for estimating PVR is to divide tricuspid regurgitation velocity (TRV) by the RVOT time velocity integral (TVI) ( 3: PVR = 10 × (TRV/RVOT TVI) + 0.16 Although the actual regression formula is more complex, this simple method provides a reasonable estimate of PVR ( Fig. 9-10). A cutoff value of 0.2 for TRV/RVOT TVI separates a group with PVR greater than 2 Wood units. Shandas and colleagues ( 16) used color M-mode–derived propagation velocity of the pulmonary artery flow to estimate PVR. The slope of the aliasing line on the color M mode of the main pulmonary artery flow decreases as PVR increases.

Mitral Inflow Velocity Pattern in Pulmonary Hypertension Pulmonary pressure usually is increased in pati ents with increased LV filling pressures. When LV filling pressures are increased, the mitral inflow velocity pattern becomes restrictive (↑E velocity, ↓A velocity, E/A >2.0, and ↓deceleration time). Therefore, it is safe to assume that P.149

pulmonary hypertension is related to a pulmonary process if mitral

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techom inflow shows a nonrestrictive diastolic filling pattern ( 17). RV pressure overload may induce LV filling abnormality because of the shift of the ventricular septum. In patients with chronic obst ructive pulmonary disease, mitral inflow velocity may demonstrate a respiratory variation similar to the degree of variation seen in constrictive pericarditis; however, the respiratory change in superior vena cava systolic forward flow velocities is 20 cm/ s or less in constriction and is much higher or even monophasic with inspiration in chronic obstructive pulmonary disease (see Chapter 17).

Figure 9-9 Estimation of pulmonary artery pressure from tricuspid regurgitation (TR) velocity ( left), right ventricular outflow tract ( RVOT) flow velocity acceleration time ( middle), and pulmonary regurgitation ( PR) velocity (right).

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Figure 9-10 Calculation of pulmonary vascular resistance (PVR) from tricuspid regurgitation ( TR) peak velocity ( TRV) and RVOT TVI. TRV/RVOT TVI ratio >2 indicates PVR >2 Wood units. A: Calculation of PVR in two different patients. The two panels (A and B) on the left are from a patient with normal PVR and the two panels ( A and B) on the right are from a patient with in creased PVR. For each patient, panel A indicates TR velocity and panel B, RVOT velocity. MnPG, mean pressure gradient; PG, peak pressure gradient; RVOT, right ventricular outflow tract; TVI, time velocity integral; v, TR velocity; VTI, velocity time integral (RVOT TVI). B: Correlation between catheter-derived PVR and echocardiographically derived PVR. (From Abbas et al. [2]. Used with permission.)

Hepatic Vein Velocity Pattern in Pulmonary Hypertension A characteristic velocity patter n in hepatic venous flow is seen in patients with pulmonary hypertension. There is a prominent atrial flow reversal in the hepatic vein caused by increased diastolic pressure and decreased compliance of the RV (see Fig. 8-16). There is very little respirat ory variation of atrial flow reversal in pulmonary hypertension, unlike the variation seen in restrictive cardiomyopathy or constrictive pericarditis.

Cor Pulmonale and Pulmonary Embolism Transthoracic Echocardiography

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techom With echocardiography, it may be difficult to distinguish between acute cor pulmonale (i.e., pulmonary embolism) and chronic obstructive lung disease. RV hypertrophy is common in chronic cor pulmonale. In both forms, the right chambers are dilated and ther e is 2D and Doppler echocardiographic evidence of RV pressure overload, as described herein. The LV cavity is relatively small and hyperdynamic unless an abnormality is also present on the left side of the heart. A still frame from the subcostal 2D echocar diographic image of a patient who had hemodynamic collapse after an orthopedic operation is shown in Figure 9-11. The chambers on the right side are dilated and the ventricular septum is deviated to the left because of increased RV pressure from acute pulm onary embolism. This RV strain pattern is P.150

normalized after pulmonary hypertension resolves with anticoagulation therapy ( 18,19). A similar normalization has been noted after pulmonary thromboendarterectomy in patients with chronic thromboembolic pu lmonary hypertension ( 20).

Figure 9-11 Subcostal two-dimensional echocardiogram demonstrating a dilated right ventricle ( RV) and right atrium (RA), with the ventricular septum ( VS) deviated to the left, in a patient who had cardiac arrest. When the dilated right chambers are detected in the setting of an acute hemodynamic event, pulmonary embolus should be considered. An RV infarct

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is almost always associated with infarction of the inferoseptal region of the left ventricle ( LV).

Occasionally, thrombi-in-transit are detected in the chambers on the right side of the heart ( 21). In the international cooperative pulmonary embolism registry, this finding was observed in 42 (4%) of 1,135 patients with pulmonary embolism who had echocardiography studi es. These thrombi are highly mobile and have the appearance of popcorn or a snake ( Figs. 9-12 and 9-13). The mobile mass comes from en bloc embolization of venous thrombi cast. Patients inevitably have pulmonary embolism and should receive vigorous anticoa gulation, thrombolytic therapy, or even surgical removal of the embolus. The mortality of these patients is higher when treated with heparin (23.5% - 28.6%) than with a thrombolytic agent (11.3% - 20.8%) ( 22). Therapeutic results are monitored by repeated echocardiography examinations. For LA thrombi due to paradoxical emboli, thrombolytic therapy is relatively contraindicated; surgical removal is the most effective treatment. A similar echocardiographic appearance has been noted in patients with intravenou s leiomyomatosis that originated from an endometrial tumor (see Fig. 18-5). The same kind of thrombus material is responsible for paradoxical embolus when the foramen ovale is patent (see Fig. 18-15). It has been observed that PASP returns to normal values within 1 month after treatment of pulmonary embolism. The risk of persistent pulmonary hypertension and RV dysfunction has been noted to be increased in patients whose PASP is more than 50 mm Hg at the time of diagnosis of pulmonary embolism and in whom P ASP does not normalize within 1 month, by echocardiography ( 23).

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Figure 9-12 Apex-down apical view demonstrating mobile thrombi in the right chamber. The shape of the mass changes because of its highly mobile nature. A: During systole, mobile thrombi have the shape of a snake. B: During diastole, the mass assumes the shape of popcorn as it traverses the tricuspid valve. Ao, aorta; LV, left ventricle; RA, right atrium; RV, right ventricle.

Prospectively performed echocardiography studies in 209 consecutive patients who had acute pulmonary embolism demonstrated that 31% of normotensive patients did have RV dysfunction (RV dilatation, paradoxical septal motion, or tricuspid regurgitation velocity >2.8 m/s) and 10% of them developed shock and 5% died in hospital (18). Conversely, normotensive patients without echocardiographic RV dysfunction had a benign course. In P.151

this patient population, alteplase in conjunction with heparin improved clinical outcome ( 22). Alteplase was given in this study as an infusion at a rate of at least 1,000 U/h to maintain activated partial thromboplastin time at 2 to 2.5 times the upper normal limit.

Figure 9-13 A and B: Separate frames from horizontal transesophageal echocardiographic imaging of mobile right atrial thrombi -in-transit (arrow in A; arrows in B). The configuration of the thrombi is dynamic. In all patients with pulmonary embolism, varying degrees of this phenomenon probably exist. When the thrombi are large, they remain in the

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right chambers longer than smaller thrombi -in-transit. CS, coronary sinus; RA, right atrium; RV, right ventricle.

Transesophageal Echocardiography The main pulmonary trunk and its bifurcation into right and left pulmonary arteries are well seen with TEE, as in thrombus in the proximal part of the pulmonary artery ( Fig. 9-14). As shown in Figure 9-12, thrombi -in-transit in the right chambers also are seen clearly with TEE. When transthoracic echocardiography is unable to characterize an intracardiac mass on the right side, TEE should be considered. In one study, TEE detec ted central pulmonary thromboemboli, mostly in the right pulmonary artery, in 35 of 60 patients (58%) who had severe pulmonary embolism ( 24). Although it is more difficult to visualize the left than the right pulmonary artery with TEE, even with the longit udinal plane, the sensitivity of TEE in the detection of pulmonary thrombi is 97%, with pulmonary angiography, computed tomography, autopsy, or surgery as a reference standard.

Figure 9-14 Transesophageal echocardiogram of pulmonary artery thrombus. Longitudinal plane view ( left) shows the right pulmonary artery ( RPA) containing a large thrombus ( arrow). Horizontal plane basal view ( right) shows the right pulmonary artery containing thrombu s (arrows). Ao, aorta; SVC, superior vena cava.

When RA pressure is increased (RV infarct, pulmonary hypertension, constrictive pericarditis), there may be a marked right-to-left shunt through the patent foramen ovale, resulting in severe hypoxemia. Because the entire atrial septum is seen clearly

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techom with TEE, patients with refractory hypoxemia associated with increased RA pressure should undergo TEE and color flow imaging.

Chronic Thromboembolic Pulmonary Hypertension Chronic thromboembolic pulmonary hy pertension results from a single or multiple pulmonary thromboemboli. It occurs in about 4% of patients with acute pulmonary embolism ( 25). In chronic thromboembolic pulmonary hypertension, thromboemboli do not resolve; instead, they form endothelial and f ibrotic obstructions in the pulmonary vascular bed ( 26). Chronic thromboembolic pulmonary hypertension is not caused by thromboembolic obliteration alone, but by vascular remodeling, cytokines, and vasculotrophic mediators ( 26). Pulmonary thromboendarterec tomy is bilateral endarterectomy in which the thrombus and adjacent medial layer are meticulously dissected. Echocardiography examinations before and after the procedure have demonstrated a marked decrease in PASP and tricuspid regurgitation as well as improvement in RV function ( 20,27).

Figure 9-15 A: Computed tomogram showing right superior pulmonary vein stenosis ( arrow) with narrowing of the ostium. B: Continuous wave Doppler (transesophageal echocardiography) (65° and clockwise rotation) demonstrates peak velocity from the pulmonary vein stenosis of 1.5 m/s and a mean gradient of 8 mm Hg.

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Evaluation of the Pulmonary Veins Normally, four pulmo nary veins (two from the right side and two from the left side) are connected with the LA. Congenitally, from one to all four pulmonary veins can be connected with or drain into the right side of the heart instead of the left side. The anomalous venous connection can occur in isolation or in association with other congenital defects. Although transthoracic echocardiography may be sufficient to visualize the connections of all four pulmonary veins, TEE provides better visualization of the pulmonary vein. The best surface echocardiographic view for visualizing the connections of all four pulmonary veins with the LA is the suprasternal short -axis view. Color flow imaging can help identify pulmonary vein drainage into the LA. This view is also best for visualizi ng anomalous connections with the RA or superior vena cava. One of the pulmonary veins may drain into the vertical vein, which connects with the innominate vein; this is also best seen from the suprasternal view. Color flow imaging demonstrates flow toward the transducer position in the vertical vein, next to the aorta.

Figure 9-16 A: Transesophageal echocardiographic view ( left) of left pulmonary veins (*), with stenosis of the vein on the right treated with a stent ( arrows). Color flow imaging ( right) shows increased flow velocity. LA, left atrium. B: Continuous wave Doppler recorded peak pulmonary vein velocity of 1.8 m/s. Mean gradient is 10 mm Hg.

TEE demonstrates all four pulmonary veins in all patients. Right pulmonary veins are seen from a 60° to 70° transducer position with the probe rotated clockwise, and left pulmonary veins are seen from 120° to 140° with the probe rotated counterclockwise.

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techom Doppler and color flow imaging of the pulmonary veins is useful in assessing the severity of mitra l regurgitation, diastolic filling pressures, and pulmonary vein stenosis.

Pulmonary Vein Stenosis Pulmonary vein stenosis may be associated with congenital defects, but it is a rare acquired condition. Catheter treatment of atrial arrhythmia in the region of pulmonary vein may result in hemodynamically significant pulmonary P.153

stenosis (28). Packer and colleagues ( 28) at our institution have described the clinical presentation, investigation, and management of pulmonary vein stenosis complicating the ablation procedure for atrial fibrillation. On spiral computed tomography, the diameter of the narrowest lumen of the affected pulmonary veins was 3 ± 2 mm, compared with a normal lumen of 13 ± 3 mm, at a mean gradient of 12 ± 5 mm Hg ( Fig. 9-15). The best treatment is percutaneous dilatation or stent placement. Actual narrowing of the pulmonary vein may be difficult to visualize with surface 2D echocardiography, but increased flow velocity from a stenotic pulmonary vein is easily recognized with color f low imaging, followed by Doppler examination from an apical, or sometimes parasternal, view. All four pulmonary veins are clearly visualized and their hemodynamics are easily assessed with TEE ( Fig. 9-16) and intracardiac echocardiography. Increasing use o f intracardiac ultrasonography during an ablation procedure has reduced the incidence of pulmonary vein stenosis.

References 1. Rich S, Dantzker DR, Ayres SM, et al. Primary pulmonary hypertension: A national prospective study. Annals of Internal Medicine, 1987;107:216–223. 2. Abbas AE, Fortuin FD, Schiller NB, et al. A simple method for noninvasive estimation of pulmonary vascular resistance. Journal of the American College of Cardiology, 2003;41:1021–1027. 3. Scapellato F, Temporelli PL, Eleuteri E, e t al. Accurate noninvasive estimation of pulmonary vascular resistance by Doppler echocardiography in patients with chronic heart failure. Journal of the American College of Cardiology, 2001;37:1813–1819. 385

techom 4. Weyman AE, Dillon JC, Feigenbaum H, et al. Ech ocardiographic patterns of pulmonic valve motion with pulmonary hypertension. Circulation, 1974;50:905–910. 5. Nanda NC, Gramiak R, Robinson TI, et al. Echocardiographic evaluation of pulmonary hypertension. Circulation, 1974;50:575–581. 6. Yock PG, Popp RL. Noninvasive estimation of right ventricular systolic pressure by Doppler ultrasound in patients with tricuspid regurgitation. Circulation, 1984;70:657–662. 7. Currie PJ, Seward JB, Chan KL, et al. Continuous wave Doppler determination of right ven tricular pressure: A simultaneous Doppler-catheterization study in 127 patients. Journal of the American College of Cardiology, 1985; 6:750–756. 8. Hatle L, Angelsen BA, Tromsdal A. Non -invasive estimation of pulmonary artery systolic pressure with Doppl er ultrasound. British Heart Journal, 1981;45:157–165. 9. Kircher BJ, Himelman RB, Schiller NB. Noninvasive estimation of right atrial pressure from the inspiratory collapse of the inferior vena cava. American Journal of Cardiology, 1990;66:493–496. 10. Bossone E, Rubenfire M, Bach DS, et al. Range of tricuspid regurgitation velocity at rest and during exercise in normal adult men: Implications for the diagnosis of pulmonary hypertension. Journal of the American College of Cardiology, 1999;33:1662–166 6. 11. Masuyama T, Kodama K, Kitabatake A, et al. Continuous -wave Doppler echocardiographic detection of pulmonary regurgitation and its application to noninvasive estimation of pulmonary artery pressure. Circulation, 1986; 74:484–492. 12. Ristow B, Ahme d S, Wang L, et al. Pulmonary regurgitation end-diastolic gradient is a Doppler marker of cardiac status: Data from the Heart and Soul Study. Journal of the American Society of Echocardiography, 2005;18: 885–891. 13. Mahan G, Dabestani A, Gardin J, et al . Estimation of pulmonary artery pressure by pulsed Doppler echocardiography [abstract]. Circulation, 1983; 68 Suppl III:III 367. 14. Chan KL, Currie PJ, Seward JB, et al. Comparison of three Doppler ultrasound methods in the prediction of pulmonary artery pressure. Journal of the American College of Cardiology, 1987;9:549–554.

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techom 15. Borgeson DD, Seward JB, Miller FA Jr, et al. Frequency of Doppler measurable pulmonary artery pressures. Journal of the American Society of Echocardiography, 1996;9:832–837. 16. Shandas R, Weinberg C, Ivy DD, et al. Development of a noninvasive ultrasound color M -mode means of estimating pulmonary vascular resistance in pediatric pulmonary hypertension: Mathematical analysis, invitro validation, and preliminary clinical studie s. Circulation, 2001;104:908–913. 17. Enriquez-Sarano M, Rossi A, Seward JB, et al. Determinants of pulmonary hypertension in left ventricular dysfunction. Journal of the American College of Cardiology, 1997;29:153–159. 18. Grifoni S, Olivotto I, Cecch ini P, et al. Short -term clinical outcome of patients with acute pulmonary embolism, normal blood pressure, and echocardiographic right ventricular dysfunction. Circulation, 2000;101:2817–2822. 19. Goldhaber SZ. Thrombolysis for pulmonary embolism. New England Journal of Medicine, 2002;347:1131–1132. 20. Sadeghi HM, Kimura BJ, Raisinghani A, et al. Does lowering pulmonary arterial pressure eliminate severe functional tricuspid regurgitation? Insights from pulmonary thromboendarterectomy. Journal of the American College of Cardiology, 2004;44:126–132. 21. Proano M, Oh JK, Frye RL, et al. Successful treatment of pulmonary embolism and associated mobile right atrial thrombus with use of a central thrombolytic infusion. Mayo Clinic Proceedings, 1988;63:118 1–1185. 22. Konstantinides S, Geibel A, Heusel G, et al., Management Strategies and Prognosis of Pulmonary Embolism -3 Trial Investigators. Heparin plus alteplase compared with heparin alone in patients with submassive pulmonary embolism. New England Journal of Medicine, 2002;347:1143–1150. 23. Ribeiro A, Lindmarker P, Johnsson H, et al. Pulmonary embolism: One -year follow-up with echocardiography doppler and five-year survival analysis. Circulation, 1999;99:1325–1330. 24. Wittlich N, Erbel R, Eichler A, et al. Detection of central pulmonary artery thromboemboli by transesophageal echocardiography in patients with severe pulmonary embolism. Journal of the American Society of Echocardiography, 1992;5:515–524.

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techom 25. Lang IM. Chronic thromboembolic pulmona ry hypertension–not so rare after all. New England Journal of Medicine, 2004;350:2236–2238. 26. Pengo V, Lensing AW, Prins MH, et al., Thromboembolic Pulmonary Hypertension Study Group. Incidence of chronic thromboembolic pulmonary hypertension after pulmonary embolism. New England Journal of Medicine, 2004;350:2257–2264. 27. Verzosa GC, McCully RB, Oh JK, et al. Effects of pulmonary thromboendarterectomy on right -sided echocardiographic parameters in patients with chronic thromboembolic pulmonary hypertension. Mayo Clinic Proceedings, 2006;81:777–782. 28. Packer DL, Keelan P, Munger TM, et al. Clinical presentation, investigation, and management of pulmonary vein stenosis complicating ablation for atrial fibrillation. Circulation, 2005;111:546–55 4.

13. 10 - Coronary Artery Disease and Acute Myocardial Infarction 10 Coronary Artery Disease and Acute Myocardial Infarction Echocardiography is the most commonly used and most practical imaging technique for the evaluation of patients who have coronary artery disease, chest pain, or acute myocardial infarction. Knowledge of global and regional systolic function and diastolic function is helpful in establishing the diagnosis, management strategy, and prognosis of patients who have coronary artery disease or who have had an acute myocardial infarction. Myocardial perfusion and contractility become abnormal immediately after the onset of ischemia. The resulting perfusion defect and regional wall motion abnormality (RWMA) can be detected readily with echocardiography, even before other ischemic manifestations. The treatment of acute myocardial infarction with thrombolysis or percutaneous coronary intervention (or both) has changed outcome and natural history of myocardial infarction. Without prompt diagnosis and early surgical intervention, mechanical complications of acute myocardial infarction are often fatal. Echocardiography, including transesophageal echocardiography (TEE), should be able 388

techom to identify most, if not all, mechanical complications of myocardial infarction. Some patients who have an acute myocardial infarction have no abnormalities in the epicardial coronary arteries ( 1). Echocardiography can still identify structural and functional changes associated with acute myocardial infarction in these patients. Exercise or pharmacologic stress echocardiography is valuable in predicting myocardial viability and prognosis as well as in detecting coronary artery disease (this is discussed in Chapter 11). Therefore, echocardiography has an important role, from the diagnosis of coronary artery disease, early detection of acute myocardial infarction (even in the absence of typical electrocardiographic [ECG] evidence), evaluation of RWMAs and viability after reperfusion therapy, detection of postinfarction mechani cal and functional complications, evaluation of unstable hemodynamics, and assessment of myocardial viability to prognostic risk stratification.

Evaluation of Myocardial Wall Motion The immediate manifestation of myocardial ischemia is a decrease in or cessation of myocardial contractility (systolic thickening), even before the occurrence of ST -segment changes or the development of symptoms. Ischemic myocardium may continue to demonstrate some degree of passive forward motion because of the pulling actio n of adjacent nonischemic muscle, but the contractility (systolic thickening) of the ischemic myocardial segments is decreased (hypokinesis) or absent (akinesis). Normally, left ventricular (LV) free wall thickness increases more than 40% during systole. I n normal subjects, the percentage of thickening of the ventricular septum is somewhat less than that of the free wall of the LV. Hypokinesis is defined as systolic wall thickening less than 30%, and akinesis is defined as wall thickening less than 10%. Dyskinesis is defined as a myocardial segment moving outward during systole, usually in association with systolic wall thinning. P.155

With multiple tomographic imaging planes, two -dimensional (2D) echocardiography allows visualization of all LV wall segmen ts. For purposes of regional wall motion analysis, the LV is divided into several segments. The American Society of Echocardiography has

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techom recommended a 16 -segment model ( 2) (see Fig. 7-14). Optionally, the apical tip is added as a 17th segment. Each segment is assigned a score on the basis of its contractility as assessed visually: normal = 1, hypokinesis = 2, akinesis = 3, dyskinesis = 4, and aneurysm = 5. On the basis of this wall motion analysis scheme, a wall motion score index (WMSI) is calculated to semiquantitate the extent of regional wall motion abnormalities:

A normally contracting LV has a WMSI of 1 (each of the 16 segments receives a wall motion score of 1; hence, the total score is 16 and WMSI is 16/16 = 1). The larger the infarct the higher th e WMSI because wall motion abnormalities become more severe. What does the WMSI indicate? Because the echocardiographic analysis of wall motion abnormality is subjective and the reduction of systolic myocardial thickening is not proportional to the incremental amount of infarcted or ischemic myocardial tissue ( 3), the correlation of the WMSI with the actual size of the myocardial infarct or the perfusion defect may not be good in the case of acute myocardial infarction. When a 2D echocardiographic examinati on was performed simultaneously with an injection of sestamibi in patients with acute myocardial infarction with ST -segment elevation on the ECG, the overall correlation between the WMSI and the perfusion defect was good ( 4). Patients with WMSI greater than 1.7 had a perfusion defect larger than 20%. The correlation was better in patients with an anterior wall myocardial infarction than in those with an inferior or lateral wall myocardial infarction with a smaller infarct size. However, it is possible to ha ve relatively normal myocardial contractility when there is a myocardial perfusion defect. Also, the reverse is true, depending on the clinical situation. Without a previous ischemic insult, a small subendocardial perfusion can be present when no visible contractility abnormality is evident. However, the myocardium may remain akinetic for a period of time after coronary reperfusion. Therefore, knowledge of both myocardial contractility and perfusion is vital for the management of the subset of patients with coronary artery disease. Another interesting subset of patients with acute myocardial infarction is the group with normal coronary arteries, for example, patients with apical ballooning syndrome, subarachnoid hemorrhage, or pheochromocytoma or those who have had electroconvulsive therapy ( 1,5,6,7). In these situations, marked wall motion abnormalities are present acutely but perfusion

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Figure 10-1 A: Parasternal long -axis (left) and apical long axis (right) views of the left ventricle ( LV) showing a thinned and akinetic inferolateral segment at the base ( arrows). It is difficult to demonstrate regional wall motion abnormalities in a still frame, but the configuration of the region is clearly abnormal. B: Apical four-chamber (left) and two-chamber (right) views demonstrating a dilated apical aneurysm or ballooning (arrows) in a 55-year-old woman with stress induced apical ballooning syndrome. LA, left atrium.

Technical Caveats A reliable regional wall motion analysis is among the most challenging tasks in echocardiography. All available windows and tomographic planes should be used to visualize all the LV segments (Fig. 10-1 A). Apical short - and long-axis views are especially useful in evaluating the apical third of the LV ( Fig. 10-1 B). Continuous scanning from the apical four -chamber to the apical long-axis to the apical two -chamber view allows complete visualization of all LV segments. In patients who have chronic obstructive pulmonary disease or who are obese, a lower frequency (2.0–2.5 MHz) transducer should be used to optimize the definition of the endocardium, and the subcostal window may

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techom provide adequate visualization of the LV segments. A new imaging method that uses th e principle of harmonic resonance (native harmonic imaging) can improve visualization of the endocardium (Fig. 10-2). In patients with a good apical window, the use of higher frequency transducers, with adjustment of the focal zone to the near region, may enhance the definition of the apical endocardium, help delineate apical wall motion abnormalities, and differentiate thrombus from apical trabeculation. The assessment of regional wall motion on echocardiography is limited when visualization of the LV endo cardium is not adequate. Several new modalities may enhance the ability to analyze regional wall motion. For example, the intravenous administration of contrast agent may enhance endocardial definition (see Chapter 6), and colorization of 2D echocardiograp hic images may improve visualization of the endocardial border. Newer ultrasound units hold promise in this regard, with more advanced technology to enhance visualization of the endocardium. Second harmonic imaging, initially created for contrast echocardi ography, improves visualization of cardiac structures as well as endocardial definition.

Evaluation of Chest Pain Syndrome Not all patients with prolonged chest pain resulting from myocardial ischemia or infarction present with typical ECG changes. More than 50% of patients with myocardial infarction have nonspecific findings on the initial ECG. Rapid assay of isoenzymes of creatine kinase (CK -MB) is reliable in detecting myocardial infarction within the first 6 hours after the onset of chest pain (8; however, the sensitivity of CK -MB isoenzymes assays may not be satisfactory if the assay is performed within 4 hours after the onset of chest pain. Troponin T and troponin I are more sensitive markers of necrotic myocardial tissue ( 9). More recently, plasma m yeloperoxidase a leukocyte enzyme, has been found to predict the risk of myocardial infarction in patients presenting to an emergency department with chest pain ( 10). The level of myeloperoxidase is increased in culprit lesions that P.156

have fissured o r ruptured in patients with sudden death from cardiac causes. Also, an increased level of myeloperoxidase independently predicted major cardiac events in the ensuing 1 month and 6-month periods.

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Figure 10-2 Demonstration of better visualization of the left ventricular (LV) endocardial border by native harmonic imaging. Parasternal long -axis views (top) and short-axis views (bottom) were scanned by fundamental imaging (2.5 MHz; left) and by native harmonic im aging (right) for comparison. LA, left atrium; RV, right ventricle; VS, ventricular septum.

Figure 10-3 A: Top, Color M-mode image, with yellow indicating systolic shortening ( s) and blue-white indicating diastolic lengthening ( d) in strain rate imaging. The time point of transition from shortening to lengthening (contraction to relaxation) is indicated by the solid black line. Middle, Strain rate tracing. *, Systolic wave; solid arrow, late diastolic wave; open arrow, early diastolic wave. Bottom, Electrocardiographic trace. An example of the time to onset of relaxation (T R ) (electrocardiogram R wave to the transition point) is illustrated at the bottom of the strain rate tracing. The dotted lines ( top) separate the septum into apical, mid, and basal segments. B:

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Strain rate color M -mode image illustrating a decrease in T R from baseline to peak stress in the nonischemic basal segment (black arrow) and minimal T R change in the ischemic apical segment (white arrow). (From Abraham et al [16]. Used with permission.)

The main advantages of echocardiography are that it can be performed in the emergency department and its findings are available immediately. As mentioned, myocardial contractility diminishes or ceases immediately after ischemia or infarction and is manifested as an RWMA that, in most patients, is readily identified with 2D echocardiography. Therefore, the use of RWMAs as a marker of myocardial infarction in patients with prolonged chest pain and nondiagnostic ECG findings is attractive. The absence of LV wall motion abnormalities usually excludes the presence of myocardial ischemia. Also, although the presence of RWMAs has a high sensitivity for detecting myocardial infarction, the positive predic tive value is about 30% because RWMAs are not specific for acute myocardial infarction and some patients have unstable angina without myocardial damage. However, echocardiography may not be helpful or cost -effective if patients have a low to intermediate r isk of acute myocardial infarction. Occasionally, echocardiography may be useful in detecting a potentially fatal cause of chest pain syndrome, such as pulmonary embolism, aortic dissection, or cardiac tamponade. The incidence of these findings is small, b ut anticoagulation or thrombolytic therapy in a subset of these patients may have a disastrous clinical outcome. The approach outlined here requires that the echocardiography examination and interpretation in the emergency department be prompt. Images can be interpreted at a distant site with the use of digital echocardiography, but having appropriately trained personnel available to perform echocardiography in the emergency department is a challenge. A 2D echocardiographic analysis of RWMAs is helpful diagnostically and clinically even in patients with classic chest pain and ST segment elevation on the ECG. The amount of myocardium at risk can be estimated by calculating the WMSI. A WMSI greater than 1.7 usually suggests a perfusion defect larger than 20% and increased complications unless the wall motion abnormalities are reversed with reperfusion therapy. Several days after reperfusion therapy, regional wall motion analysis is useful in assessing functional recovery, although myocardial contrast perfusion

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echocardiography can predict functional recovery soon after reperfusion therapy ( 11,12). A biphasic response during exercise echocardiography early after myocardial infarction also predicts myocardial viability ( 13). The amount of myocardium at risk from the affected artery also may determine which patients receive the greatest benefit from acute interventional therapy. Patients with a large amount of myocardium at risk (usually an anterior wal l myocardial infarction) will derive more benefit from reperfusion therapy than those with a small amount of myocardium at risk. When a patient presents with an ST-segment elevation myocardial infarction, the affected myocardium is akinetic or dyskinetic. After the myocardium has been reperfused successfully within an appropriate time (usually within 4 hours), it becomes more contractile on subsequent 2D echocardiography studies. Acute myocardial infarction may be aborted in a subset of patients if the ischemic duration is short. Serial echocardiography studies have demonstrated that the improvement in regional myocardial contractility is evident within 24 to 48 hours and that the improvement continues for several days to months. Therefore, follow -up 2D echocardiographic imaging is useful in detecting reperfused myocardial segments and infarct expansion. Persistent akinesis does not always indicate failed reperfusion. When the myocardium remains akinetic while being viable, low dose dobutamine or contrast ech ocardiography may be helpful in demonstrating its viability (see Chapter 11). Enlargement or remodeling of the LV, one of the strongest predictors of a cardiac event after myocardial infarction ( 14, is readily assessed with serial 2D echocardiography and c an be predicted by the lack of myocardial perfusion. Strain measurements have been used to identify acutely ischemic myocardium. In a study of patients undergoing elective coronary angioplasty, systolic strain was reduced and postsystolic strain was increased but delayed ( 15). Relaxation of ischemic myocardial segments is impaired and as a consequence, the physiologic early diastolic thinning and lengthening are replaced by ongoing postsystolic thickening and shortening. Therefore, it may be possible that t he abnormal regional deformation (i.e., reduction of systolic strain) or strain rate can be used as a marker of acute

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Acute Myocardial Infarction In many institutions world -wide, primary percutaneous coronary intervention (PCI) is the treatment of choice for acute myocardial infarction and mortality after acute myocardial infarction has decreased significantly. The role of echocardiograph y has evolved as the management strategy of acute myocardial infarction has changed. Its current role can be classified as follows: 1) diagnosis and exclusion of acute myocardial infarction in patients with prolonged chest pain and nondiagnostic ECG findin gs, 2) estimation of the amount of myocardium at risk and final infarct size after reperfusion therapy, 3) evaluation of unstable hemodynamics, 4) detection of infarct complications, 5) evaluation of myocardial viability, and 6) risk stratification. Theref ore, at various stages of acute myocardial infarction, echocardiography is important in providing anatomical, functional, and hemodynamic information.

Mechanical Complications and Cardiogenic Shock Because patients who have cardiogenic shock after myocardi al infarction have a poor prognosis unless the cause is reversible, it is of paramount clinical importance to identify promptly the underlying cause so that proper treatment can be given. In a study of an international registry from 19 medical centers, the cause of cardiogenic shock after myocardial infarction in 251 patients was severe LV failure in 85%, mechanical complications in 8%, right ventricular (RV) infarct in 2%, and other comorbid conditions in 5% (17). Two-dimensional and Doppler echocardiograp hy with color flow imaging are useful for promptly identifying the cause in these patients, especially in checking for mechanical complications. Echocardiography performed soon after acute myocardial infarction and shock showed that the severity of mitral regurgitation and LV ejection fraction (LVEF) were the only independent predictors of survival (18). In addition, TEE should be performed promptly in patients in whom precordial echocardiography may not be possible or if images obtained in the intensive ca re unit are suboptimal

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techom (19). The presence of normal systolic function in a critically ill or hemodynamically unstable patient should immediately lead to suspicion of a mechanical complication. Acute and chronic complications of myocardial infarction are li sted in Table 10-1.

Figure 10-4 Transthoracic parasternal short -axis (A) and apical four-chamber (B) views showing a dilated right ventricle (RV) and right atrium ( RA) in a patient with an RV infarct from an inferior wall myocardial infarction, indicated by an arrow pointing to thinned akinetic inferior and inferoseptal segments. C: Transesophageal four -chamber view demonstrating RV infarct. The chambers on the right s ide are markedly dilated, and the atrial septum ( AS) is deviated toward the left atrium (LA) because of increased RA pressure. A Swan -Ganz catheter and temporary pacemaker leads ( arrowheads) are seen in RA. D: Injection of contrast agent into a vein in the right arm opacifies the left -sided cardiac chambers immediately after opacification of the RA. E: Long-axis view of a transesophageal

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examination ( left) showing the atrial septum and patent foramen ovale ( arrow) in a patient with RV infarct and hypoxemia. Color flow imaging ( right) showing continuous right-to-left shunt (arrow) via a patent foramen ovale that was responsible for the patient's hypoxemia in the setting of RV infarct. A, anterior wall; L, lateral wall; LV, left ventricle; P, posterior wall; VS, ventricular septum.

Left Ventricular Failure and Remodeling Compared with 10 years ago in our coronary care unit, cardiogenic shock or heart failure due to LV systolic dysfunction is now less common after the first myocardial infarction, thanks to the tremendous clinical success with thrombolytic therapy and PCI. However, if cardiogenic shock develops after myocardial infarction, the mortality rate remains extremely high. Urgent coronary revascularization improves the outcome ( 20), but the mortality rate is still 40% to 50%. A more common clinical scenario is congestive heart failure and poor outcome due to progressive LV remodeling that is stimulated by the initial mechanical damage to the LV and subsequent neurohormonal modulation. With LV remodeling, the LV becomes larger and more spherical (i.e., more dilatation along the short axis of the LV), LVEF decreases, and mitral leaflets are displaced more apically, allowing increasing degrees of mitral regurgitation: all these features result in a worsening of heart failure and death. Clinical trials have demonstrated that β -blockade, angiotensin -converting enzyme (ACE) inhibitor, and biventricular pacing therapy ameliorate or reverse LV remodeling ( 21, 22, 23, 24). Ongoing trials are addressing the importance of surgical revascularization, surgical ventricular resection, passive constraint device, and mitral valve procedure in this patient population. Echocardiography is essential in managing these patients, and it assists clinical trials in LV remodeling by providing regional wall motion analysis and detailed information about LV size and volume, myocardial viability, LV filling pressures, severity of mitral regurgitation, and pulmonary artery systolic pressure.

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Figure 10-5 A: Cross section of a h eart with a lateral wall rupture that resulted in fatal hemopericardium. B: Transthoracic subcostal view demonstrating hemopericardium with gelatinous echodense material ( small arrow) in the pericardium in a hypotensive patient with a recent myocardial infarction. The pericardial effusion ( PE) was drained urgently, and the myocardial rupture was repaired. LV, left ventricle; RV, right ventricle.

Table 10-1 Complications of myocardial infarction

Acute phase LV systolic dysfunction Rupture Free wall rupture Ventricular septal defect Papillary muscle rupture Subepicardial aneurysm Mitral regurgitation LV dilatation Papillary muscle dysfunction Papillary muscle rupture LV thrombus Pericardial effusion/ta mponade RV infarct LVOT obstruction Chronic phase

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Infarct expansion Ventricular aneurysm True aneurysm Pseudoaneurysm LV thrombus

LV, left ventricle; LVOT, left ventricular outflow tract; RV, right ventricle.

Right Ventricular Infarct The RV frequently is involved in acute myocardial infarction; however, a hemodynamically significant RV infarct P.159

is infrequent and almost always associated with inferior wall myocardial infarction ( 25). However, once a patient de velops cardiogenic shock due to RV infarct, mortality is as high as for cardiogenic shock due to LV infarct ( 26). Revascularization improves survival. Patients who have an RV infarct present with increased jugular venous pressure but clear lung fields. The y may become hypotensive after the administration of nitroglycerin or develop shock that requires inotropic support and the administration of fluids. Echocardiographically, the RV is dilated and hypokinetic to akinetic ( Fig. 10-4). The apical portion of th e RV is supplied by the left anterior descending coronary artery P.160

and may contract normally while the basal to mid -RV free walls become affected in an RV infarct. The right atrium (RA) is also dilated, and tricuspid regurgitation becomes significant as a result of dilatation of the tricuspid anulus. Because RV systolic pressure is not increased, peak tricuspid regurgitation velocity is not high, usually less than 2 m/s. Tissue Doppler imaging of the tricuspid valve anulus may be helpful in identifyin g depressed RV function in patients with inferior wall myocardial infarction. In patients with a patent foramen ovale (PFO)an RV infarct creates an optimal clinical setting for a clinically significant right -to-left shunt through the PFO because of abnorma l RV compliance and markedly increased

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techom RA pressure. If a patient presents with hypoxemia after inferior wall myocardial infarction, an RV infarct and right -to-left shunt through a PFO should be strongly considered. This diagnosis can be confirmed with cont rast echocardiography (peripheral venous injection of agitated saline). Following opacification of the RA, the contrast medium enters the LA through the PFO. This situation is best assessed with TEE ( Fig. 10-4). In this clinical setting, the PFO and shunt can be closed with a closure device.

Figure 10-6 A: Gross pathology specimen showing a pseudoaneurysm at the level of the midinferolateral segment. B: Two-dimensional imaging ( left) of a free wall rupture (arrowhead) resulting in a false aneurysm ( FA) (pseudoaneurysm). The pulsed wave Doppler image ( right) shows to -and-fro blood flow velocities. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

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Figure 10-7 Echocardiography examination of a 54 -year-old man who had a myocardi al infarction 5 months earlier caused by complete occlusion of the diagonal artery. He had a syncopal spell 3 weeks after the acute myocardial infarction, and echocardiography showed a small amount of pericardial effusion. He came to Mayo Clinic for furthe r cardiac evaluation, and because chest radiography showed an abnormal cardiac contour, echocardiography was performed. A: An apical four chamber view showed apical dilatation consistent with an aneurysm cavity. In this view, the aneurysm appears to be a true aneurysm, with a relatively large neck. B: An apical twochamber view showed an abrupt discontinuity of the anterior wall (arrows) communicating with a large cavity that appeared to be a pseudoaneurysm ( PsA). The aneurysm cavity was pulsatile during sy stole in real -time imaging. C: Parasternal short-axis view also showing the tear or rupture of the anterolateral wall of the left ventricle ( LV) communicating with a PsA cavity. The space between the arrows is the mouth of the aneurysm cavity, which is relatively large. The myocardial rupture was repaired surgically. The rupture was found to be contained by the epicardial layer of the LV and pericardium. This entity has been termed subepicardial aneurysm. LA, left atrium; RA, right atrium.

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Free Wall Rupture and Pseudoaneurysm Cardiac free wall rupture usually is a fatal complication of acute myocardial infarction ( Fig. 10-5 A) that occurs in about 1% of all patients with myocardial infarction. It accounts for up to 7% of all infarct-related deaths. Typically, the rupture produces a sudden hemodynamic collapse due to cardiac tamponade (from hemopericardium) and electromechanical dissociation. Most ruptures occur within the first week after the infarction (me dian time, 4 days), and they are more common in women and elderly patients. Patients with rupture have less severe coronary artery disease and usually have a small myocardial infarction. Another clinical situation that potentially enhances cardiac rupture is the use of thrombolytic therapy (usually more than 10 hours after the onset of chest pain), presumably because of a hemorrhagic infarct. Although patients with infarct expansion are at higher risk for cardiac rupture, no specific echocardiographic featu res have been found to predict this highly fatal complication. Echocardiographic diagnosis of cardiac rupture depends on a high degree of clinical acumen because a subset of patients may present subacutely with syncope, hypotension, recurrent chest pain, o r emesis (or some combination of these) ( 27). A meticulous search by the echocardiographer for the site of rupture is mandatory if a region of thin myocardium or a small amount of pericardial effusion is present, particularly if a loculated effusion or clo t is detected ( Fig. 10-5 B). Detection of a free wall rupture in these patients allows surgical repair, with a survival rate greater than 50%. Not uncommonly, transthoracic 2D echocardiography may not be able to show the site of a rupture but only demonstr ate a pericardial effusion with or without the Doppler characteristics of pericardial tamponade. The presence of pericardial effusion alone is not sufficient to diagnose a free -wall rupture because pericardial effusion is relatively common after acute myoc ardial infarction. Myocardial contrast echocardiography and color flow imaging may help identify the site of rupture. Negative echocardiographic findings should not exclude myocardial rupture if clinical suspicion is high. In this case, another imaging tec hnique, such as magnetic resonance imaging, should be considered. In some cases, a pseudoaneurysm forms after a free wall rupture is contained within a limited portion of the pericardial space (most frequently in the posterior wall, followed by the lateral and apical wall) ( Fig. 10-6 403

techom A). A pseudoaneurysm is usually characterized by a small neck communication ( Fig. 10-6 B) that connects the LV and aneurysmal cavity (the ratio of the diameter of entry and the maximal diameter of the pseudoaneurysm is

anterior

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Pulmonar

Hypotensio

y edema

n

Hemodynami

O 2 sat. stepup

V wave

Dynamic

cs

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on PCWP

LVOT

>10%

tracing

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Fluids, β-

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α-agonist

LVOT, left ventricular outflow tract; PA, pulmonary artery; PCWP, pulmonary capillary wedge pressure; RA, right atrium; sat., saturation.

Ventricular Septal Rupture Ventricular septal rupture occurs in 1% to 3% of patients after myocardial infarction, and it occurs during the early phase of acute infarction (within the first week). As in free wall rupture, ventricular septal rupture is more common in elderly women who have not had a previous myocardial infarction. Nearly half of the patients in whom infarct -related ventricular septal rupture develops have single -vessel coronary artery disease. The typical clinical presentation is a new systolic murmur, with abrupt and progressive hemodynamic deterioration. The differential diagnosis of a new systolic murmur in patients with acute myocardial infarction includes infarct -related ventricular septal rupture, papillary muscle dysfunction or rupture, pericardial rub, acute LV outflow tract (LVOT) obstruction ( Fig. 10-10), and

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techom free wall rupture ( Table 10-2). After physical examination, echocardiography is the next logical noninvasive diagnostic procedure for all patients with a new murmur, especially for those who are hemodynami cally unstable. Infarct -related ventricular septal defect is diagnosed by the demonstration of a disrupted ventricular septum with a left -to-right shunt ( Fig. 10-11). The defect is always located in the region of thinned myocardium with dyskinetic motion. The diagnosis can be established in 90% of cases with a transthoracic 2D echocardiography examination. TEE may be necessary in a small subgroup of patients with a suboptimal precordial study ( Fig. 10-9). Peak flow velocity across the rupture measured with continuous wave Doppler echocardiography can be used to estimate RV systolic pressure (Fig. 10-11 E). When the rupture is in the inferoseptum, the myocardial infarction usually involves the RV, which portends a poor prognosis. An inferoseptal ventricular s eptal rupture can be a serpiginous septal tear, and an anteroapical septal ventricular septal rupture may evolve into an LV free wall rupture. Other transducer positions may be helpful in identifying a ventricular septal defect ( Fig. 10-12).

Figure 10-10 Transesophageal systolic frame of long -axis view in a 72-year-old woman with chest pain, hypotension, and systolic murmur. Left, Note large apical aneurysm, hyperdynamic inferobasal area ( upward arrow ) resulting in systolic anterior motion of the mit ral valve (downward arrow ), and dynamic left ventricular ( LV) outflow tract obstruction. Right, With infusion of phenylephrine (α -agonist), LV outflow tract obstruction ( single arrow) is less and hemodynamics are improved. Apical aneurysm ( three arrows) is not improved. This patient had only a mild degree of coronary disease. Her

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presentation can be classified as an apical ballooning syndrome, complicated by LV outflow tract obstruction. Ao, aorta; LA, left atrium; VS, ventricular septum.

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Currentl y, the therapeutic approach to an infarct -related ventricular septal rupture is urgent surgical intervention ( 32). Without a repair, the rupture is almost always fatal. Until the time of surgery, the patient's condition should be stabilized by afterload reduction (nitroprusside) and intra -aortic balloon pump counterpulsation. Closure device has been used in this situation, but no large experience with the device has been reported.

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Figure 10-11 Echocardiographic findings and postinfarction ventricular septal rupture. A: Transthoracic apical four chamber view demonstrating rupture ( arrow) of the ventricular septum ( VS) in a patient with anteroapical myocardial infarction. B: Left, Zoomed ventricu lar septal rupture ( arrow) and, right, color flow imaging demonstrating a shunt from the left ventricle ( LV) to the right ventricle ( RV). C: Transesophageal transverse view with the transducer in the midesophagus position demonstrating an apical anterosept al ventricular septal rupture ( arrowheads). This was the first ventricular septal rupture detected with transesophageal echocardiography at Mayo Clinic; the patient was an 81 -yearold woman with an anterior wall infarct and new systolic murmur. D: Transesophageal transgastric view of the LV demonstrating a serpiginous tear of the ventricular septum. Left, Tear in the left side of the ventricular septum ( single arrow in LV), with dissection into the myocardial cavity at that level; the right side of the sept um was intact ( three arrows). Right, Tear in the right side of the ventricular septum, more toward the apical level ( arrow). E: Continuous wave Doppler recording from the parasternal position of an infarct -related ventricular septal defect. The peak systol ic flow velocity is 3 m/s, corresponding to a 36 -mm-Hg pressure gradient between the LV and RV. Systolic blood pressure was 90 mm Hg; hence, RV systolic pressure = 90 - 36 = 54 mm Hg. There is a continuous shunt through the ventricular septal defect except during early diastole. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle; VS, ventricular septum.

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Figure 10-12 A: Transthoracic subcostal view showing a large inferoventricular septal defect ( arrow). B: Color flow imaging shows a shunt from the left to right ventricle via the ventricular septal defect. C: Continuous wave Doppler recording demonstrates high -velocity systolic flow ( yellow arrow) through the ventricular septal defect, indicating that RV sys tolic pressure is not markedly increased. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

Papillary Muscle Rupture Mitral regurgitation is common after acute myocardial infarction. Among 206 patients entering the Thrombolysis in Myocardial Infarction (TIMI) phase I trial, 13% had mitral regurgitation ( 33). In a study in Olmsted County, Minnesota, mitral regurgitation was present in 50% of patients after the first myocardial infarction, being mild in 38% and moderate to severe i n the other 12% ( 34). The incidence may be more common (up to 50% to 60%) if transient mitral regurgitation is included. In the TIMI -I trial, the presence of early mitral regurgitation independently predicted 1 year cardiovascular mortality, but a murmur o f mitral regurgitation was heard in fewer than 10% of the patients. In patients with cardiogenic shock after acute myocardial infarction, the presence of mitral regurgitation predicts a poor outcome ( 18). In the Olmsted County study, mitral regurgitation a lso predicted heart failure and mortality ( 34).

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cavity and mitral anulus dilatation, 2) papillary muscle dysfunction, 3) papillary muscle rupture, and 4) acute systolic anterior motion of the mitral valve. Therapeutically, it is important to recognize the exact underlying cause of ischemic mitral regurgitation because papillary muscle rupture mandates urgent replacement or rep air of the mitral valve, but mitral regurgitation due to papillary muscle dysfunction or anulus dilatation may improve with afterload reduction or coronary revascularization (or both). However, according to a large clinical study, acute reperfusion with thrombolysis or coronary angioplasty may not reliably reverse severe mitral regurgitation. Mitral regurgitation due to acute systolic anterior motion is managed with fluids, a β -blocker, or occasionally a pure α -agonist. Hemodynamically, papillary muscle r upture is the most serious complication involving the mitral valve. The patients usually have a small infarct in the distribution of the right or circumflex coronary artery. Because the posteromedial papillary muscle is supplied by a single coronary artery (in contrast to the dual supply of the anterolateral papillary muscle), it ruptures 6 to 10 times more often than the anterolateral papillary muscle. Echocardiography is the best way to diagnose papillary muscle dysfunction and rupture (Fig. 10-13). Rupture of a papillary muscle can be partial (incomplete) or complete. The severity of mitral regurgitation is assessed with Doppler color flow imaging. Because patients with severe mitral regurgitation usually present with hemodynamic decompensation, TEE may b e necessary to establish the diagnosis clearly and to assess the severity of mitral regurgitation ( Fig. 1014). After papillary muscle rupture has been diagnosed, urgent mitral valve replacement with or without coronary revascularization is necessary for s urvival. The long -term survival rate is satisfactory after successful surgical treatment.

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Figure 10-13 Apical long-axis view on transthoracic examination demonstrating partial rupture of the papillary muscle (arrow). Incidentally, a large amount of pleural effusion (PL) was noted. In real time, the inferolateral wall was akinetic and the anteroseptum was hyperdynamic. Ao, aorta; LA, left atrium; LV, left ventricle.

Figure 10-14 Transesophageal echocardiographic (TEE) images demonstrating rupture and dysfunction of papillary muscle with severe mitral valve regurgitation. A: Left, This was the first complete rupture of papillary muscle diagnosed with TEE at Mayo Clinic. Transverse view (using monoplane) demonstrates

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a ruptured papillary muscle prola psing into the left atrium ( LA) during diastole and attached to the posterior mitral leaflet (arrow in LA); arrow in left ventricle ( LV) indicates the anterior mitral leaflet. Right, Color flow imaging shows severe mitral regurgitation with a broad mitral regurgitation ( MR) jet. RA, right atrium; RV, right ventricle. B: Multiplane TEE image with the transducer at zero degree. This demonstrates a ruptured papillary muscle ( arrow) that is still attached to both mitral leaflets. C: It was difficult to assess t he severity of MR with surface echocardiography in an elderly woman with her first inferolateral acute myocardial infarction and cardiogenic shock but global systolic function was normal. TEE showed severe MR (left) caused by papillary muscle dysfunction a nd an akinetic inferolateral wall. Pulsed wave Doppler echocardiography (right) of the pulmonary vein shows systolic flow reversal ( SR), indicating severe mitral regurgitation. Coronary angiography showed complete occlusion of the left circumflex coronary artery. The patient underwent urgent mitral valve repair and recovered satisfactorily. ( A From Patel AM, Miller FA Jr, Khandheria BK, et al. Role of transesophageal echocardiography in the diagnosis of papillary muscle rupture secondary to myocardial infa rction. American Heart Journal, 1989; 118:1330–1333 . Used with permission.)

Figure 10-15 Apex-down, apical four -chamber view showing a large apical aneurysm. The apex is thinned and dilated, with

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dyskinetic motion in real time. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

Figure 10-16 A and B: Example of a pedunculated mobile apical thrombus ( arrow in A and Th in B) in a patient with an anteroapical infarct. The mobile nature of the thrombus can be appreciated by the varying shape of the thrombus in two separate frames. This appearance suggests a high probability of embolization. LA, left atrium; LV, left ventricle; RV, right ventricle.

Ischemic Mitral Regurgitation Ischemic mitral regurgitation refers to chronic mitral regurgitation caused by coronary artery disease. As in the acute phase of myocardial infarction, chronic ischemic mitral regurgitation has been found to be an important prognostic indicator ( 35). Even a mild degree of mitral regurgitation P.166

has been associated with increased mortality ( 36). After 5 years, total mortality and cardiac mortality for patients with ischemic mitral regurgitation ( 62% ± 5% and 50% ± 6%, respectively) were higher than for those without ischemic mitral regurgitation (39% ± 6% and 30% ± 5%, respectively). An effective regurgitant orifice of 20 mm 2 or more and a regurgitant volume of 30 mL or more were associated with increased mortality. Ischemic mitral regurgitation was not related to ejection fraction. The major determinant of the effective regurgitant orifice was mitral deformation, that is, sys tolic mitral valvular tenting area ( 37). This

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techom study by Yiu and colleagues also showed that tenting area is determined by the apical and posterior displacement of the papillary muscles and by the WMSI of the segments supporting the papillary muscles. Whethe r reducing mitral regurgitation surgically or with a percutaneous device procedure will improve the patient's quality of life or survival has not been determined by a clinical trial. The continuous remodeling process also has an important role in clinical outcome (38,39).

Acute Dynamic Left Ventricular Outflow Tract Obstruction Dynamic LVOT obstruction traditionally has been associated with hypertrophic cardiomyopathy. However, it can also develop after acute myocardial infarction and should be considered i n all patients who have a new murmur or unstable hemodynamics (or both) ( Fig. 10-10). Acute dynamic LVOT obstruction is related to the compensatory hyperdynamic motion of the posterior and inferolateral walls that results in systolic anterior motion of the mitral leaflet and also causes mitral regurgitation as well as the obstruction ( 40). Acute dynamic LVOT obstruction is more common in elderly women who have basal septal hypertrophy due to hypertension after anterior wall myocardial infarction. However, i t has occurred without myocardial infarction in patients who were hypovolumic or were treated with an inotropic agent. It has been noted in one -third of patients with apical ballooning syndrome (41). Patients with acute LVOT obstruction can develop severel y unstable hemodynamics, including shock and pulmonary edema. The most appropriate management includes fluids, β -blockers, αagonists, and avoidance of vasodilators and inotropics.

Pericardial Effusion and Tamponade Hemodynamically insignificant pericard ial effusion is common after myocardial infarction, especially after a large transmural anterior infarct. It is treated symptomatically; however, cardiac rupture may present as cardiac tamponade. In this situation, the pericardial sac may be filled with a gelatinous-appearing clot ( Fig. 10-5 B). If this occurs, urgent cardiac surgery is needed, and emergency pericardiocentesis may be required to stabilize the patient's condition until surgery. Rarely, after an acute myocardial infarction, constrictive peric arditis develops because of inflammation of the pericardium.

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True Ventricular Aneurysm and Thrombus A ventricular aneurysm is characterized by myocardial thinning and bulging motion during systole ( Fig. 10-15). Aneurysm formation is related to transmural m yocardial infarction and is found most frequently at the apex, followed by the inferobasal area. The apical view is the best window to visualize an apical aneurysm. An inferobasal aneurysm is visualized best from a parasternal long or apical two-chamber vi ew. A ventricular aneurysm is the consequence of infarct expansion, which indicates a poor prognosis. Ventricular aneurysms frequently harbor a thrombus and can be the focus of malignant ventricular arrhythmias. Because of concern about a potential embolic event, patients with a large apical infarct or a ventricular aneurysm are given anticoagulant therapy for at least 6 months after an infarct, at which time the chance for systemic embolism diminishes. The frequency of apical thrombus has decreased with th rombolytic therapy and therapeutic heparinization during hospitalization. Unless apical wall motion improves with reperfusion therapy, patients with an apical infarct remain at higher risk for developing thrombus after anticoagulant therapy is stopped. Two -dimensional echocardiography has become the most practical and reliable imaging modality for detecting LV thrombus. It is important to differentiate thrombus from chordae or artifacts frequently seen at the apex ( Fig. 10-16). Characteristically, a thrombu s has a nonhomogeneous echo density with a margin distinct from the underlying wall, which is akinetic to dyskinetic. A pedunculated thrombus has a greater chance of embolization than a sessile or a laminated thrombus. Contrast echocardiography is also hel pful in detecting LV thrombus (see Chapter 6). P.167

Acute Myocardial Infarction with Normal Coronary Arteries, Including “Tako-Tsubo” or Apical Ballooning Syndrome

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techom Not uncommonly, patients who present with acute myocardial infarction do not have coronary artery stenosis demonstrated on subsequent coronary angiography. These patients may have typical ST-segment elevation on ECG and increased levels of troponin or CK-MB. Echocardiography demonstrates typical regional wall motion abnormalities. Also, these patients can develop complications of acute myocardial infarction similar to those of patients with coronary artery disease. Clinical situations in which this scenario is seen include coronary spasm, subarachnoid hemorrhage, pheochromocytoma, and ap ical ballooning syndrome (1,5,41). The apical segment is usually involved, and acute LVOT obstruction has occurred in this setting. Characteristically, patients with sudden onset of subarachnoid hemorrhage present with T wave inversion on the ECG and, less frequently, ST -segment elevation. In these patients, echocardiography demonstrates regional and global myocardial dysfunction. However, the myocardial dysfunction resolves in a few days. Patients in whom myocardial dysfunction develops after subarachnoid hemorrhage have been found to have a higher catecholamine level. Increased P.168

cardiac troponin I has been associated with an increased risk of cardiac complications and death after subarachnoid hemorrhage (42). Apical ballooning syndrome was initially described as “tako-tsubo,” or ampulla cardiomyopathy, by Satoh and colleagues (41). (Tako-tsubo is an octopus -catching device that has a narrow neck.) With a ballooned apex and hyperdynamically contracting basal segment, the LV looks like a tako -tsubo (Fig. 1017). The Mayo Clinic experience with apical ballooning syndrome in 16 patients demonstrated the following ( 7: 1) all were postmenopausal women (mean age, 71 years), 2) all had a mild increase in troponin T and CK -MB levels despite extensive apica l akinesis to dyskinesis, 3) most patients presented with ST -segment elevation and few developed LVOT obstruction, 4) the initial LVEF was 0.395 and returned to normal (mean, 0.60) in 8 days, and 5) significant stress, either psychological or physical stre ss, was identified in almost all patients. These patients can have very unstable hemodynamics and should be supported in the usual manner because almost all of them recover fully. In a few patients with stress-induced cardiomyopathy, only mid -ventricular involvement has been observed with a normally contracting apex

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techom (43). Unless coronary spasm is identified, patients with apical ballooning syndrome should be treated with β -blockers.

Diastolic Function Myocardial ischemia alters diastolic function of the LV. The most prominent initial diastolic abnormality due to ischemia is prolonged and delayed myocardial relaxation. Relaxation becomes slower and delayed, resulting in prolongation of the isovolumic relaxation time (IVRT) and a lower transmitral pressure gradient at the time of mitral valve opening, which decreases early rapid filling (E) of the LV. The deceleration time (DT) of the E velocity is prolonged because of continued slow relaxation with an incompletely emptied LA; this results in augmented LA co ntraction (increased A velocity), which augments LV filling. The typical mitral flow pattern of a relaxation abnormality (↓E, ↑DT, ↑A, ↓E/A) is seen during transient myocardial ischemia (Fig. 10-18) and in patients with coronary artery disease ( 43). With myocardial infarction, the mitral flow velocity pattern depends on the interaction of various factors: relaxation abnormalities, ventricular compliance, LA pressure, loading conditions, heart rate, medications, and pericardial compliance in the sett ing of acute cardiac dilatation. Therefore, no particular mitral inflow pattern is seen consistently in patients with myocardial infarction. Although numerous factors influence transmitral Doppler velocities, increased LA pressure is one of the most import ant determinants and produces a restrictive diastolic filling pattern (↑E, ↓DT, ↓A, ↑E/A). Patients with acute myocardial infarction who demonstrate a restrictive filling pattern on transmitral Doppler echocardiography are more likely to experience P.169

heart failure from severe LV systolic dysfunction or severe underlying coronary artery disease (or both). Mitral deceleration time has been found to be a strong prognostic parameter of LV remodeling and survival after acute myocardial infarction ( 44, 45). Another diastolic index for LV filling pressure, the E/E′ ratio, was also found to be a strong predictor for survival after acute myocardial infarction ( 46,47).

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Figure 10-17 Left ventriculography during acute and subacute stages of apical ballooning syndrome. During the acute stage, the left ventricle looks like a balloon because of apical akinesis, but it returns to normal in a few days. (From Tsuchihashi et al [5]. Used with permission.)

Figure 10-18 Mitral inflow ( top) and anulus velocity ( bottom) at baseline ( left) and with chest pain due to ischemia ( right). With chest pain, mitral inflow becomes restrictive because of

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increased filling pressure. However, mitral anulu s velocities do not change greatly.

Risk Stratification After a patient has had a myocardial infarction, the most powerful prognostic indicators are the degree of systolic dysfunction, LV volume, the extent of coronary artery disease, mitral regurgitation, diastolic function, and the presence of heart failure. Therefore, it is reasonable to predict that patients who have a high WMSI have a greater chance of subsequently developing cardiac events. We have demonstrated that most of the patients with Killip class II -IV heart failure after acute myocardial infarction had a WMSI of 1.7 or higher. In addition to the WMSI, restrictive Doppler filling variables derived from mitral inflow velocities correlate well with the incidence of postinfarct heart failure and LV filling pressures (44,45). E/E′, a reliable variable for estimating pulmonary capillary wedge pressure, has been found to be a strong predictor of long-term outcome after acute myocardial infarction ( 46,47). LA volume, a surrogate for chronic diastolic dysfunction and chronic increase in LA pressure, is also a strong predictor for outcome after acute myocardial infarction ( 48). Echocardiographic variables that are affected by filling pressures determine the short -term prognosis (e.g., D T and E/E′), but echocardiographic variables that indicate chronic changes (e.g., LV volume and LA volume) determine the more long -term prognosis ( Fig. 10-19). Stress echocardiography is sensitive for detecting residual ischemia, myocardial viability, an d multivessel disease soon after myocardial infarction occurs. Usually, however, patients are unable to exercise adequately soon after an acute myocardial infarction. Many studies have demonstrated that stress echocardiography with dobutamine can be perfor med safely soon after acute myocardial infarction (3 to 5 days) and can provide predictable stress to the heart ( 49). Carlos and colleagues ( 49) demonstrated that the following information on dobutamine stress echocardiography was predictive of future adve rse outcome: 1) lack of myocardial viability (i.e., no increase in wall motion of the infarcted segment with a low dose of dobutamine) and 2) involvement of four or more segments with acute myocardial infarction (i.e., ≥25% of the LV). The myocardium rem ains akinetic for a period of time (days to weeks) after successful reperfusion of an occluded coronary artery.

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techom Demonstration of viability by augmentation of contractility (with dobutamine echocardiography) or demonstration of perfusion (with contrast echocardiography) predicts functional recovery. Dobutamine echocardiography and contrast echocardiography have similar sensitivity and specificity for predicting fractional recovery, although myocardial perfusion echocardiography is better for evaluating the a nterior wall than the inferior or lateral wall.

Figure 10-19 A: Both left atrial volume and deceleration time (DT) of mitral inflow are strong predictors of survival after myocardial infarction. A short DT (≤140 ms) predicts increased mortality in the short term (3 months), and increased left atrial volume index ( LAVI) (>32 mL/m2) is associated with increased mortality with longer follow -up. B: E/E′ >15, indicative of increased left ventricular ( LV) filling pressure, has been found to be associated w ith increased mortality after acute myocardial infarction, independent of underlying left ventricular ejection fraction ( EF). (B From Hillis et al [45]. Used with permission.)

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Figure 10-20 A: Parasternal long -axis view in 27-year-old man showing enlarged coronary sinus ( arrow). One of the causes of enlarged coronary sinus is a coronary fistula draining into the sinus. B: Left, Parasternal short -axis shows large coronary sinus (CS) and a tubular structure resembling a coronary artery (arrow). Right, Color flow imaging shows turbulent flow in CS. Ao, aorta; LA, left atrium; LV, left ventricle; RV, right ventricle.

In summary, patients at increased risk for future cardiac events after acute myocardial infarction can be identified by 1) systolic dysfunction (LVEF 0.75 cm 2 . Most patients with a ratio 0.85 cm 2 /m 2



Moderate: 0.60 < EOA ≤ 0.85 cm 2 /m 2



Severe: EOA ≤0.60 cm 2 /m 2

Moderate and severe degrees of PPM have been associated with increased mortality, which was higher in patient s with an LV ejection fraction less than 40% ( 14,15). At Mayo Clinic, for patients with severe mismatch, 5 -year survival rates (72% ± 6%) and 8-year survival rates (41% ± 8%) were significantly less than for patients with moderate mismatch (80% ± 3% and 65% ± 5%) or no hemodynamically significant mismatch (85% ± 3% and 74% ± 5%) ( 13). The following three -step approach is recommended to prevent PPM: 

Calculate the patient's body surface area (BSA)



Calculate the minimally acceptable EOA of the aortic prosthesis: BSA Ã — 0.85 cm 2



Choose and implant an aortic prosthesis with an EOA larger than the EOA calculated in step 2

Calculation of Effective Prosthetic Orifice Area The PHT method overestimates the area of a mitral prosthesis. The constant 220 (see Chapter 12) was derived for stenotic lesions of a native mitral valve and not for calculating the EOA of a mitral prosthesis. If there is no clinically significant aortic or mitral

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techom regurgitation, the continuity equation is a better method for determining t he area of mitral and aortic prostheses ( 4):

where MP is the mitral prosthesis and MP TVI is the time velocity integral of mitral prosthesis inflow velocity obtained with continuous wave Doppler echocardiography. The stenotic mitral valve area can also b e calculated by the PISA (proximal isovelocity surface area) method, as shown in Figure 139 for a patient who developed obstruction at the level of the mitral anulus. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle. The area of an aortic prosthesis can be estimated by the product of the TVI ratio (between the LVOT and aortic prosthesis) and the area of the LVOT, using the continuity equation:

where AP is the aortic prosthesis and SROD is the sewing -ring outer diameter. P.232

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The LVOT area is calculated from the outer diameter of the sewing ring. Aortic prosthesis TVI is obtained from the continuous wave Doppler velocity of the aortic prosthesis. The effective prosthesis area and LVOT TVI/AP TVI calculated from normal m itral and aortic prostheses, respectively, are shown in Tables 13-1, 13-2, 13-3 and 13-4.

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Figure 13-5 Continuous wave Doppler spectra in a patient with severe mitral valve ( MV) prosthetic regurgitation who has mitral and aortic prostheses. Left, The mitral velocity is increased to 3 m/s, but its pressure half -time is normal (60 milliseconds), indicating increased flow across the mitral prosthesis without obstruction. Right, The velocity through the aortic prosthesis is relatively low (1.6 m/s), indicating that the increased mitral flow velocity is due to mitral valve regurgitation rather than to a high systemic cardiac output. If mitral flow velocity is increased because of increased systemic cardiac output, the peak velocity across the aortic pr osthesis is expected to increase as well. AV, aortic valve.

Figure 13-6 A: Transesophageal echocardiogram showing a large thrombus ( arrows) attached to the left atrial ( LA) surface of a mechanical mitral prosthesis, causing an obstruction. Ao,

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aorta; LV, left ventricle. B: Continuous wave Doppler recording across the obstructed mitral prosthesis. Peak mitral prosthesis velocity is higher than 2 m/s and pressure half -time, hence, deceleration time ( DT), is prolonged. (Pressure half -time = 0.29 × DT.)

Figure 13-7 A: Longitudinal transesophageal view of a St. Jude Medical tricuspid valve prosthesis ( arrow). The disks of the prosthesis failed to move because of thrombotic obstruction. Ao, aorta; LA, left atrium; RA, right atrium. B: Continuous wave Doppler echocardiography examination from the apex showed peak velocity across the tricuspid valve prosthesis to be close to 2 m/s, with a slight respiratory variation that is typical for a tricuspid valve prosthesis. The velocity and mean gradient returned to baseline after 2 days of treatment with continuous infusion of streptokinase. After thrombolytic therapy, peak velocity was 1 m/s, with a mean gradient of 4 mm Hg.

Thrombolytic Therapy for Obstruction of Prosthetic Valves The formation of thrombus is responsible for 90% of obstructed prosthetic valves, with or without additional pannus formation.

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techom Inadequate anticoagulation has been noted in 48% to 92% of patients with prosthetic valve obstruction. Thrombus may be visualized wit h TEE, and its size is important in deciding on the optimal treatment strategy. Unless the thrombus is large (>5 mm), thrombolytic therapy appears to be a reasonable treatment for left sided as well as for right -sided heart prosthetic valve obstruction (16,17). According to a meta -analysis, the initial success rate is 80% to 85% and the rate of recurrent obstruction is 18% ( 18). The efficacy of different thrombolytic agents for valve obstruction and their risks are listed in Tables 13-6 and 13-7. The decisi on of whether to treat with thrombolysis or surgery should be made on the basis of each patient's clinical condition, functional status, valve location, and comorbid status. The management of patients who have prosthetic valve obstruction can be facilitate d if TEE can separate thrombus from pannus formation. Prosthetic valve obstruction due to thrombus can be predicted by inadequate anticoagulation, a soft mass seen on TEE, and a video intensity ratio (video intensity of mass/prosthetic valve) less than 0.7 (19).

Figure 13-8 A: Continuous wave Doppler examination of an obstructed mechanical mitral valve ( MV) prosthesis. Peak velocity was 2.2 m/s, with a pressure half -time of 290 milliseconds. DT, deceleration time. B: At the time of operation, the thrombus as well as pannus formation ( arrows) was identified along the sewing ring. C: The patient had a second mitral valve replacement, and postoperative continuous wave Doppler examination showed a peak velocity of 1.6 m/s ,

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with a mean gradient ( MG) of 4 mm Hg and a pressure half time (PHT) of 80 milliseconds.

After mechanical valve replacement, the addition of a low dose of aspirin to standard oral anticoagulation may reduce thromboembolic events, but it increases bleedin g P.234

complications ( 20,21). The current recommendations for adding aspirin to warfarin (Coumadin) therapy for patients with prosthetic heart valves are as follows ( 21): 

Patients with a mechanical valve who have a thromboembolic event despite adequate anticoagulation



Patients who have a caged ball or caged disk valve (international normalized ratio [INR] target, 3.0; range, 2.5–3.5)



Patients who have a mechanical valve and additional risk factors (INR target, 3.0; range, 2.5–3.5), including previous thromboembolism, atrial fibrillation, coronary P.235

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heart disease, a large left atrium (LA), LA thrombus, ball valve, more than one mechanical prosthetic valve, or a mechanical prosthetic valve in the mitral position 

A lower level of anticoagul ation (INR, 2.5; range, 2.0–3.0) with a low dose of aspirin instead of a target INR of 3.0 in patients with a tilting disk or bileaflet mechanical valve in the mitral position or a bileaflet mechanical valve in the aortic position plus atrial fibrillatio n.

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Table 13-6 Efficacy of thrombolytic agents used for valve obstruction, stratified by valve position Agent

Tissue-Type Plasminoge Streptokinase

Position

Mitral

Urokinase

n Activator

No. a

%

No. a

%

No. a

%

75/88

85

10/2

43

7/11

64

73

1/1

10

3

Aortic

24/32

11/1

75

5

0

Tricuspid

18/20

90

3/5

60

Pulmonar

5/5

10

1/1

10

y

Total

0

122/14

67

10/1

67

0

25/4

84 b

5

a

2/3

57

4

5

Number of patients in whom therapy was successful of

total number treated. b

P 1,767 pg/mL) were associated with an increased risk for all -cause mortality (7.0% vs. 21.6%) (18). Because of the good correlation between Doppler diastolic filling variables and NT -proBNP, the combination of information may have a mor e powerful prognostic implication than information from either source alone.

Echocardiography in the Management of Dilated Cardiomyopathy Proper timing of diastolic filling is important in optimizing cardiac output (Fig. 15-5). If the PR interval becomes prolonged (>200 milliseconds), atrial contraction may occur before early diastolic filling is completed. If the PR interval is too short (60–100 milliseconds), the atrium may contract at the same time as the ventricle. Therefore, by optimizing the PR int erval with the guidance of Doppler echocardiography, mitral inflow may increase cardiac output and the patient's symptoms may improve ( 19).

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techom Atrioventricular optimization is also important after a biventricular pacing P.254

device has been placed in patie nts who have mechanical dyssynchrony. The optimal atrioventricular delay can be achieved by identifying an interval that produces nonfused mitral E and A velocities without truncating the duration of A velocity. This can be done empirically by reviewing mi tral inflow velocities on various atrioventricular delays or by the method described by Ritter and colleagues (20) (see Chapter 5 and Fig. 5-11): SAV optimal = SAV s h o r t + d where d = (SAV l o n g + QA l o n g ) - (SAV s h o r t + QA s h o r t ) and SAV is sensed atrioventricular (AV) delay.

Figure 15-2 A: Mitral inflow pulsed wave Doppler recording. Mitral E velocity (50 cm/s) is similar to A velocity, and deceleration time ( DT) is not shortened. B: Tissue Doppler recording of the septal mitral anulus, showing reduced systolic velocity (S′), early diastolic velocity ( E′), and prominent positive velocity (toward the apex) during isovolumic relaxation (IVR). E/E′ = 50/6 = 8, indicating no marked increase in pulmonary capillary wedge pressure or filling pressure. C: Color M-mode of mitral inflow in dilated cardiomyopathy. Flow propagation velocity was calculated by measuring the slope of

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the mitral inflow excursion from the mitral anulus to the ape x. It was severely reduced (slope = 3.38 cm/0.204 s = 16.5 cm/s), indicating severe impairment of myocardial relaxation. (Normal propagation velocity is ≥50 cm/s.)

Left bundle branch block is common in patients with dilated cardiomyopathy. Intraventricular dyssynchrony created by a left bundle branch block results in ineffective cardiac contraction and heart failure ( 21,22). Tissue Doppler imaging and other modified techniques (tissue tracking, tissue synchronization imaging, or strain imagi ng) are able to quantify the degree of intraventricular dyssynchrony. The initial data suggest that patients with a greater dyssynchrony receive more benefit from cardiac resynchronization therapy than those with less dyssynchrony ( 23,24). Numerous variabl es can be quantified with echocardiography as a measure of mechanical dyssynchrony ( Fig. 15-6). Initial clinical experience suggests that intraventricular mechanical dyssynchrony (defined as more than a 60 -millisecond difference in time to peak tissue Doppler systolic velocity) between lateral and septal basal segments (25), more than a 100 -millisecond maximal difference in time to peak systolic velocities from 12 segments, or more than 33 milliseconds of standard deviation derived from 12 basal and mid level segments of LV best predicts who will have a good response to biventricular pacing ( 26). However, it is often difficult to identify the timing of peak systolic velocity, and there may be multiple systolic velocities when recorded by tissue Doppler echocardiography. It appears from our prospective data that dyssynchrony measured by strain imaging does provide better predictive value for identifying responders than dyssynchrony by tissue velocity ( 27). Which echocardiographic variables are most helpful in predicting a positive response P.255

to cardiac resynchronization requires additional clinical investigation.

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Figure 15-3 A: Two-dimensional parasternal long -axis view of typical dilated cardiomyopathy ( left) and pulsed wave Doppler velocity recording (right) of mitral valve ( MV) inflow showing a relaxation abnormality pattern with increased A velocity. Patients with this type of diastolic filling pattern usually have minimal to mild symptoms, despite severe left ventricular ( LV) systolic dysfunction. Two-dimensional parasternal long -axis view (B), and apical view ( C) of typical dilated cardiomyopathy (left) and MV inflow velocity pattern ( right) of restrictive physiology, with a markedly decreased A velocity and an increased E/A ratio. Deceleration tim e (DT) of mitral E velocity is shortened. Patients with this type of diastolic filling have increased filling pressure and symptomatic congestive heart failure. LA, left atrium; RA, right atrium; RV, right ventricle.

The use of a passive constraint device has been reported to minimize LV remodeling or even to result in reverse remodeling (28). Echocardiography is essential for identifying patients with dilated cardiomyopathy who are appropriate for these innovative therapies and for monitoring their respon ses. A randomized clinical trial (ACORN) was performed to assess a cardiac support device in patients with dilated cardiomyopathy. As the echocardiography core laboratory, the Mayo Clinic Echocardiography Laboratory measured all echocardiographic data. The se data showed that the decrease in LV volume and improvement in the sphericity index of the patients with the ACORN device were significantly more than those of patients without the device.

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Figure 15-4 Parasternal long -axis view of dilated cardiomyopathy. Mitral tenting ( dotted area) is only 2.66 cm 2 despite the markedly dilated left ventricular cavity. Color flow imaging showed only a mild degree of mitral regurgitation.

Mitral regurgitation frequently accompanies dilated cardiomyopathy, and its severity contributes to a worse clinical outcome. Reverse remodeling by medical or device therapy (or both) improves not only LV function but also mitral regurgitation. Some new devices are aimed at correcting mitral regurgitation without addressing progre ssive LV dilatation. Whether this approach directed toward mitral regurgitation alone improves the hemodynamics and survival of patients needs to be assessed in large clinical trials. According to a retrospective review of 419 patients with dilated or isch emic cardiomyopathy, mitral valve annuloplasty for moderate to severe mitral regurgitation had no clearly demonstrable mortality benefit ( 29). A prospective randomized controlled trial is warranted for this population. By reliably measuring structural, fun ctional, and hemodynamic variables, echocardiography is uniquely suited to monitoring the progression of dilated cardiomyopathy. Reverse remodeling has been attempted by surgical anterior ventricular endocardial restoration (SAVER), introduced in 1984 (30). It results in a characteristic P.256

echocardiographic appearance ( Fig. 15-7). This procedure is most suitable for patients who have a large LV (LV end -systolic volume ≥60 mL/m 2 ), scarred akinetic apex, and normally contracting

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Figure 15-5 A: Mitral flow velocity curve and simultaneous left atrial (LA) and left ventricular (LV) pressure curves in a 76 year-old man with a long PR interval and severe LV dysfunction (ejection fraction, 25%) due to severe coronary artery disease. He has severe New York Heart Association functional class IV symptoms. Left, Atrial pacing with anterograde native conduction and a long atrioventricular delay. There is an increase in LV pressure above LA pressure during atrial relaxation in mid -diastole (arrowhead), culminating in a shortening of diastolic filling time and onset of di astolic regurgitation. The baseline cardiac output ( CO) is 3.0 L/min. Center, Atrioventricular ( AV) pacing at a short AV interval of 60 milliseconds. Diastolic filling occurs through all of diastole. Atrial contraction now occurs simultaneously with LV contraction, resulting in a lower CO than on the left. Note that mean LA pressure increased from 31 mm Hg ( left) to 42 mm Hg (center). Right, AV pacing at the optimal AV interval of 180 milliseconds. The relation of atrial contraction to the onset of ventricular contraction is now optimal (see text), resulting in diastolic filling throughout the entire diastolic filling period. An appropriate relation exists between mechanical LA and LV contraction so that mean LA pressure is maintained at a low level (34 mm Hg), with LA contraction occurring just before LV contraction. This causes an increase in LV end -diastolic pressure to 43 mm Hg. CO has in creased to 5.2 L/min. B: Continuous wave Doppler image of mitral regurgitation signal and simultaneous LA and LV pressure curves in a patient with a

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long PR interval. Left, Normal sinus rhythm ( NSR) with a long intrinsic PR interval. Diastolic mitral regur gitation (arrowheads) is due to an increase in LV pressure above LA pressure before ventricular contraction. Center, P-synchronous pacing with a short AV interval of 60 milliseconds. Diastolic mitral regurgitation is no longer present, but there is a decre ase in CO from that on the left from an atrial contraction that is ineffective because it occurs during ventricular contraction. Right, P-synchronous pacing at the optimal AV interval (100 milliseconds). Diastolic mitral regurgitation is no longer present. LV diastolic pressure increases appropriately at the onset of ventricular contraction. LV pressure has increased from 30 mm Hg ( left) to 43 mm Hg ( right). (From Nishimura et al [19]. Used with permission.)

Figure 15-6 Measurement of intraventricular dyssynchrony with tissue Doppler imaging. A: Tissue Doppler recording of septal (yellow) and lateral ( blue) wall velocity at baseline in a patient with congestive heart failure, a left ventricular ejection fraction of 25%, and a left bundle branch block. There is a substantial difference in their peak ejection velocities ( arrows). B: After biventricular pacing, tissue velocities from the septal and lateral wall are superimposable ( arrow). AVC, aortic valve closure; AVO, aortic valve opening.

Hypertrophic Cardiomyopathy Two-Dimensional and M-Mode Echocardiography

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techom Hypertrophic cardiomyopathy is a genetic disorder caused by a missense mutation in 1 of at least 10 genes that encode the proteins of the cardiac sarcomere ( 5). Mutations P.257

associated with hypertrophic cardiomyopathy are scattered throughout sarcomeric genes, with mutations in the gene encoding the β-myosin heavy chain representing one of the most common genetic causes of hypertrophic cardiomyopathy ( 31). The phenotypic expression of hypertrophic cardiomyopathy, which occurs in 1 of every 500 adults, includes massive hypertrophy involving primarily the ventricular septum.

Figure 15-7 Apical four-chamber view showing the typical appearance of surgical anterior ventricular endocardial restoration (SAVER). Arrows, a patch used in SAVER procedure. LA, left atrium; LV, left ventricle.

Although asymmetric septal hypertrophy is the most common type of morphologic pattern, hypertrophic cardiomyopathy can present with concentric, apical, or free wall LV hypertrophy ( 5,32,33,34) (Fig. 15-8). When the basal septum is hypertrophied and bulging, the LVOT becomes narrowed, providing a substrate for dynamic obstruction. The velocity of blood flow across the narrowed LVOT increases and produces the Venturi effect. Consequently, the mitral leaflets and support apparatus are drawn toward the septum (i.e., systolic anterior motion), obstructing the LV OT (Fig. 15-9). This obstruction is dynamic and depends on the loading conditions and LV size and contractility. When aortic flow is interrupted by

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Figure 15-8 A: Parasternal long-axis view of hypertrophic cardiomyopathy (nonobstructive variant). The ventricular septum ( VS) is asymmetrically hypertrophied compared with the posterior wall ( PW). The left atrium ( LA) is mildly enlarged. LV, left ventricle; MV, mitral valve; OT, outflow tract; RV, right ventricle. B: Diastolic and systolic frames of the parasternal short-axis view. The entire VS is uniformly and markedly thickened, as is the anterolateral LV free wall. Note that the posteroinferior wall is of normal thickness. A lso note the abnormal texture of the involved myocardium. The principal difference from another form of hypertrophic cardiomyopathy is no obstruction of resting LV outflow tract.

M-mode echocardiography is useful in documenting asymmetric septal hypertrophy, systolic anterior motion of the mitral valve (see Fig. 2-19 B), and midsystolic aortic valve closure. Asymmetric septal hypertrophy is also seen in RV hypertrophy, hypertension , and inferior wall myocardial infarction with preceding LV hypertrophy. Systolic anterior motion of the mitral valve can be seen also in other hyperdynamic cardiac conditions. Two dimensional (2D) echocardiography is the method of choice for establishing the diagnosis of hypertrophic cardiomyopathy. Furthermore, detailed morphologic characterization is provided by 2D echocardiographic imaging. The most frequent morphologic variety of hypertrophic cardiomyopathy consists of diffuse

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techom hypertrophy of the ventri cular septum and anterolateral free wall (70%–75% of cases), followed by basal septal hypertrophy (10%–15% of cases), concentric hypertrophy (5% of cases), apical hypertrophy (15 mm). Although increased wall thickness seen on two -dimensional (2D) echocardiography is the hallmark of cardiac amyloidosis, the diagnosis cannot be excluded when wall thickness is not increased. Amyloid deposits in the he art are diffuse and involve the valves, myocardium, interatrial septum, and pericardium ( 3). It is common to detect multivalvular regurgitation due to diffuse amyloid

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techom deposits in the cardiac valves. Amyloid deposits make the myocardium sparkle on 2D echoca rdiography; this produces a beautiful image, but the sparkling appearance alone is not diagnostic of cardiac amyloidosis with harmonic imaging because the sparkling appearance is common in patients who do not have cardiac amyloidosis. Other conditions may produce similar echocardiographic features, for example, hypertensive disease (especially in patients with renal failure), glycogen storage disease (4), and hypertrophic cardiomyopathy. Patients with cardiac amyloidosis usually have a low QRS voltage or a pseudoinfarct pattern on the electrocardiogram (ECG) ( Fig. 16-3), whereas those with LV hypertrophy, hypertrophic cardiomyopathy, or glycogen storage disease have increased QRS voltages of the LV hypertrophy pattern (Fig. 16-4). Although it can be difficul t with 2D echocardiography to differentiate infiltrative cardiomyopathy, such as Fabry disease, from hypertrophic cardiomyopathy or P.275

other forms of LV hypertrophy, the echocardiographic binary appearance of the LV endocardial border, reflecting compartmentalization of endomyocardial glycosphingolipids, may be helpful in diagnosing Fabry disease ( 5) (Fig. 16-4 right). During an early stage of cardiac amyloidosis, systolic function can be hyperdynamic, and it is not uncommon to see systolic anterior motion of the mitral valve and intracavitary obstruction, as in hypertrophic cardiomyopathy ( 6). As the disease progresses, however, systolic function gradually deteriorates.

Table 16-1 Echocardiographic features of cardiac manifestations of systemic illnesses

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Amyloidosis Increased LV and RV wall thickness (moderate to marked) Normal LV cavity size Gradual deterioration of ventricular systolic function Granular appearance of myocardium (abnormal texture) Pericardial effusion Spectrum of diastolic dysfunction Thickening of the valves and multivalvular regurgitation Ankylosing spondylitis Dilatation of the aortic anulus Dilatation of sinuses of Valsalva Thickened aortic valve with aortic regurgitation Carcinoid Thickening and retraction of tricuspid valve with severe tricuspid regurgitation Tricuspid stenosis, usually mild Pulmonary valve thickening and retraction with pulmonic stenosis RV volume overload Thickening of valves on left side (600 mg/m 2 ) and cyclophosphamide (>6.2 g/m 2 ) (15). In addition, pericardial effusion or tamponade may develop after cyclophosphamide therapy. Severe LV systolic dy sfunction has been reported also in bulimic patients who ingested ipecac (16). 664

techom Emetine, the principal component of ipecac, causes mitochondrial damage by inhibiting oxidative phosphorylation. Long -term highdose corticosteroid therapy may result in LV syst olic dysfunction. Cardiac function can be suppressed by phenothiazine and tricyclic antidepressants.

Figure 16-8 Gross pathologic specimen of carcinoid heart disease. A: The pulmonic valve leaflets are thickened, retracted, and shortened, with a fixed opening. Note the fibrous endocardial plaque ( arrows). B: The tricuspid valve leaflets and chordae are thickened and retracted. (From Click RL, Olson LJ, Edwards WD, et al. Echocardiography and systemic diseases. Journal of the American Society of Echocardiography , 1994;7:201–216 . Used with permission.)

Long-term use of chloroquine (>1,000 g) may result in infiltrative cardiomyopathy similar to Fabry disease, with the following echocardiographic features ( Fig. 16-13): 1) increased LV wall thickness with or without increased RV wall thickness, 2) biatrial enlargement, 3) restrictive diastolic filling, and 4) valvular regurgitation. Chloroquine is taken up by lysosomes, a nd abnormal lysosomal enzymatic activities cause the accumulation of glycogen and phospholipids ( 17). Light microscopy findings include vacuolated cytoplasm of myocytes ( Fig. 16-14). These changes develop preferentially in the ventricular septum, which may explain the conduction abnormality in this disorder ( 17). These abnormalities resolve after treatment with chloroquine is discontinued. Cardiac valves may be affected by drug toxicity. Ergot alkaloids may produce valvular lesions similar to those of rheum atic or

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techom carcinoid (or both) valvular disease ( 18). The 2D echocardiographic findings are similar to those for the P.280

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abnormalities already mentioned, but microscopic examination shows fibrous plaque stuck on relatively normal valve tissue in patients who have taken ergot alkaloids. Anorectic drugs have been implicated as causes of valvulopathy or pulmonary hypertension (or both). In Europe in the late 1960s and early 1970s, aminorex was found to cause pulmonary hypertension. Connolly and colle agues (19) reported on 24 patients who took “fen -phen” and were found to have aortic, mitral, or tricuspid regurgitation ( Fig. 16-15). Subsequent studies have documented an P.282

8% to 30% prevalence of valvular regurgitation in patients who took “ fen-phen” for various lengths of time ( 20,21). Valvular regurgitation or pulmonary hypertension has been identified in patients who took the medication for less than 1 month. It is recommended that patients who have taken fenfluramine or dexfenfluramine with or without phentermine have an echocardiography examination if symptoms or signs of valvular regurgitation develop. Valvular regurgitation is considered to be associated with “fen -phen” when echocardiography demonstrates mild aortic regurgitation or a moderate degree of mitral regurgitation. Aortic regurgitation is more common than mitral regurgitation. A similar regurgitant lesion of the tricuspid and mitral valves has been reported in patients who took pergolide (22).

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Figure 16-9 Microscopic surgical pathology specimens. A: Tricuspid leaflets with “stuck -on” plaque along the ventricular aspect. B: A pulmonary cusp with carcinoid plaque. (From Simula et al [11]. Used with permission of Mayo Foundation for Medical Education and Research.)

Figure 16-10 A (left): Two-dimensional systolic frame of the right ventricular ( RV) inflow view showing carcinoid involvement of the tricuspid valve ( TV). The anterior and septal tricuspid leaflets do not coapt because of retraction and thickening, which results in severe tricuspid regurgitation. Right, Color flow imaging shows severe tricuspid regurgitation. RA, right atrium. B: Continuous wave Doppler signal of

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tricuspid flow in carcinoid heart disease. The systolic tricuspid regurgitation velocity is 2.5 m/s, which is higher than expected for pure severe tricuspid regurgitation. If RA pressure is assumed to be 20 mm Hg, RV systolic pressure is 45 mm Hg because of the mild degree of pulmonary stenosis in carcinoid. Concavity (arrows) of the downslope of tricuspid regurgitation corresponds to the “V† wave because of severe regurgitation. Diastolic inflow velocity is increased because of severe tricuspid regurgitation. C: Parasternal short-axis view at the level of the pulmonary valve showi ng carcinoid involvement of the pulmonary valve. The pulmonary valve anulus ( arrow) is retracted and narrowed, and the valve is diminutive. Ao, aorta; PA, pulmonary artery. D: Continuous wave Doppler signal from the narrowed pulmonary valve shows mild stenosis, with a peak systolic velocity of 2 m/s and a regurgitant signal with a short deceleration time due to rapid equalization ( downward arrow ) of the RV and pulmonary artery diastolic pressures before the onset of QRS. There is also diastolic flow ( upward arrow) across the pulmonary valve because of a rapid increase in RV diastolic pressure.

Figure 16-11 Subcostal view in a patient with metastatic carcinoid. A: A large mass in the liver is a metastatic tumor (Met) from carcinoid. B: Color flow imaging shows yellow -

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orange flow in the hepatic vein during systole, characteristic for severe tricuspid regurgitation. IVC, inferior vena cava. C: Pulsed wave Doppler rec ording from the hepatic vein shows marked systolic flow reversal ( arrows).

Figure 16-12 A: Myocardial metastases ( M) in the left ventricular (LV) wall of a 61-year-old man who also had carcinoid involvement of the tricuspid and pulmonary valves. This was confirmed pathologically. B: Metastasis in the right ventricular outflow tract. Ao, aorta. (A From Pandya et al [12]. Used with permission.)

Figure 16-13 Parasternal long -axis (A) and apical four chamber (B) views from a 38 -year-old woman with lupus that was treated with chloroquine. The echocardiographic appearance resembles that of hypertrophic cardiomyopathy. The mitral valve (arrows) is also thick, affected by chloroquine.

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LA, left atrium; LV, left ventricle; PW, posterior wall; RA, right atrium; RV, right ventricle; VS, ventricular septum.

Figure 16-14 Light (A) and electron ( B) microscopy examination of right ventricular endocardial biopsy tissue showing, A, vacuolization, and B, left, myelinoid bodies and, right, curvilinear bodies ( A: Hematoxyln-eosin, medium power; B [left]: × 10,000 and right, × 35,000).

Hemochromatosis Idiopathic hemochromatosis, an autosomal recessive disease, is an iron-overload disorder associated with mutation of the HFE gene located on chromosome 6 ( 23). The incidence of this disorder is 2 3/1,000 population. It is characterized by large deposits of iron in various organs, including the heart, liver, testes, and pancreas. When the heart is involved, the disease is usually in an advanced stage, with multiorgan involvement. The severity of myocardial dysfunction is proportional to the amount of iron de posited in the myocardium. Myocardial deposits of excessive iron interfere with myocardial cellular function and result in LV dilatation and systolic dysfunction, as in dilated cardiomyopathy ( Fig. 16-16). P.283

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Progressive congestive heart failu re is the most frequent cause of death of patients with hemochromatosis. Therefore, if a patient

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techom presents with heart failure and features of dilated cardiomyopathy of unknown cause, the iron level, iron -binding capacity, and ferritin level should be determ ined. The typical 2D echocardiographic findings of cardiac hemochromatosis include mild LV dilatation, LV systolic dysfunction, normal wall thickness, normal heart valves, and biatrial enlargement ( 24). Dilatation of the heart chambers produces various deg rees of mitral and tricuspid valve regurgitation. When a patient presents with congestive heart failure, the LV diastolic filling pattern is usually restrictive and the morphologic features are those of dilated cardiomyopathy. These typical echocardiograph ic features were found in 37% of patients with hemochromatosis evaluated at Mayo Clinic ( 24). Most of the patients with these echocardiographic findings died within 6 months after the echocardiography study. The LV dysfunction can be reversed, sometimes co mpletely, with chronic phlebotomies. Serial echocardiography examinations are useful for monitoring the response of LV function.

Figure 16-15 A: Gross specimen of an explanted mitral valve from a 45-year-old woman who took “fen -phen” for 11 months. The leaflets and chordae are glistening and thickened. B: Low-power view of a section of the resected mitral valve from a 44-year-old woman who took “fen -phen” for 12 months. Note the intact valve structure, with “stuck -on”

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plaques (arrows). (Elastic-van Gieson stain; à — 36.) C (left): Typical echocardiographic features of the mitral valve associated with “fen -phen” treatment. Both the aortic valve (AV) and mitral valve ( MV) are thickened. The anterior mitral leaflet ( arrow) shows doming during diastole, resembling a rheumatic MV. Right, Color flow imaging shows severe aortic regurgitation ( AR). LA, left atrium; RV, right ventricle. ( B From Connolly et al [19]. Used with permission.)

Figure 16-16 Hemochromatosis. A: Histologic section of myocardial biopsy specimen showing iron ( black stain ) within the myocardial cells ( arrows). B: Gross pathology specimen with the reddish brown rust appearance and dilated cardiac chambers characteristic of cardiac hemochromatosis. LV, left ventricle; RV, right ventricle. (From Click RL, Olson LJ, Edwards WD, et al. Echocardiography and systemic diseases. Journal of the American Society of Echocardiography , 1994;7:201–216 . Used with permission.)

Hypereosinophilic Syndrome Hypereosinophilic syndrome is defined as a persistent (>6 months) eosinophilia with more than 1,500 eosinophils/mm 3 and evidence of organ involvement. Cardiac involvement in hypereosinophilic syndrome is common and involves both the right and left sides of the heart, with endocardial thickening of the inflow areas and thrombotic-fibrotic obliteration of the ventricular apices ( Fig. 1617). Of 51 patients (mean age, 44 ± 18 years) with hypereosinophilia evaluated at Mayo Clinic, 29 had the

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techom characteristic ec hocardiographic findings ( 25). These findings include limited motion of the posterior mitral leaflet (resulting in mitral regurgitation of varying severity) in combination with thickening of the inferobasal LV wall, endocardial thrombotic fibrotic lesion, and biventricular apical obliteration by thrombus. Myocardial contrast imaging demonstrates the characteristic apical thrombus (16,17). The obliteration of the apical cavity and eosinophilic involvement of the endocardium decrease ventricular compliance and limit ventricular diastolic filling, producing restrictive physiology pattern on pulsed wave Doppler echocardiography and strain imaging ( 26). Rarely, acute hypereosinophilic crisis produces diffuse myocarditis, with dilatation of the ventricular cavit y and a marked decrease in systolic function. Patients usually die of severe heart failure or uncontrollable ventricular arrhythmias.

Figure 16-17 Left: Apical four-chamber view from a young woman with hypereosinophilic syndrome, showing apical obliteration of the left ventricle ( LV) and right ventricle ( RV) because of deposits of thrombus and eosinophils. The underlying myocardial contractility is not impaired. This condition should be differentiated from apical hypertrophic cardiomyopathy, in which the apical cavity is obliterated by hypertrophied myocardium but still has a slitlike cavity inside the hyperdynamic myocardium. Right, Myocardial contrast shows black wedge -shaped thrombus ( arrows) in the LV apex, which has good perfusion. It is very differe nt from apical hypertrophic cardiomyopathy. LA, left atrium; RA, right atrium.

Radiation-Induced Cardiac Diseases

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techom Radiation to the mediastinum can damage the coronary arteries, pericardium, valves, or myocardium and result in proximal coronary stenosis, pericardial effusion, constrictive pericarditis, a regurgitant valve, restrictive cardiomyopathy, or a combination o f these. Radiation -induced valve damage is manifested as thickening and regurgitation of any valve, although the tricuspid valve is involved most frequently. A more severe cardiac manifestation is failure of the right side of the heart from constrictive pe ricarditis or restrictive cardiomyopathy (or both). Radiation -induced constriction has the worst prognosis, even after pericardiectomy. Two-dimensional and Doppler echocardiography features of constriction and restriction are discussed in detail in Chapter 17.

Renal Failure Patients who have chronic renal failure are usually hypertensive, and the most prominent echocardiographic finding is increased LV wall thickness related to LV hypertrophy. The myocardial texture in LV hypertrophy appears similar to that of cardiac amyloidosis, but these two conditions can be distinguished. Chronic renal failure is associated with LV hypertrophy, and cardiac amyloidosis is associated with decreased voltage on ECG. Although systolic function is normal in the early stage of chronic renal failure, diastolic function is abnormal, with decreased myocardial relaxation. As the disease progresses with decreased compliance of the myocardium, the LV filling pressure increases and the diastolic filling pattern may become pseudonormal ized or even restrictive. Also, LV systolic function may decrease with long -standing hypertension. Small amounts of pericardial effusion are common, especially in patients undergoing long -term hemodialysis. Chronic renal failure commonly causes valvular sc lerosis with calcification; the mitral anulus is also calcified.

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Figure 16-18 Typical two-dimensional echocardiographic findings in scleroderma or CREST syndrome. A: A circumferential pericardial effusion ( PE) with an enlarged right ventricle (RV) due to pulmonary hypertension. LA, left atrium; LV, left ventricle. B: A flattened ventricular septum ( VS) creates a D-shaped LV; also note enlargement of the RV and a circumferential PE. The patient had clinical and Doppler echocardiographic evidence of cardiac tamponade. However, the RV did not collapse during early diastole because of pulmonary hypertension.

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Sarcoidosis Sarcoidosis is a granulomatous disease of unknown cause involving multiple organs. Its most important manifestation is caused by pulmonary involvement, resulting in diffuse pulmonary fibrosis, right-sided heart failure, and pulmonary hypertension ( 26). Cardiac involvement is uncommon, occurring in fewer than 20% of patients. The myocardium is involved by noncaseating granulomas, producing myocardial fibrosis and regional wall motion abnormalities. The fibrosis occurs predominantly at the mid and basal levels of the LV, although global involvement may occur. Thinning and aneurysmal formation develop, mainly at the basal inferior an d lateral portions of the LV. Therefore, the 2D echocardiographic features include a dilated LV with regional wall motion abnormalities, especially at the mid and basal levels of the LV (27). A posterior basal aneurysm may be seen. These echocardiographic features were found in 14% of the patients with sarcoidosis who were evaluated at Mayo Clinic, and the symptoms of congestive heart failure were more common in these patients (27). Although angiotensin -converting enzyme (ACE) levels are commonly used to di agnose sarcoidosis, most patients who had the echocardiographic features of cardiac involvement had normal ACE levels and noncaseating granulomas in the endomyocardial biopsy specimen. Therefore, normal ACE levels do not exclude active cardiac sarcoidosis and should not deter one from obtaining endomyocardial biopsy specimens to make the diagnosis.

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techom Wegener granulomatosis is characterized by a necrotizing granulomatous lesion of the respiratory tract, vasculitis, and glomerulonephritis . It can involve other organs, including the heart. Atypical regional wall motion abnormalities and aortic valve regurgitation have been reported ( 28).

Scleroderma The most common cardiac abnormality associated with scleroderma is a pericardial lesion, whi ch has been reported in up to 78% of patients (29). Cardiac tamponade that requires pericardiocentesis rarely develops, although pericardial effusion is common. Pulmonary hypertension is a prominent feature of scleroderma ( Fig. 16-18) and the cause of a patient's shortness of breath. Tricuspid regurgitation velocity should be reported in all patients with scleroderma. The myocardium may be involved by fibrosis or sclerosis, resulting in systolic and diastolic dysfunction. Therefore, an evaluation of globa l systolic and diastolic function should be an essential part of the echocardiography examination of patients who have scleroderma.

Sepsis Frequently, LV dilatation and decreased LV ejection fraction (LVEF) are observed in patients with sepsis and septic s hock (30,31). In patients who survive, the LV dilatation and systolic dysfunction are reversible. The cause of myocardial dysfunction in sepsis is not clear. It may be related to a circulating myocardial depressant, such as an endotoxin, tumor necrosis fac tor, or an interleukin. It has been suggested that the activation of caspase -3 is important in endotoxin-induced cardiomyocyte dysfunction, which may be related to a change in the calcium myofilament response, contractile protein cleavage, and sarcoma diso rganization (32). Therefore, in patients with sepsis, echocardiography frequently shows a dilated LV with a decreased LVEF. Stroke P.286

volume may be maintained (normal LV outflow tract time velocity integral and velocity) or reduced. Certain infections result in characteristic cardiac and echocardiographic abnormalities: an intracardiac mass in echinococcosis or tuberculosis, pericarditis in a viral or bacterial infection or in tuberculosis, and a ventricular aneurysm in Chagas disease.

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Chagas Disease Chagas disease (American trypanosomiasis) is little known in North America but is endemic in all Latin American countries. In infected patients, heart muscle is invaded by the protozoan parasite Trypanosoma cruzi . This produces characteristic abnormalities: biventricular enlargement, ventricular aneurysms, thinning of the ventricular wall, and mural thrombi ( 33). The conduction system is also affected, causing conduction abnormalities. With an increasing number of persons who are infected with T. cruzi immigrating to North America, it is important for physicians and sonographers to be familiar with the echocardiographic manifestations of this infection.

Spondyloarthropathies and Vasculitis Spondyloarthropathy with cardiac involvement includes ankylosing spondylitis and Reiter syndrome. Cardiac manifestations of ankylosing spondylitis include aortic regurgitation, pericardial effusion, and conduction abnormalities. Aortic regurgitation results from thickening of the aortic valve cusps, displacement of the cusps by the fibrous tissue bump, and dilatation of the aortic root. Patients with ankylosing spondylitis may need aortic valve replacement because of severe aortic valve regurgitation. Aortic regurgitation with dilatation of the aorta is found also in patients who have Reiter syndrome or psoriatic arthritis. Behçet syndrome can cause thickening of the aortic wall at the aortic root, resulting in severe aortic regurgitation ( 34).

Systemic Lupus Erythematosus Lupus is a systemic disease characterized by antinuclear antibodies, which produce immune complexes that cause inflammation of various organs. The most common cardiac involvement is pericarditis, found in more than two -thirds of patients with lupus. Thus, the detection of pericardial effusion on echocardiography is one of the diagnostic criteria for systemic lupus erythematosus. Despite the frequent presence of pericardial effusion, tamponade and constrictive pericarditis are uncommon. The myocardium may be involved by vasculitis, resulting in myocarditis, but clinically important LV diastolic dysfunction is rare. Another characteristic cardiac lesion is Libman -Sacks endocarditis, with a verrucous valvular lesion generally involving the mitral valve ( 35). It usually is found on the basal portion of the

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techom mitral valve but can extend to the chordal structure or papillary muscles (Fig. 16-19). The aortic valve typically is not involved in Libman-Sacks endocarditis. These lesions are difficult to see on TTE, but detection is enhanced with TEE. Metastatic tumo rs also involve cardiac valves, producing lesions similar to those in Libman-Sacks endocarditis. This condition is called marantic endocarditis; it occurs most commonly with Hodgkin disease and adenocarcinoma of the lung, pancreas, stomach, and colon (see Chapter 18).

Figure 16-19 Libman-Sacks endocarditis in a 36 -year-old woman with systemic lupus erythematosus and no clinical evidence of bacterial endocarditis. The diastolic frame of the horizontal transesophageal echocardiographic view of the mitral valve shows large verrucous v egetations ( arrows). LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

Genetic Diseases Several genetic disorders have characteristic cardiovascular manifestations. The major cardiovascular abnormalities that are inherited genetically are described elsewhere (hypertrophic cardiomyopathy, Marfan syndrome, and dilated cardiomyopathy). The more uncommon genetic disorders with cardiac manifestations that we encounter in the echocardiography laboratory are described below. A more detailed description can be found in Alizad and Seward ( 36).

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techom Friedreich ataxia is an autosomal recessive spinocerebellar degeneration. The myocardium is involved in 95% of patients. The most frequent finding is increased LV wall thickness ( 37), which also occurs in patients with LEOPARD syndrome ( L, lentigines; E, ECG conduction defect; O, ocular hypertelorism; P, pulmonary valve stenosis; A, abnormalities of genitalia; R, retardation; D, deafness). Skin pigmentation is of neural crest origin, and the hypertrophic cardiomyopathy in LEOPARD syndrome may be related to excessive levels of catecholamine. P.287

Pheochromocytoma is a catecholamine -secreting tumor usually located in the adrenal gland. It occasionally is inherited as an autosomal dominant trait. An excess of catecholamine produces dilated or hypertrophic cardiomyopathy. An acute episode may cause chest pain or myocardial ischemia, which is manifested as a regional wall motion abnormality on echocardiography. A characteristic tumor has been found n ear the left atrioventricular groove ( Chapter 18). Noonan syndrome has several echocardiographic findings: LV hypertrophy, pulmonary valve stenosis, secundum atrial septal defect, constrictive pericarditis, dilation of the ascending aorta, and a partial at rioventricular canal defect. Fabry disease is an X -linked recessive sphingolipidosis that results in the accumulation of glycosphingolipids in the lysosomes of tissues because of the lack of α -galactosidase A. Its echocardiographic characteristics include increased thickness of the myocardial wall, myocardial dysfunction, and a thick mitral valve. Without phenotypic manifestations, tissue Doppler imaging may allow early detection of Fabry cardiomyopathy in patients with a genetic predisposition to the dise ase (38). Pompe disease is the classic glycogen storage disease due to the deficiency of α -glucosidase. The progressive deposition of glycogen in the myocardium is manifested as thick myocardial walls with a tumor-like appearance of the papillary muscles. Osler-Weber-Rendu disease, also called hereditary hemorrhagic telangiectasia, is characterized by widespread dermal, mucosal, and visceral telangiectases and hemorrhage. Pulmonary atrioventricular fistula is common and can be diagnosed with

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techom contrast echocardiography. TEE can localize an isolated fistula of a specific pulmonary venous connection. Ehlers-Danlos syndrome consists of hyperextensible skin, hypermobile joints, and easy bruising. Major cardiac abnormalities are aortic root dilatation, mitral and aortic valve prolapse, and aneurysm of the sinus of Valsalva. Rarely, dilatation of the innominate artery and aneurysm of the membranous ventricular septum have been reported. Marfan syndrome is a systemic connective tissue disease, and cardiovascular comp lications are common. Mitral valve prolapse is the most common cardiac abnormality, followed by aortic root dilatation, aortic regurgitation, and aortic dissection. Prophylactic β-blockade is recommended as well as aortic root replacement with or without aortic valve replacement when the aortic dimension reaches 50 to 55 mm. Morquio syndrome is due to the deficiency of Nacetylgalactosamine -6-sulfatase. Patients present with dwarfism, corneal clouding, deafness, and valvular abnormalities such as mitral stenosis, aortic stenosis, and aortic regurgitation. Syndrome myxoma is an inherited condition characterized by cutaneous lentiginosis, blue nevi, peripheral tumors, and endocrine neoplasms as well as cardiac myxoma (Carney complex). Myxoma occurs in young p ersons (50

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125 mm Hg. VTI (=TVI), time velocity integral. Since the 1980s, the primary treatment for isolated pulmonary valve stenosis has been catheter -based balloon valvuloplasty. Clinical results have been excellent, with most patients having a response to a single dilation.

Leaflet mobility is critical for the success of valve repair in Ebstein anomaly. Repair consists of creating a monocusp valve. The repair relies on the anterior leaflet contacting the interventricular septum in systole to form a functional monocusp valve. Anatomic features that are favorable for repair include the following:

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A large mobile anterior leaflet capable of coapting with the septum (Fig. 20-37); the leading edge of the leaflet is very important and must be freely mobile.

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Absence of direct muscular insertions that limit or distort the motion of the valve (direct muscular insertions are shown in Figure 20-38).

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A single central regurgitant jet ( Fig. 20-39). Multiple origins of regurgitation ( Fig. 20-38) or fenestrations in the leaflet tissue markedly decrease the chance for successful repair.

In the most advanced cases of Ebstein anomaly, virtually no mobile tricuspid valve tissu e is present ( Fig. 20-40). These patients often have the most severely dysfunctional myocardium and the most deformed valves. Valve repair is not possible in these cases. Our approach leans toward early valve replacement in an attempt to preserve as much m yocardial function as possible.

Tetralogy of Fallot Tetralogy of Fallot is the most common form of cyanotic congenital heart disease, occurring in 4% to 9% of patients with CHD. This malformation results from anterior malalignment of the infundibular (RVOT) portion of the interventricular septum. The malali gnment creates the four cardinal features of the defect: 1) pulmonary and subpulmonary stenoses, 2) VSD, 3) override of the aortic valve anulus (over the VSD), and 4) RV hypertrophy. These features are shown in Figure 20-41. This anomaly results in P.358

mixing of the venous flow streams at the level of the VSD. The patients are cyanotic because of this and the decrease in PA blood flow caused by the coexisting subpulmonary and pulmonary stenoses.

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Figure 20-34 Discrete subaortic stenosis. A: Parasternal long axis systolic frame shows a circumferential fibrous membrane (34) narrowing the left ventricular ( LV) outflow tract. The membrane is immediately below the aortic valve anulus and attaches to the septum and anterior leaflet of the mitral v alve. B: Continuous wave Doppler echocardiogram showing a moderate outflow gradient (mean gradient, 34 mm Hg). (A and B: Transthoracic echocardiograms.) Note: These obstructive membranes or ridges are often associated with hypertrophy of the basal ventricular septum. As a result, septal myectomy and myotomy in addition to resection of the membrane are often required to eliminate the obstruction. Aortic valve regurgitation can occur in these patients because of either the turbulent outflow jet or the direct distortion of the valve (when the membrane attaches to the valve leaflets). C and D: Longitudinal plane transesophageal echocardiograms (TEEs) of a discrete, obstructive subaortic membrane. In patients with limited transthoracic windows, TEE provides excellent visualization of this area. These TEE images show a discrete, circumferential subaortic membrane ( arrow in C) that causes

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severe outflow obstruction. The obstruction begins at the ridge, below the valve anulus, as shown in the color flow image ( D). When the basal ventricular septum is thickened or posteriorly displaced, the “length† of the obstructive zone can increase. In these cases, a tunnel of obstruction is created. Tunnel subaortic stenosis can be difficult to relieve with simple resection and may require complex LV outflow enlargement procedures, such as the Konno -Rastan operation and its modifications. Thus, the length of the obstructive subaortic zone should be quantified to facilitate surgical planning. Note that many patients with subaortic stenosis also have abnormal aortic valves. It usually is not possible to differentiate subvalvular obstruction from t he valvular stenosis by Doppler hemodynamics. Therefore, one must rely on two -dimensional images (degree of anular or LV outflow tract hypoplasia, presence of leaflet thickening, degree of leaflet excursion) to determine whether intervention is required fo r one or both lesions. A, anterior; Ao, aorta; LA, left atrium; RV, right ventricle; S, superior.

Surgical techniques used to treat tetralogy of Fallot have evolved and now rarely include palliative procedures, such as the Blalock Taussig shunt. Instead, primary repair is preferred in most cases. Definitive repair includes patch closure of the VSD, resection of obstructive subpulmonary muscle, further enlargement of the subpulmonary outflow tract (usually with a transanular patch), and relief of pulmonary valve stenosis. Currently, most patients have this type of repair before they are 12 months old.

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Figure 20-35 A: Four-chamber view of an anatomic specimen showing a severe form of Ebstein anomaly. No functional valve tissue is present within the anatomic inflow tract. The mobile segments of the valve are displaced anteriorly and apically and are out of the plane of the image. The right heart is globally enlarged and the vestiges of the anterior tricuspid valve (TV) leaflet are attached at multiple points ( arrows) to the walls of the right ventricle. The area between the anatomic TV anulus and the coaptation point of the functional TV leaflets is the atrialized portion of the right ventricle ( aRV). The anatomic anulus (35) is adjacent to the right atrioventricular groove. B: Apical four-chamber echocardiographic view showing features of severe Ebstein anomaly, with dis placement and tethering of the septal ( arrow) and anterior TV leaflets. The septal insertion of the TV is closer to the apex (farther from the atrioventricular groove) than normal (Fig. 20-36). The right ventricular (RV) free wall is thin, demonstrating that both the valve and myocardium are abnormal in these patients. Although the anterior leaflet is more developed in this case than in the anatomic specimen ( A), there are two areas of direct papillary muscle insertion that impair leaflet mobility (35). T his type of papillary muscle attachment reduces the likelihood of successful valve repair in this patient. LA, left atrium; LV, left ventricle; RA, right atrium.

Figure 20-36 Displacement index in Ebstein anomaly. The septal insertion of the tricuspid valve is always slightly apical to that of the mitral valve. A: This relation in the normal heart.

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B: Excessive apical displacement seen in Ebstein anomaly. Arrows, the mitral and tricuspid septal insertions. The linear distance between these two points is divided by the patient's body surface area to obtain the displacement index. AML, anterior mitral leaflet; L, left; LV, left ventricle; RA, right atrium; RV, right ventricle; S, superior; STL, septal tricuspid leaflet.

Figure 20-37 Ebstein anomaly with a repairable tricuspid valve. Apical four -chamber images from mid -diastole (A), midsystole ( B), and end-systole (C). Successful creation of a monocusp repair depends on the mobility of the anterior leaflet (arrow). In the patient her e, the anterior leaflet is freely mobile, including its leading edge, and no muscular insertions limit or distort the motion of the valve. The regurgitant jet originated only from the gap in coaptation between the anterior leaflet and the remnant of the se ptal leaflet. The leading edge of the valve reaches a point close enough to the septum that, given the degree of anular dilation, annuloplasty can “advance” it to a point where it will coapt with the septum. The evaluation of leaflet mobility must be m ade by imaging the valve within the anatomic inflow tract. To be certain that the imaging plane is sufficiently posterior, the mitral valve anulus and leaflets should also be visible in the frame. The outflow tracts should not be visible at all. Many Ebste in valves have mobile segments anterior to this true inlet plane. Unless the inlet portion of the anterior leaflet is free, these valves do not create adequate valves after repair, partly because the

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annuloplasty does not affect the motion of the outlet po rtion of the valve and the amount of right ventricular ( RV) myocardium distal to these severely displaced valves is often only a small portion of the RV (frequently only the infundibulum). L, left; LV, left ventricle; RA, right atrium; S, superior.

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Transanular patch repair avoids the problem of conduits and prosthetic valves in growing children, but it leaves these patients without a functional pulmonary valve ( Fig. 20-42). The resulting pulmonary regurgitation is well tolerated by most pat ients, at least throughout childhood. A growing body of evidence suggests that many patients will require pulmonary valve insertions in adulthood. The optimal timing for this intervention is debated.

Figure 20-38 Poor candidate for valve repair in Ebste in anomaly. Although the anterior leaflet has some mobility, there is a direct muscular insertion of a free wall papillary muscle into the anterior leaflet ( arrow in A). This will limit the motion of the leaflet. More importantly, the anterior leaflet has multiple fenestrations, causing at least three separate jets of tricuspid regurgitation ( arrows in B). The multiple points of

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regurgitation and limited systolic mobility made this patient a poor candidate for repair. These multiple jets often are due to segments of the leaflet that are either unsupported by chordae or have free wall attachments that are not immediately evident. Once the jets have been recognized, focused two dimensional scans in the areas will often show the underlying abnormality responsible for the regurgitation. L, left; LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle; S, superior.

Figure 20-39 A and B: Apical four-chamber images of a valve with anatomy similar to that of the valve in the patient in Figure 20-37. The anterior leaflet is freely mobile ( A), and color flow mapping ( B) shows only a single central jet of tricuspid regurgitation. The severity of the enlargement of the right heart makes the displacement of the tricuspid valve seem less prominent, b ut the displacement index in this case was 20 mm/m 2 . The patient subsequently had successful valve repair, with only mild residual tricuspid regurgitation. L, left; LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle; S, superior.

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Complete Transposition of the Great Arteries 828

techom Complete transposition is the most common form of cyanotic CHD that presents in a neonate (second most frequent overall). Abnormal septation of the truncus arteriosus results in connection of the pulmonary artery to the LV and of the aorta to the RV (ventricular-arterial discordance). The typical anatomy of this discordant arterial connection is shown in Figure 20-43. These babies uniformly are cyanotic, although they may not be in distress while the PDA and foramen ovale provide adequate mixing of the venous flow streams. This condition creates two circulations in parallel (instead of one circulation in series), with systemic venous blood being returned to the aorta and pulmonary venous flow being directed back to the pulmonary arteries. The PDA or septal d efects (or both) are required to allow mixing of the flow streams. Without such mixing, an adequate amount of oxygen is not delivered to the tissues and the baby becomes acidotic and does not survive.

Figure 20-40 Apical four-chamber image of one of the most advanced forms of Ebstein anomaly. The right heart is markedly dilated (anulus diameter, 50 mm). Right ventricular function was severely depressed. There is no evidence of any mobile valve tissue in the inflow tract. The anterior leaflet is attached completely to the free wall, beginning just 2 cm below the anatomic anulus ( arrow). No septal leaflet tissue is seen. The native valve tissue was displaced to the entrance of the right ventricular outflow tract (the infundibular orifice). This valve was not suitable for repair. The remnants of the tricuspid valve were resected to avoid right ventricular outflow

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obstruction, and a bioprosthesis was placed at the anatomic anulus, restoring the “functional† right ventricle to a volume adequate for supporting the circulation. aRV, atrialized portion of the right ventricle; L, left; LA, left atrium; LV, left ventricle; RA, right atrium; S, superior.

Before surgical treatment, echocardiography is generally the only cardiac imaging test required to evaluate a baby who has complete transposition of the great arteries ( Fig. 20-43). In addition to defining these classic features of a discordant ventricular -arterial connection, the preoperative examination must also defin e the status of the PDA, the ventricular and atrial septae, and the anatomy of the proximal coronary arteries. Abnormal origins or branching patterns of the coronary arteries can increase the risk of the arterial switch operation, but if these anomalies ar e recognized in advance, the procedure can be modified to minimize their effect. Currently, the most common surgical procedure used to treat complete transposition of the great arteries is the arterial switch operation. This procedure involves transection of both arterial roots above their arterial sinuses. The coronary arteries are then harvested from the anterior arterial root (associated with the RVOT) and transferred and anastomosed to the posterior root (associated with the LVOT). The pulmonary arteria l confluence and distal main pulmonary artery are moved (pulled) into a position anterior to the native aorta. The distal end of the transected native ascending aorta is then connected to the posterior root, creating the neo-aorta. Finally, the main pulmon ary artery is reconstructed using a patch (often taken from a homograft) creating the neopulmonary artery. As a result of these maneuvers, the great arteries have a unique echocardiographic appearance. Before neonatal arterial switch operations became feas ible, the primary surgical approach to complete transposition of the great arteries was to divert the systemic P.362

and pulmonary veins through the RA and LA to the AV valve associated with the opposite ventricle. Two widely used techniques were the Mustard and Senning operations ( Fig. 20-44). The surgical techniques are quite different, but the echocardiographic appearance of both are very similar. Because arterial switch operations have been applied widely only since the 1980s, many 830

techom adult patients who had these operations are still alive. The atrial baffles created by these operations reroute oxygenated and deoxygenated blood returning to the heart so it is directed to the appropriate arterial root. However, this was achieved by using the tricuspid valve and RV to support the aortic circulation. The most important late complication of these procedures is RV myocardial failure, often associated with severe tricuspid regurgitation. Because the right heart is supporting the aortic circulation, this becomes clinically analogous to LV failure and mitral regurgitation seen in patients without CHD. Although some degree of RV failure is present in most adults after a Mustard or Senning operation, the clinical course for these patients is quite variable. Valve rep air and replacement can be performed, but progressive RV dysfunction may lead to cardiac transplantation in many patients. Other common late postoperative problems include obstruction of one or more venous pathways. Pulmonary venous obstruction is not comm on and is difficult to relieve completely. It was more frequent after the Senning operation than the Mustard procedure. However, systemic venous compromise is often seen in patients after the Mustard operation, especially involving the SVC pathway.

Figure 20-41 Tetralogy of Fallot. A: Typical parasternal long axis appearance of the ventricular septal defect and aortic override in tetralogy of Fallot. The aortic valve is located centrally over the muscular interventricular septum (50%

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override). In this plane, the ventricular septal defect (41) is between the septum and valve. This long -axis image is typical of both the major defects involving conotruncal malformations: tetralogy of Fallot and truncus arteriosus. The connection of the pulmonary arterie s distinguishes the two lesions. In tetralogy of Fallot, the right ventricular outflow tract and pulmonary valve are stenotic but connect to the right ventricle (RV). In truncus arteriosus, the overriding semilunar valve is the only outlet for both ventric les, and the pulmonary arteries arise as branches from the proximal truncal artery (usually just beyond the sinotubular junction). B: The biphasic Doppler pattern is characteristic of dynamic obstruction. C and D show the subpulmonary stenosis caused by th e anteriorly deviated outlet septum ( arrow). Ao, aorta; LA, left atrium; LV, left ventricle; RA, right atrium.

Congenitally Corrected Transposition of the Great Arteries Despite this lesion being named for the abnormal connections and position of the grea t arteries, it is better thought of as an abnormality of ventricular development and position. Embryonic ventricular looping is abnormal in patients with congenitally corrected transposition of the great arteries. This results in the morphologically RV mat uring on the left side of the heart and becoming associated with the LA and pulmonary veins. The morphologic LV develops on the right side of the heart and becomes associated with the RA and vena cavae. This reversed connection of the atria to the ventricl es is referred to as atrial ventricular discordance ( Fig. 20-45). Although congenitally corrected transposition of the great arteries and complete transposition of the great arteries have similar names, their anatomic and physiologic features are very diff erent. The discordant connections inherent in congenitally corrected transposition of the great arteries result in the venous flow streams being routed to the appropriate arteries but through the “wrong” ventricles. The RA connects discordantly to the morphologic (anatomic) LV, which, in turn, is discordantly connected P.363

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to the pulmonary artery. The left -heart connections are similarly discordant, with the pulmonary venous flow being routed through the LA to the morphologic RV, which is discordantly connected to the aorta.

Figure 20-42 Echocardiographic findings in a patient after repair of tetralogy of Fallot with a transanular right ventricular outflow tract patch. A: Parasternal long -axis image. The ventricular septal defect (VSD) p atch has created complete continuity between the left ventricle ( LV) and aorta (Ao). The patch attaches to the muscular septum apically and to the infundibular septum superiorly. This not only closes the communication between the LV and right ventricle ( RV) but also eliminates the aortic override. B: Apical four-chamber view shows an enlarged, but not hypertrophied, RV. The left atrium (LA) and right atrium ( RA) are not dilated, suggesting that filling pressures and tricuspid valve function remain relativel y normal in this patient (only trivial tricuspid regurgitation was detected at the time of the examination). C-E: Parasternal short-axis images at the base of the heart. C: Two-dimensional scan shows the VSD patch (42), and enlarged RV outflow tract. The transanular patch has dilated over time (stretched by the repetitive jet of regurgitation). As a result, the RV outflow tract has the appearance of a moderate aneurysm. D: Most of the pulmonary valve was removed at the time of repair, leaving

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only a remnant of one leaflet attached to the medial anulus (across from the arrow marking the lateral edge of the native anulus). E: Diastolic color flow image of the same area. Severe (free) pulmonary regurgitation is confirmed by the broad color flow jet (arrow).

In the absence of other abnormalities, these patients are not cyanotic. In fact, if there are no other defects, the condition may not be diagnosed in many patients until adulthood. Problems arise in these patients because the inappropriate ventricle (the morphologic RV) supports the aortic circulation. The morphologic RV and tricuspid valve do not tolerate aortic pressure loads as well as the morphologic LV and mitral valve. Consequently, the most common late complications in patients with congenitally correc ted transposition of the great arteries are systemic AV regurgitation (Fig. 20-45) and ventricular dysfunction. Patients with congenitally corrected transposition of the great arteries also have an increased frequency of complete heart block (both congenit al and acquired). The abnormal looping of the ventricles during fetal development creates an abnormality of the conduction system (anterior deviation of the AV node). The ventricular looping abnormality seen in congenitally corrected transposition of the g reat arteries is often associated with abnormal development or septation of the great arteries and conotruncus region. In classic congenitally corrected transposition of the great arteries, this results in a second discordant connection with malpositioned arterial roots. The aortic valve is anterior and to the left of the pulmonary valve and is connected to the left sided morphologic RV. This anterior and leftward position of the aorta is the reason this malformation is abbreviated as “L TGA.” The resul t of both the atrial -ventricular and the ventricular-arterial connections being discordant is the “congenital correction† that is the physiologic hallmark of this malformation.

Univentricular Atrioventricular Connections Some of the most complex congen ital cardiac malformations involve a univentricular AV connection ( Fig. 20-46). These hearts can also be thought of as functionally single

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ventricles (univentricular hearts). The terms single ventricle and univentricular are misnomers because all h uman hearts will have components of both an RV and LV. What distinguishes these patients from those with biventricular hearts is one of two anatomic variables. Either one of the ventricles is too small to be used as a circulatory pump or a coexistence of l esions makes it impossible to divide the two circulations surgically (such as major straddling of an AV valve).

Figure 20-43 A: Anatomic specimen showing the anatomy typical of complete transposition of the great arteries. The great arteries originate from an inappropriate ventricle: the aorta (A) from the right ventricle ( RV) and the pulmonary artery (P) from the left ventricle ( LV). The arteries follow a parallel course, and the aorta and aortic valve are positioned to the right and anterior of the pulmonary artery and valve. This heart also has several small mid -muscular ventricular septal

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defects. B-E: Echocardiographic images from a neonate with complete transposition of the great arteries before surgical treatment with an arterial switch operation. B: Parasternal short-axis image at the base showing the classic arrangement of the semilunar valves in this defect. The aortic val ve is anterior and to the right of the pulmonary valve. C: Parasternal long-axis image showing the parallel relation of the great arteries. The pulmonary artery ( PA) courses posteriorly after exiting the LV. Both semilunar valves can be seen in long axis in this plane. This never occurs when the great arteries are normally positioned. Note, slight modifications of the imaging plane in this area will show the origin and initial branching pattern of the coronary arteries from the aortic sinuses that face the pulmonary valve. Coronary arterial definition is an important part of the initial evaluation of a neonate who has complete transposition of the great arteries. This is because the coronary arterial transfer is the component of the arterial switch operation that is associated with the greatest difficulty and risk. D: This subcostal image confirms that the right -sided great artery is the aorta ( Ao) (vertical course with no proximal branches). E: Subcostal four -chamber image with angulation posterior to the ao rta. It demonstrates that the posterior great artery (connected to LV) bifurcates into a right and left pulmonary artery, confirming the presence of ventriculoarterial discordance. A, Ao, aorta; LA, left atrium; LV, left ventricle; P, PA, pulmonary artery; RA, right atrium; RV, right ventricle.

As a result of the mixing of the venous returns within the ventricle, all the patients are cyanotic. Newborns with univentricular AV connections and severe pulmonary stenosis may be dependent on the ductus arteriosus to provide pulmonary artery blood flow. In other patients, the ductus may be needed to supply aortic flow (when there is severe subaortic stenosis or coarctation). An intravenous infusion of prostaglandin is used to maintain ductal patency in these patients, and this has markedly decreased the need for emergent surgical palliation of neonates with these complex defects. Even when palliative procedures are required, they usually can be delayed safely until the child is a few days to a week old. The echocardiographic appearance of three common anatomic forms of univentricular AV connection are shown in Figure 20-46.

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techom Because these hearts do not tolerate surgical septation into a biventricular repair, other palliative strategies have been developed. The most definitive surgical procedure currently available for these patients is the Fontan operation. P.365

Many technical variations have been used to create “Fontan circulations.” The unifying feature of this operation is the creation of a right -heart bypass. The systemic venous return is diverted from the ventricle and is baffled directly into the pulmonary arteries. This eliminates the mixing of systemic and pulmonary venous bloo d that occurred within the single ventricular chamber and relieves cyanosis. It also eliminates the excess volume load on the single ventricle by restoring the circulation to one in which the pulmonary and systemic flows are in series rather than in combin ation. Because the pulmonary circulation has no ventricular pump to drive its flow, a successful Fontan operation depends on the patient having pulmonary arteries of adequate size and low pulmonary arteriolar resistance. Also, the systolic and diastolic fu nctions of the single ventricle must be preserved. Increased ventricular filling pressures impede flow through the lungs by increasing the total pulmonary vascular resistance.

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Figure 20-44 Senning operation for complete transposition of the great arteries. A: Anatomic specimen showing the apical four-chamber anatomy. The pulmonary venous pathway ( PV) is widely patent. The pulmonary venous flow sweeps through the baffle from the posterior an d leftward pulmonary veins to the anterior and rightward tricuspid valve. The area of “atrium” just above the mitral valve anulus ( arrow) is the confluence of the systemic venous pathways (inferior and superior venae cavae). The actual superior vena ca va pathway is anterior to this plane and not visible. The dark circle at the inferior aspect of the confluence leads to the inferior vena cava. B and C: Apical four-chamber echocardiographic images from a 16-year-old patient. The plane is comparable to tha t in A. B: Two-dimensional image showing a dilated right atrium and right ventricle ( RV) (with RV hypertrophy). The pulmonary veins (PV) have been baffled to the tricuspid valve, and this pathway appears widely patent. C: Color flow Doppler imaging is useful to confirm laminar flow through the reconstruction and to detect stenoses or residual shunts. In this case, flow from the pulmonary veins to the RV is unobstructed and no residual shunts are seen. D and F: The anatomy of an atrial switch operation for complete transposition of the great arteries in a 30-year-old man. The apical four -chamber views usually are the most informative initial scans ( D and E) for evaluation of the venous reconstructions after either a Mustard or Senning operation. The pulmonary vein pathway ( PV in D) is usually visualized in the same plane as the internal cardiac crux and atrioventricular valves (as in D). Flow travels horizontally from the left-sided pulmonary veins to the RV inlet. In this vi ew, the narrowest point in the pathway is often centered over (or just to the right of) the plane of the interventricular septum. After the pulmonary vein pathway has been identified, posterior angulation of the scan plane will demonstrate the inferior ven a caval (IVC) portion of the reconstruction ( E). The pathway from the IVC to the mitral valve also has a primarily horizontal course. The superior vena caval pathway is not usually visible from the apex. This pathway follows a more superior to inferior and leftward course, nearly parallel with the posterior wall of the ascending aorta. In young patients, a combination of parasternal long -axis (angled toward the patient's right, as in F; 44, superior vena cava pathway), right parasternal sagittal,

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and suprasternal coronal views are necessary to visualize completely this part of the repair. In many mature patients, the superior vena caval pathway is not visible on any surface scans and transesophageal echocardiography is required to assess this pathway. A, anterior; IVC, inferior vena cava; L, left; LA, left atrium; LV, left ventricle; PV, pulmonary vein S, superior; SV, superior vena cava.

Figure 20-45 Congenitally corrected transposition of the great arteries. A: A “four-chamber view” of a normal heart. B: Same view as in A, but the heart is from a patient with congenitally corrected transposition of the great arteries. This specimen shows the unique septal insertions of the two atrioventricular valves encountered with a discordant atrioventricular (AV) connection. The septal leaflet of the morphologic tricuspid valve always inserts onto the ventricular septum at a point closer to the cardiac apex than does the anterior leaflet of the morphologic mitral valve. The left AV valve has a septal insertion that is apical in relation to the insertion of the right AV valve, confirming that it is anatomically a tricuspid valve ( arrow). Because the AV valves develop from their ventricles, the morphologic right ventricle

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(mRV) is always connected t o a morphologic tricuspid valve and vice versa. Thus, images of only the septal AV valve insertions allow for confident echocardiographic identification of not only the type of AV valve present but also the morphology of the underlying ventricle. This rela tion is easily demonstrated in apical four-chamber echocardiographic images of the internal cardiac crux. C: Two-dimensional systolic apical four -chamber image from an adult with congenitally corrected transposition of the great arteries. Note the anatomy of the internal cardiac crux (arrow). The septal insertion of the left AV valve is slightly apical to that of the right AV valve ( arrow). This relation is one of the anatomic hallmarks of congenitally corrected transposition of the great arteries. It is th e most reliable echocardiographic finding for identifying the morphology of the ventricle associated with the AV valve and discordant AV connections. In this case, the moderator band (45) can also be seen within the left -sided ventricle, further confirming its status as a morphologically “right† ventricle (mRV). D: A systolic color flow image of the left AV valve of the same patient as in C. The patient had severe left AV valve regurgitation, one of the most important causes of cardiac morbidity in thes e patients. Systemic ventricular dysfunction and arrhythmias are also common in these patients. Note that this patient also had an implantable cardiac defibrillator; the leads are visible in the right atrium ( RA) (C) and the right -sided morphologic LV ( mLV). L, left; LA, left atrium; LV, left ventricle; RV, right ventricle; S, superior.

Figure 20-46 A-C: Echocardiographic images of three common types of univentricular atrioventricular (AV) connection. These

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hearts are often classified as functional single ventricles. A: Double-inlet AV connection. Although this connection can be seen with either a dominan t left ventricle ( LV) or right ventricle morphology, double inlet to an LV is by far the more common. In this case, the left atrium ( LA), right atrium ( RA), and AV valves are committed to a ventricle that has distinct papillary muscles and relatively fine trabeculations, LV morphology. The right ventricular remnant is anterior to the plane of imaging and gives rise to one of the great arteries. This remnant usually consists of only the infundibulum and is always too small to act as an independent pump in a patient with double inlet LV. B and C: Single-inlet connections. This is usually associated with atresia (absence) of one of the AV valves. The most common examples of this connection are hypoplastic left heart syndrome and tricuspid atresia. B: An example of tricuspid valve atresia. The apical “floor† of the RA (arrow) shows no evidence of a valve and there is no right ventricular inlet. The only outlet from the RA is across the atrial septum. Similar to double -inlet LV, the right ventricular remnant i s anterior and usually gives rise to one of the great arteries. The size of this remnant is more variable in tricuspid atresia than in double -inlet LV and is related to the size of the ventricular septal defect connecting it to the LV cavity and the adequacy of the arterial outlet. C: A subcostal “four†chamber view from a neonate with hypoplastic left heart syndrome. The LV is extremely diminutive in this case (46), where both the mitral and aortic valves were atretic. The LA is moderately hypoplastic and the right -heart chambers are enlarged. The ascending aorta is always small in these patients and there is always a coexisting coarctation. All these patients require a patent ductus arteriosus to provide blood flow to the systemic circulation. RV, right ventricle.

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References 841

techom 1. Tynan MJ, Becker AE, Macartney FJ, et al. Nomenclature and classification of congenital heart disease. British Heart Journal, 1979;41:544–553. 2. Huhta JC, Hagler DJ, Seward JB, et al. Two -dimensional echocardiographic assessment of dextrocardia: A segmental approach. American Journal of Cardiology, 1982;50:1351–1360. 3. Freedom RM. The “anthropology† of the segmental approach to the diagnosis of complex congenital heart disease. Cardiovascular an d Interventional Radiology, 1984;7:121–123. 4. Van Praagh R. The segmental approach clarified. Cardiovascular and Interventional Radiology, 1984;7:320–325. 5. Weinberg PM. Systematic approach to diagnosis and coding of pediatric cardiac disease. Pediat ric Cardiology, 1986;7:35–48. 6. Hagler DJ. Echocardiographic segmental approach to complex congenital heart disease in the neonate. Echocardiography, 1991;8:467–475. 7. Henry WL, DeMaria A, Gramiak R, et al. Report of the American Society of Echocardi ography Committee on Nomenclature and Standards in Two -dimensional Echocardiography. Circulation, 1980;62:212–217. 8. Buskens E, Grobbee DE, Frohn -Mulder IM, et al. Efficacy of routine fetal ultrasound screening for congenital heart disease in normal pregnancy. Circulation, 1996;94:67–72. 9. Rychik J, Ayres N, Cuneo B, et al. American Society of Echocardiography guidelines and standards for performance of the fetal echocardiogram. Journal of the American Society of Echocardiography, 2004;17:803–810. 10. Carvalho JS, Mavrides E, Shinebourne EA, et al. Improving the effectiveness of routine prenatal screening for major congenital heart defects. Heart, 2002;88:387–391. 11. El-Najdawi EK, Driscoll DJ, Puga FJ, et al. Operation for partial atrioventricula r septal defect: A forty -year review. Journal of Thoracic and Cardiovascular Surgery, 2000;119:880–890. 12. Silvilairat S, Cabalka AK, Cetta F, et al. Abdominal aortic pulsation and pulse delay in coarctation of the aorta: Pulse wave Doppler analysis rel iably reflects severity [abstract]. Journal of the American Society of Echocardiography, 2005;18:563.

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techom 13. Bengur AR, Snider AR, Serwer GA, et al. Usefulness of the Doppler mean gradient in evaluation of children with aortic valve stenosis and comparison to gradient at catheterization. American Journal of Cardiology, 1989;64:756–761. 14. Bengur AR, Snider AR, Meliones JN, et al. Doppler evaluation of aortic valve area in children with aortic stenosis. Journal of the American College of Cardiology, 1991;18: 1499–1505. 15. Currie PJ, Hagler DJ, Seward JB, et al. Instantaneous pressure gradient: A simultaneous Doppler and dual catheter correlative study. Journal of the American College of Cardiology, 1986;7:800–806. 16. Lima CO, Sahn DJ, Valdes -Cruz LM, et al. Noninvasive prediction of transvalvular pressure gradient in patients with pulmonary stenosis by quantitative two -dimensional echocardiographic Doppler studies. Circulation, 1983;67:866–871. 17. Silvilairat S, Cabalka AK, Cetta F, et al. Echocardiogr aphic assessment of isolated pulmonary valve stenosis: Which outpatient Doppler gradient has the most clinical validity? Journal of the American Society of Echocardiography, 2005;18:1137–1142. 18. Silvilairat S, Cabalka AK, Cetta F, et al. Outpatient echocardiographic assessment of complex pulmonary outflow stenosis: Doppler mean gradient is superior to the maximum instantaneous gradient. Journal of the American Society of Echocardiography, 2005;18:1143–1148. 19. Sasson Z, Yock PG, Hatle LK, et al. D oppler echocardiographic determination of the pressure gradient in hypertrophic cardiomyopathy. Journal of the American College of Cardiology, 1988;11:752–756. 20. Shiina A, Seward JB, Edwards WD, et al. Two -dimensional echocardiographic spectrum of Ebst ein's anomaly: Detailed anatomic assessment. Journal of the American College of Cardiology, 1984;3:356–370 21. Gussenhoven EJ, Stewart PA, Becker AE, et al. “Offsetting† of the septal tricuspid leaflet in normal hearts and in hearts with Ebstein's an omaly: Anatomic and echographic correlation. American Journal of Cardiology, 1984;54:172–176.

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24. 21 - Intraoperative Echocardiography 21 Intraoperative Echocardiography Roger L. Click Jae K. Oh Intraoperative transesophageal echocardiography (IOTEE) has become a routine addition to most cardiac operations (1,2,3,4,5,6,7,8,9,10). Echocardiography was introduced into the cardiac operating room in 1972 with epicardial scanning ( 11). Although epicardial scanning is still used in a few specific situations (12), IOTEE has become the more commonly used method for visualizing cardiac structures in the operating room. The Mayo Clinic experience with IOTEE over the past 13 years is summarized in Figure 21-1. The surgical volume increased steadily during these years , and more surgeons are using IOTEE for more operations. Initially, IOTEE was used in about one -third of all cardiac operations; currently, it is performed in more than 90% of all cardiac operations.

Iotee Application Reasons for performing IOTEE are the f ollowing: 1) prebypass—to confirm the preoperative findings and the reason for the operation and to screen for any new findings that may alter the surgical plan, 2) postbypass—to check the surgical result and to screen for any new abnormalities that ma y require further intervention or return to cardiopulmonary bypass, 3) to minimize cardiovascular complications during cardiac and noncardiac operations by monitoring left ventricular (LV) function and wall motion, and 4) to identify any cardiovascular fac tors that may be responsible in patients who become hemodynamically unstable in the operating room. IOTEE involves multiple disciplines and requires cooperation among anesthesiologists, cardiologists, and surgeons. Because the anesthesiologist is in charge of the patient's hemodynamic condition and airway, the transesophageal probe is usually inserted by the anesthesiologist. If he or she is comfortable with performing transesophageal echocardiography (TEE), baseline TEE data can be

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techom obtained and reviewed in conjunction with a cardiologist echocardiographer. The anesthesiologist routinely monitors for air in the cardiac chambers or regional wall motion abnormalities. In cases of valve or congenital heart surgery at Mayo Clinic, the cardiologist-echocardiographer usually is actively involved from the beginning of the operation.

Implementation Routine TEE is performed prebypass in all patients. Further attention is then focused on the specific surgical referral. Prebypass TEE findings are then discussed with the cardiac surgeon and anesthesiologist. Any new findings are reviewed with the surgeon to determine if the surgical plan needs to be altered. After the patient comes off the bypass pump, IOTEE is repeated to assess the results of the operation. The postbypa ss echocardiographic findings are discussed with the surgeon. When the structural or hemodynamic results are considered inadequate, a second pump run may be initiated to revise the operation, after which the results are again evaluated with echocardiograph y. However, it is not realistic to attempt perfect repair in all surgical cases. If a hemodynamically insignificant lesion remains, it is better to leave it than to return and revise the repair. Occasionally, it is difficult to determine the long -term outcome of mild abnormalities shown on IOTEE that are not immediately causing hemodynamic abnormalities. Therefore, postbypass, it is important to P.369

wait until after the hemodynamics have stabilized and are optimal before making final decisions on the ba sis of IOTEE.

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Figure 21-1 Distribution of intraoperative transesophageal echocardiograms ( IOTEE) performed at Mayo Clinic from 1991 to 2003. The total number of cases for each year and the separate adult and congenital cases are shown. The total number of pump cases for each year and the percentage of those having IOTEE are shown.

Indications The case distribution for adult and congenital cases is shown in Figures 21-2 and 21-3, respectively. Initially, in our experience, the adult distribution of surgical cases having IOTEE was very similar each year, with predominantly valve surgery, that is, with repair and replacement, accounting for more than half of the adult cases in which IOTEE was used ( Fig. 21-2). In contrast, in the past 3 years, the use of IOTEE has increased for coronary artery bypass graft (CABG) surgery, up from 11% of all adult cases in 1998 to 23% of all cases in 2003 ( Fig. 21-2). This increased use of IOTEE in CABG surgery results from the surgeon's comfort with IOTEE and firsthand knowledge of the impact of IOTEE in even routine cardiac surgical cases ( 13).

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Figure 21-2 Surgical case distribution of adult intraoperative transesophageal echocardiograms performed at Mayo Clinic in 1998 and 2003. The percentages represent the portion of all intraoperative transesophageal echocardiograms that year that had that surgical proc edure. AV, aortic valve; CABG, coronary artery bypass grafting; HOCM, hypertrophic obstructive cardiomyopathy; Misc, miscellaneous, MV, mitral valve.

Currently at Mayo Clinic, IOTEE is requested for nearly all adult patients undergoing the following cardiovascular procedures: all valve repairs, suspicion of clinically significant mitral valve regurgitation in patients having aortic valve replacement, ao rta repair for dissection or aneurysm, myectomy procedure for hypertrophic obstructive cardiomyopathy (HOCM), repair of an intracardiac shunt, removal of an intracardiac mass, all congenital cases, P.370

and in most patients having routine valve replacem ent or CABG.

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Figure 21-3 Distribution of congenital intraoperative transesophageal echocardiograms performed at Mayo Clinic in 2003. Each percentage value represents the percentage of congenital cases having that surgical procedure. ASD, atrial septal defect; AV, atrioventricular; Coarc, coarctation; Misc, miscellaneous; PA, pulmonary artery; RV, right ventricle; RVOT rec, RV outflow tract reconstruction; VSD, ventricular septal defect.

Practical guidelines for performing IOTEE were published in 1999 (14). Indications for IOTEE were divided in three categories, depending on evidence at the time for the impact of IOTEE on a given surgical procedure. Since then, numerous articles have supported the use of IOTEE in almost all types of ca rdiac surgery (15,16,17,18,19,20,21,22,23,24,25,26). IOTEE has been used in all congenital surgical cases at Mayo Clinic since pediatric probes became available. The number of congenital cases has remained constant ( Fig. 21-1). The distribution of types of congenital cases is shown in Figure 21-3, and it also has been constant.

Impact of Iotee

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techom At Mayo Clinic and other institutions, the impact of IOTEE has been evaluated (1,3). We have analyzed and continue to prospectively analyze our IOTEE practice in rega rd to its usefulness for the surgical practice and, in particular, alterations of the surgical practice or decisions in the operating room based on IOTEE. In 2000, we published our first 5 -year experience with more than 3,000 adult cases ( 1). Prebypass, ne w findings were found in 15% of patients, altering surgery in 14%; postbypass, new information was found in 6%, altering surgery or management in 4%. The overall impact was 18% ( Fig. 21-4). Figure 21-4 shows the overall impact of IOTEE on surgery in all ca ses and in HOCM, aorta valve surgery, mass removal, CABG, aortic surgery, and valve surgery for endocarditis. Even for patients having only CABG, the overall impact was 5%. The impact of IOTEE prebypass is illustrated in Figures 21-5, 21-6 and 21-7 and the postbypass impact, in Figures 21-8 and 21-9.

Figure 21-4 Overall (all cases) impact of intraoperative transesophageal echocardiography on adult surgical procedures and six specific procedures. The percentages include new prebypass and postbypass echocardiographic findings that were the basis for altering the su rgical procedure or management. AVR, aortic valve replacement; CABG, coronary artery bypass grafting; HOCM, hypertrophic obstructive cardiomyopathy; SBE, subacute bacterial endocarditis.

Cost analysis has also shown IOTEE to be a valued adjunct to cardiovascular surgery ( 27). In our own analysis, if one considers the cost of IOTEE versus the cost of a redo operation to correct something missed, only two or three cases per 100 need have an

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or the number of broken chordae tendinae, and has little impact on the final surgical decision (28) (Fig. 21-10).

Figure 21-5 Intraoperative transesophageal echocardiography before surgical removal of right atrial ( RA) myxoma (thick arrows). In addition, a left atrial ( LA) myxoma (thin arrow) was an unexpected new finding.

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Figure 21-6 New prebypass finding in a patient undergoing mitral valve repair. A: Flail posterior mitral valve leaflet (arrow). B: Mass in area of left atrial appendage ( arrow); C: zoom of mass ( arrow). D: Fibrotic thrombus ( arrow) found and removed.

Figure 21-7 A: Preoperative transesophageal echocardiogram shows a para-aortic valve abscess space ( arrow) in a patient with a history of endocarditis. B: Color flow Doppler echocardiogram shows flow into the space ( arrow). C: Intraoperative transesophageal echoc ardiography performed 1

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week later at the time of surgery shows a new aortic -to-left atrium fistula ( arrow) seen on a color flow Doppler image.

Figure 21-8 A: Large left atrial ( LA) myxoma (arrow) prolapsing through the mitral valve. LV, left ventricle; RA, right atrium; RV, right ventricle. B: Myxoma (arrows) being removed. Intraoperative transesophageal echocardiogram after removal of myxoma showing substantial residual mitral regurgitation ( arrows) (C) and after mitral valve annulopla sty showing no mitral regurgitation ( D).

Mitral Valve Repair Currently at Mayo Clinic, the mitral valve is repaired rather than replaced in more than 95% of patients who have a regurgitant mitral valve lesion. Myxomatous degeneration (prolapse, flail with or without ruptured chordae tendineae) is responsible for mitral regurgitation in 70% of patients undergoing mitral valve repair (23). Other causes include myocardial ischemia, anulus dilations, papillary muscle dysfunction, cleft mitral leaflet, and, les s commonly, rheumatic disease or endocarditis. Valve repair usually is not recommended for an active endocarditic lesion or for a patient with a hemodynamically unstable condition (i.e., a patient with hypotension or in shock with papillary muscle dysfunct ion or 852

techom rupture). Compared with mitral valve replacement, repair is associated with lower short - and long-term mortality (29,30,31). There is not an increased need for a repeat mitral valve procedure in comparison with mitral valve replacement. In addition, longterm anticoagulation is unnecessary, and there is less risk of infective endocarditis. Reconstructive cardiac surgery is an individualized procedure, and its outcome is less predictable than that of valve replacement. After the patient is anesthetize d, the TEE probe is inserted to obtain baseline data about mitral valve morphology, severity of mitral regurgitation, global systolic function, and other cardiovascular abnormalities (e.g., patent foramen ovale, intracardiac mass, or tricuspid regurgitatio n). The posterior mitral leaflet is involved more frequently than the anterior leaflet in patients with myxomatous degeneration. The success rate for satisfactory mitral valve repair is higher for posterior leaflet prolapse or flail segment than for anteri or or bileaflet involvement (23). It is important for the echocardiographer to understand mitral valve anatomy. Prebypass, the echocardiographer will confirm the leaflet or scallop (or both) involved and P.373

any new lesion. Although this is important information to give to surgeons, they usually do not have difficulty identifying the abnormality after the valve has been exposed. However, after surgical repair and after IOTEE has been performed postbypass, any residual regurgitation, if significant, will usually require a second pump run. It is very helpful for the surgeon to know where the valve leaks, that is, in the medial, middle, or lateral portion, so that attention can focus on that area during the second pump run and repair. A series of diagrams illustrating scallop identification are shown in Figure 21-11. The following description is an adaptation of two previously published articles (32,33). Identifying the three scallops is best done in two steps. Ste p 1: at 0 degrees multiplane TEE, you can easily identify whether the involved leaflet is anterior, posterior, or bileaflet, but because you are cutting across the valve from anterior to posterior, it is difficult in this plane to determine medial from lat eral. Step 2: next, the probe is rotated to about 60 to 75 degrees. This is the commissural view in which three scallops are seen: the posterior medial scallop, the

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Figure 21-9 New intraoperative transesophageal echocardiographic finding postbypass. A: Prebypass echocardiogram showing mitral valve vegetations ( arrows) and valve destruction. The valve was replaced with a tissue prosthesis. B: Postbypass echocardiogram showing abn ormal tissue prosthesis (tethering of the posterior leaflet) ( arrow). C: Color flow Doppler image postbypass mitral valve replacement showing severe prosthetic regurgitation ( arrow); the patient was placed back on bypass and the valve replaced. D: Removed tissue valve showing crimped edge ( arrow) by a stitch, causing the prosthetic regurgitation.

For severe mitral regurgitation due to myxomatous degeneration, mitral valve repair consists of 1) quadrangular excision or plication of redundant or fla il tissue (especially for the posterior leaflet), 2) reconstruction of a competent mitral leaflet, 3) shortening of the chordae tendineae (if elongated) or chordal implantation (for anterior leaflet),

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and 4) ring annuloplasty. The repair procedure used to correct other causes of mitral regurgitation depends on the mechanism that causes the regurgitation, for example, perforation, cleft mitral valve, endocarditis, anulus dilatation, or ischemia.

Figure 21-10 Perforation missed by intraop erative transesophageal echocardiography. A: Long-axis prebypass echocardiographic view of the aortic valve ( AV) in a patient with a history of endocarditis. B: Prebypass color flow Doppler image shows severe aortic regurgitation ( arrowheads); no perforati on was appreciated on the intraoperative transesophageal echocardiogram. C: The surgeon found a perforation ( arrow) in the left coronary cusp. In retrospect, the smaller eccentric aortic regurgitant jet seen prebypass ( B, arrow) likely was the perforation.

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Figure 21-11 Identification of mitral valve scallops. A: First view at 0 degrees to determine if anterior leaflet ( AL) or posterior leaflet ( PL); B: Next, the probe is rotated to about 70 degrees, cutting across the valve medial to lateral, to identify the individual scallops: A2, middle portion of anterior leaflet; P1, lateral scallop; P2, middle scallop; P3, medial posterior scallop. P2 is across fr om A2 and seen when flail. C: Three panels are examples of the three posterior leaflet flail views.

Figure 21-12 Identification of mitral valve scallops. Column A: Echocardiograms of flail posterior leaflet ( PL) at 0 degrees. Column B: Drawings of flail posterior scallops ( P1 - P3) at 70

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degrees. Column C: Corresponding echocardiograms at 70 degrees identifying the involved posterior leaflet scallop. P1, lateral scallop; P2, middle scallop; P3, medial scallop.

Immediate feedback about the structural and functional results of a reconstructive procedure before chest closure provides assurance to the surgeon (when the result is good) or an opportunity to revise the repair (when it is not optimal). During the initial experience with IOTEE, revision was necessary in 10 of 143 patients (7%) who underwent mitral valve repair at Mayo Clinic (23), but this rate has decreased significantly. Significant mitral regurgitation still may be present because of systolic anterior motion of the repaired mi tral valve, with or without ring annuloplasty ( Fig. 21-13), usually in the setting of hypovolemia or hyperdynamic LV (or both). Systolic anterior motion and mitral regurgitation usually resolve with optimally restored LV volume or treatment with a β-blocker (or both) ( 34) (Fig. 21-13). Also, it needs to be reemphasized that the severity of mitral regurgitation after repair needs to be assessed under normal physiologic hemodynamic conditions.

Hypertrophic Obstructive Cardiomyopathy Myectomy for HOCM consist s of removing ventricular septal tissue through the aortic valve orifice to relieve LV outflow tract (LVOT) obstruction ( Fig. 21-14). IOTEE is useful preoperatively in determining the site of septal contact by the mitral leaflet (during systolic anterior m otion) and the thickness of the ventricular septum, which helps surgeons decide the extent and depth of the myectomy (16,22). Evaluation of mitral valve morphology and regurgitation severity is also important because a subset of patients with HOCM is prone to develop rupture of the chordae tendineae attached to a mitral leaflet. If a morphologic abnormality of the mitral valve is present, mitral valve repair is indicated in addition to myectomy. Occasionally, the right ventricular outflow tract also is obst ructed by hypertrophy, and it is easily evaluated with TEE. The actual LVOT gradient is usually best obtained P.376

from the transgastric long -axis view (120–130 degrees using

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techom multiplane TEE), but it may be obtained with the four -chamber view in some cases. At our institution, the gradient is usually measured by inserting a needle into the aorta and the LV before and after myectomy ( Fig. 21-15). Figure 21-16 shows a prebypass IOTEE assessment in a patient with HOCM. Figure 21-17 shows a postbypass IOTE E assessment after myectomy for HOCM. Postoperatively, IOTEE is useful in determining the severity of residual mitral valve regurgitation and in assessing potential complications of myectomy, such as ventricular septal defect or aortic regurgitation ( Fig. 21-18). It is common for a small shunt to occur between the resected intramyocardial vessel (septal perforator) and the LV after myectomy and should not be confused for a ventricular septal defect ( Fig. 21-19).

Figure 21-13 Systolic anterior motion (SAM ) of the mitral valve after mitral valve repair. A: Transesophageal echocardiogram showing SAM ( arrow). B: Color flow echocardiogram of mitral regurgitation ( thin arrow) associated with SAM and turbulence in the left ventricular outflow tract (thick arrow). C: Transesophageal echocardiogram after esmolol, no SAM. D: Color flow echocardiogram after esmolol, no mitral regurgitation and no turbulence in left ventricular outflow tract.

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techom Even after generous myectomy, systolic anterior motion of the mitral valve may persist, although the postoperative LVOT gradient is less. Our follow -up study demonstrated that the systolic anterior motion shown on immediate postoperative TEE disappears in most patients by the time of hospital dismissal ( 16).

Measurement of Homograft Size A homograft aortic valve is preferred for patients undergoing aortic valve replacement for infective endocarditis. The homograft is stored in a freezer and thawed before being used. IOTEE is able to measure the LVOT diameter for sizing the homogra ft before the patient is placed on cardiopulmonary bypass, which allows a homograft of correct size to be selected at the beginning of the operation and thawed ( 25). Usually, a homograft that is 1 or 2 mm smaller than the measured LVOT diameter is selected . The homograft aortic valve with a portion of the aortic root is inserted inside the patient's aortic root, and the coronary arteries are reimplanted to the donor aortic root. Familiarity with the surgical procedure allows accurate interpretation of the e chocardiographic images of normal and abnormal aortic homografts.

Figure 21-14 Surgical view of myectomy for hypertrophic obstructive cardiomyopathy. A: View of opened aortic root

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(arrow). B: Resection of obstructing basal septum (arrow). C: Portion of septum removed ( arrow).

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Detection of Atheromatous Plaque in the Aorta Patients with severe atherosclerotic changes in the ascending aorta have an increased risk of stroke after bypass surgery because of dislodgment of an atheromatous plaque by the aortic clamp. IOTEE can identify atheromatous lesions in the aorta, and the surgical technique can be modified to reduce the risk of embolization (24,25). However, epiaortic ultrasonography may be more accurate than TEE for identifying athero sclerosis (35). The ascending aorta is heavily calcified in some patients with calcific aortic stenosis, and prior knowledge of aortic calcification helps a surgeon be prepared with an alternative surgical approach. Examples of IOTEE and assessment of the aorta are shown in Figures 21-20 and 2121.

Aortic Dissection For proximal aortic dissection, IOTEE evaluates the point of intimal tear, the severity of aortic regurgitation, and the involvement of coronary arteries perioperatively. The aortic valve usually can be resuspended, rather than replaced, and the coronary arteries reimplanted. Postoperatively, the integrity of the aorta, the severity of aortic regurgitation, and ventricular wall motion are evaluated (Fig. 21-22).

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Figure 21-15 Surgical view of hemodynamic measurement of the gradient across the left ventricular outflow tract in hypertrophic obstructive cardiomyopathy. White arrow, Left ventricle pressure needle; arrow, aortic pressure needle.

Figure 21-16 Prebypass transesop hageal echocardiography and hemodynamic assessment of hypertrophic obstructive cardiomyopathy. A: A four-chamber view shows systolic anterior motion ( upper arrow) and thickened septum ( lower two arrows). B: A color flow image shows mitral regurgitation

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(upper arrow) and increased left ventricular outflow tract velocity (lower two arrows ). C: Doppler echocardiogram of left ventricular outflow tract velocity, which is 4.55 m/s ( arrow). D: Hemodynamic measurement of gradient with one pressure needle in the aorta and the other needle in the left ventricle. Arrow, post premature ventricular contraction accentuation of the gradient.

Figure 21-17 Postbypass transesophageal echocardiography and hemodynamic assessment of hypertrophic obstructive cardiomyopathy after myectomy. A: A four-chamber view shows minimal systolic anterior motion ( arrow). B: Color flow image shows mitral regurgitation ( upper arrow); left ventricular outflow tract velocity ( lower two arrows ) has been lessened. C: Doppler echocardiogram of left ventricular outflow tract velocity, Back of Book > Appendices > Appendix 1: Echocardiography laboratory, Mayo Clinic, Rochester, Minnesota—example of a final report

Appendix 1: Echocardiography laboratory, Mayo Clinic, Rochester, Minnesota—example of a final report Responsible consultant: [name] Demographics Height: 182.9 cm Weight: 83.9 kg BSA: 2.06 m 2 BMI: 25.08 Procedure start time: 02/17/2005 12:30 PM Location: GO 6S Referring provider: [name] Indication for study: CAD; other Procedure Type: Adult TTE Components: 2D, color flow Doppler, Doppler, M -mode, TDI (tissue Doppler imaging) Referral diagnosis Hemodynamics Heart rate: 107 BPM Blood pressure: 115/65 mm Hg ECG: sinus rhythm Media details Server # clinical clips -81 (number of digital clips acquired for this study)

Final impressions 1. Normal echocardiogram 2. Normal left ventricular chamber size, with ejection fraction 58% 3. Normal wall motion 4. Normal left ventricular diastolic function

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5. Normal left atrial size 6. Normal cardiac valves Findings LEFT VENTRICLE: Normal global left ventricular wall thickness. Normal left ventricular chamber size. Normal left ventricular systolic function. Calculated left ventricular ejection fraction, 58%. RIGHT VENTRICLE: Normal right ventricular size. Normal right ventricular function. ATRIA: Normal -sized atria. CARDIAC VALVES: Normal cardiac valves. Normal physiologic mitral regurgitation. Normal physiologic pulmonary regurgitation. Normal physiologic tricuspid regurgitation. Unable to detect peak tricuspid regurgitation velocity for pulmonary artery systolic pressure calculation. OTHER ECHO FINDINGS: Normal inferior vena cava. Normal scan of the aorta. No evidence of shunt at atrial level. No evidence of intracardiac mass or thrombus . No pericardial effusion. Measurements (Examples)

Ventricular septum Thickness (d), mm Posterior wall Thickness (d), mm Left ventricle Dimension (d), mm Dimension (s), mm Volume (d), mL Volume (s), mL EF, % LV mass, g LV mass index, g/m 2 Left atrium Volume by A-L method, mL Volume index by A -L method, mL/m 2 Thoracic aorta Mid ascending aorta diameter, mm Aortic valve systolic LVOT velocity, m/s LVOT TVI, cm AV velocity, m/s LVOT/AV velocity ratio

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Aortic valve area LVOT diameter, cm LV stroke volume, mL Aortic valve area, cm 2 Hemodynamics Stroke volume, mL Cardiac output, L/min Cardiac index, L/min/m 2 Mitral valve (d) E velocity, m/s A velocity, m/s E/A ratio Deceleration time, ms Medial anulus e' velocity, cm/s E/e' Pulmonary valve (s) Acceleration time, ms Extracardiac vessels Pulmonary veins Systolic velocity, m/s Diastolic velocity, m/s Atrial reversal velocity, m/s

BMI, body mass index; BPM, beats per minute; BSA, body surface area; CAD, coronary artery disease; d, diastolic; s, systolic; TTE, transthoracic echocardiography.

27.2 2. Normal values from M-mode echocardiography Men (n = 288) Women ( n = 524)

Mean SD Mean SD Age, yr 35.7

6.1 35.9 5.5 Height, m 1.77 0.06 1.63 0.06 Weight, kg 74.1 6.9 59.3 6.1 Body mass index, kg/m 2 23.5 1.6 22.1 1.7 Body surface area, m 2 1.91 0.11 1.64 0.10 Systolic blood pressure, mm Hg 117.0 9.1 110.0 10.5 Diastolic blood pressure, mm Hg 74.8 6.8 70.9 7.5 LV diastolic dimension, mm 50.8 3.6 46.1 3.0 LV systolic dimension, mm 32.9 3.4 28.9 2.8 LV wall thickness, mm b 18.1 2.0 15.5 1.5 LA dimension, mm 37.5 3.6 33.1 3.2 LA, left atrium; LV, left ventricle. a These reference values were derived from a healthy subset of the Framingham Heart Study. These values were obtained by M-mode measurement with two -dimensional echocardiographic

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LV wall thickness is the sum of the ventricular septum and

posterior wall thickness. From Lauer MS, Larson MG, Levy D. Gender -specific reference M mode values in adults: Population -derived values with consideration of the impact of height. Journal of th e American College of Cardiology , 1995;26:1039–1046. Used with permission.

27.3 3. Reference limits and partition values of left ventricular size Appendix 3: Reference limits and partition values of left ventricular size a

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diastoli

€“3.

€“3.

€“3.7

¥3.8

€“3.

€“3.

€“3.6

¥3.7

2

4

1

4

LV dimens ion

c diamet er, cm

c diamet er/BSA

918

techom

, cm/m 2

LV

2.5â

3.3â

3.5â

â‰

2.4â

3.4â

3.6â

â‰

diastoli

€“3.

€“3.

€“3.6

¥3.7

€“3.

€“3.

€“3.7

¥3.8

2

4

3

5

LV

56â€

105

118â

â‰

67â€

156

179â

â‰

diastoli

“104

–1

€“13

¥13

“155

–1

€“20

¥20

17

0

1

78

1

1

c diamet er/heig ht, cm/m

LV volume

c volume , mL

LV

35â

76â

87â€

â‰

35â

76â

87â€

â‰

diastol

€“7

€“8

“96

¥97

€“7

€“8

“96

¥97

5

6

5

6

LV

19â€

50â

60â€

â‰

22â€

59â

71â€

â‰

systolic

“49

€“59

“69

¥70

“58

€“70

“82

¥83

LV

12â

31â

37â€

â‰

12â

31â

37â€

â‰

systoli

€“3

€“3

“42

¥43

€“3

€“3

“42

¥43

0

6

0

6

ic volum e/BSA , mL/m 2

volume , mL

c volum e/BSA , mL/m 2

919

techom

BSA, body surface area; LV, left ventricular.

a

Bold italic values: Recommended and best validated.

From Lang RM, Bierig M, Devereaux RB, et al. Chamber Quantification Writing Group, American Society of Echocardiography's Guidelines and Standards Committee, European Association of Echocardiography. Recommendations for chamber quantification: A report fro m the American Society of Echocardiography's Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. Journal of the American Society of Echocardiography , 2005;18:1440–1463. Used with permission.

27.4 4. Reference limits and values and partition values of left ventricular function Appendix 4: Reference limits and values and partition values of left ventricular function a

Women

Men

Sev

Sev

Refe

Mild

Mod

erel

Refe

Mild

Mod

erel

renc

ly

erat

y

renc

ly

erat

y

e

Abn

ely

Abn

e

Abn

ely

Abn

Varia

Ran

orm

Abno

orm

Ran

orm

Abno

orm

ble

ge

al

rmal

al

ge

al

rmal

al

27â€

22â

17â€

â‰

25â€

20â

15â€

â‰

“45

€“26

“21

¤16

“43

€“24

“19

¤14

Linear metho d

End ocardi al fracti

920

techom

onal shorte ning, %

Mid

15â€

13â

11â€

â‰

14â€

12â

10â€

â‰

“23

€“14

“12

¤10

“22

€“13

“11

¤10

Eje

â‰

45â

30â€

25

mass

“150

€“17

€“18

3

“200

€“22

€“25

5

1

2

7

4

44â€

89â€

101â

â‰

50â€

103â

117â

â‰

“88

“100

€“11

¥11

“102

€“11

€“13

¥13

2

3

6

0

1

thick ness, cm

Se ptal thick ness , cm

or wall thick ness , cm

2D meth od

, g

LV mass /BSA , g/m 2

BSA, Body surface area; LV, left ventricular; 2D, 2 -dimensional.

a

Bold italic values: Recommended and best validated.

From Lang RM, Bierig M, Devereaux RB, et al. Chamber Quantification Writing Group, American Society of Echocardiography's Guidelines and Standards Committee,

923

techom

European Association of Echocardiography. Recommendations for chamber quantification: A report fro m the American Society of Echocardiography's Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. Journal of the American Society of Echocardiography , 2005;18:1440–1463. Used with permission.

27.6 6. Reference limits and partition values of right ventricular and pulmonary artery size Appendix 6: Reference limits and partition values of right ventricular and pulmonary artery size Variable

Reference

Mildly

Moderately

Severely

Range

Abnormal

Abnormal

Abnormal

2.0–2.8

2.9–3.3

3.4–3.8

≥3.9

2.7–3.3

3.4–3.7

3.8–4.1

≥4.2

7.1–7.9

8.0–8.5

8.6–9.1

≥9.2

RV dimensions

Basal RV diameter, cm

Mid-RV diameter, cm

Base-toapex length, cm

924

techom

RVOT diameters

Above

2.5–2.9

3.0–3.2

3.3–3.5

≥3.6

1.7–2.3

2.4–2.7

2.8–3.1

≥3.2

1.5–2.1

2.2–2.5

2.6–2.9

≥3.0

aortic valve, cm

Above pulmonic valve, cm

PA diameter

Below pulmonic valve, cm

PA, pulmonary artery; RV, right ventricular; RVOT, right ventricular outflow tract. Data from Foale R, Nihoyannopoulos P, McKenna W, et al. Echocardiographic measurement of the normal adult right ventricle. British Heart Journal , 1986;56:33–44. Erratum in: British Heart Journal , 1986;56:298 and British Heart Journal , 1987;57:396.

27.7 7. Reference limits and partition values of right ventricular size and function as measured in the apical four-chamber view Appendix 7: Reference limits and partition values of right ventricular size and function as measured in the apical fourchamber view 925

techom

Reference

Mildly

Moderately

Severely

Range

Abnormal

Abnormal

Abnormal

11–28

29–32

33–37

≥38

7.5–16

17–19

20–22

≥23

32–60

25–31

18–24

≤17

Variable

RV diastolic area, cm 2

RV systolic area, cm 2

RV fractional area change, %

RV, Right ventricular. Data from Weyman AE. Principles and practice of echocardiography. 2nd ed. Philadelphia: Lea & Febiger; 1994.

27.8 8. Reference limits and partition values for left atrial dimensions and volumes Appendix 8: Reference limits and partition values for left atrial dimensions and volumes a

Women

Men

Sev

Sev

Refe

Mild

Mod

erel

Refe

Mild

Mod

erel

renc

ly

erat

y

renc

ly

erat

y

e

Abn

ely

Abn

e

Abn

ely

Abn

Ran

orm

Abno

orm

Ran

orm

Abno

orm

ge

al

rmal

al

ge

al

rmal

al

926

techom

Atrial dimens ions

LA

2.7â

3.9â

4.3â

â‰

3.0â

4.1â

4.7â

â‰

diamet

€“3.

€“4.

€“4.6

¥4.7

€“4.

€“4.

€“5.2

¥5.2

er, cm

8

2

0

6

LV

1.5â

2.4â

2.7â

â‰

1.5â

2.4â

2.7â

â‰

diamet

€“2.

€“2.

€“2.9

¥3.0

€“2.

€“2.

€“2.9

¥3.0

er/BSA

3

6

3

6

RA

2.9â

4.6â

5.0â

â‰

2.9â

4.6â

5.0â

â‰

minor-

€“4.

€“4.

€“5.4

¥5.5

€“4.

€“4.

€“5.4

¥5.5

5

9

5

9

RA

1.7â

2.6â

2.9â

â‰

1.7â

2.6â

2.9â

â‰

minor-

€“2.

€“2.

€“3.1

¥3.2

€“2.

€“2.

€“3.1

¥3.2

5

8

5

8

LA

â‰

20â

30â€

â‰

20â

30â€

>40

area,

¤20

€“30

“40

¤20

€“30

“40

, cm/m 2

axis dimens ion, cm

axis dimens ion/BS A, cm/m 2

Atrial area

>40

cm 2

Atrial volume s

927

techom

LV

22â€

53â

63â€

â‰

18â€

59â

69â€

â‰

diastol

“52

€“62

“72

¥73

“58

€“68

“78

¥79

LA

22

29â

34â€

â‰

22

29â

34â€

â‰

volum

±

€“3

“39

¥40

±

€“3

“39

¥40

e/BSA

6

3

6

3

ic volume , mL

, mL/m 2

BSA, Body surface area; LA, left atrial; RA, right atrial.

a

Bold italic values: Recommended and best validated.

From Lang RM, Bierig M, Devereaux RB, et al. Chamber Quantification Writing Group, American Society of Echocardiography's Guidelines and Standards Committee, European Association of Echocardiography. Rec ommendations for chamber quantification: A report from the American Society of Echocardiography's Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. Journal of the American Society of Echocardiography , 2005;18:1440–1463. Used with permission.

27.9 9. Appendix 9

Appendix 9 The 95% confidence intervals for aortic root diameter at sinuses of Valsalva based on body surface area in children and

928

techom adolescents (A), adults 20 to 39 years old (B), and adults 40 years and older (C). From Roman MJ, Devereaux RB, Kramer -Fox R, et al. T wo-dimensional echocardiographic aortic root dimensions in normal children and adults. American Journal of Cardiology , 1989;64:507–512 . Used with permission.

27.10 10. Reference ranges for diastolic function parameters by age Appendix 10: Reference ranges for diastolic function parameters by age a

Age Groups, y

Para mete

45–

50–

55–

60–

65–

≥7

r

49

54

59

64

69

0

0.7

0.6

0.7

0.7

0.6

0.6

(0.5–

(0.5–

(0.5–

(0.5â€

(0.4–

(0.4–

0.9)

0.9)

0.9)

“0.9)

0.8)

1.0)

0.5

0.5

0.6

0.6

0.7

0.8

(0.3–

(0.4–

(0.4–

(0.4â€

(0.4–

(0.5–

0.7)

0.8)

0.9)

“0.9)

1)

1.1)

1.3

1.2

1.2

1.0

1.0

0.8

(1.0–

(0.8–

(0.7–

(0.7â€

(0.6–

(0.6–

2.0)

2.0)

1.8)

“1.6)

1.5)

1.3)

1.50

1.40

1.29

1.20

1.00

1.00

(1.0–

(1.0–

(0.83â

(0.83â

(0.75â

(0.67â

2.67)

2.33)

€“2.25)

€“2.0)

€“1.67)

€“1.60)

Mitral inflow

E, m/s

A, m/s

E/A

E/( A-E at A)

929

techom

DT, ms

Adur , ms

208

217

210

222

227

242

(180â€

(178â€

(183â€

(180â€

(188â€

(188â€

“258)

“266)

“187)

“282)

“298)

“320)

140

147

147

147

150

150

(122â€

(130â€

(127â€

(129â€

(122â€

(128â€

“170)

“172)

“173)

“172)

“180)

“183)

0.60

0.60

0.60

0.60

0.60

0.60

(0.40â

(0.40â

(0.40â

(0.40â

(0.50â

(0.40â

€“0.80)

€“0.80)

€“0.80)

€“0.80

€“0.80)

€“0.80)

Pulmo nary vein flow

PS, m/s

)

PD, m/s

0.40

0.40

0.40

0.40

0.40

0.40

(0.30â

(0.30â

(0.30â

(0.30â

(0.30â

(0.30â

€“0.60)

€“0.60)

€“0.60)

€“0.60

€“0.60)

€“0.60)

)

PS/ PD

1.25

1.40

1.40

1.50

1.60

1.67

(0.86â

(1.00â

(1.00â

(1.00â

(1.00â

(1.00â

€“2.00)

€“2.00)

€“2.00)

€“2.25

€“2.50)

€“2.50)

)

PVA

118

122

123

123

127

130

(100â€

(103â€

(105â€

(103â€

(110â€

(112â€

“140)

“142)

“157)

“160)

“152)

“170)

-25.0

-25.0

-21.6

-23.3

-21.7

-22.3

Rdur-

(-

(-

(-

(-

(-

(-

Adur,

53.3â€

51.7â€

50.0â€

51.7â€

55.0â€

51.7â€

“0)

“0)

“11.7)

“13.4)

“12.5)

“31.6)

Rdur, ms

PVA

ms

TDImitral

930

techom

anulu s

Sep tal

S

E′

0.10

0.09

0.09

0.09

0.08

0.07

, m/s

(0.07â

(0.06â

(0.05â

(0.06â

(0.05â

(0.05â

€“0.14)

€“0.14)

€“0.12)

€“0.13

€“0.11)

€“0.11)

)

A′ S

, m/s

0.10

0.10

0.11

0.11

0.11

0.11

(0.07â

(0.08â

(0.08â

(0.09â

(0.09â

(0.09â

€“0.14)

€“0.14)

€“0.15)

€“0.15

€“0.15)

€“0.15)

)

E/E ′

S

6.67

7.00

7.78

7.64

8.57

8.57

(4.62â

(4.55â

(4.62â

(5.0â€

(5.45â

(4.55â

€“11.2

€“11.6

€“13.3

“12.0)

€“13.3

€“16.6

5)

7)

3)

3)

7)

0.13

0.12

0.11

0.10

0.09

0.08

(0.09â

(0.08â

(0.07â

(0.07â

(0.07â

(0.05â

€“0.17)

€“0.16)

€“0.15)

€“0.15

€“0.12)

€“0.11)

Later al

E′L , m/s

)

A′ L

, m/s

0.11

0.11

0.11

0.12

0.12

0.12

(0.07â

(0.07â

(0.08â

(0.08â

(0.09â

(0.08â

€“0.16)

€“0.15)

€“0.16)

€“0.17

€“0.16)

€“0.18)

)

E/E ′

L

5.38

5.45

6.0

6.67

7.0

7.78

(3.75â

(3.75â

(3.85â

(4.62â

(4.17â

(5.0–

€“7.78)

€“8.89)

€“10.0)

€“8.89

€“11.2

14.0)

)

5)

Valsal va

931

techom

mane uver

VS E/A

1.00

1.00

0.80

0.71

0.60

0.57

(0.60â

(0.57â

(0.44â

(0.43â

(0.40â

(0.30â

€“1.33)

€“1.33)

€“1.25)

€“1.20

€“1.00)

€“1.00)

)

VS

1.33

1.25

1.00

1.00

0.75

0.71

E/(A-

(0.80â

(0.67â

(0.60â

(0.50â

(0.50â

(0.33â

E at

€“2.50)

€“3.00)

€“2.50)

€“2.00

€“1.67)

€“1.50)

A)

)

ΔE/

0.37

0.40 (-

0.37

0.36 (-

0.31

0.29 (-

(0–1.

0.05â€

(0–1.

0.04â€

(0–0.

0.04â€

0)

“1.0)

0)

“0.8)

64)

“0.70)

0.0 (-

0.07 (-

0.17 (-

0.13 (-

0.17 (-

0.17 (-

(A-E

1.3–

1.33â€

1.0–

0.83â€

0.58â€

0.75â€

at A)

1.0)

“0.75)

0.77)

“0.75)

“0.57)

“0.63)

0.30

0.30

0.30

0.40

0.40

0.40

(0.10â

(0.20â

(0.20â

(0.20â

(0.20â

(0.20â

€“0.50)

€“0.60)

€“0.60)

€“0.60

€“0.60)

€“0.60)

A

ΔE/

Index of myoc ardial perfor manc e

LIM P

)

A, late diastolic mitral flow velocity; A d u r , duration of late mitral flow; A â € ² L , lateral mitral anulus velocity with atrial contraction; A â € ² S , late diastolic lateral annular velocity; DT, deceleration time of early diastolic mitral flow; E, early diastolic mitr al flow velocity; E â € ² L , early diastolic lateral annular velocity; E â € ² S , early diastolic septal annular velocity; ΔE/A, change in E/A with Valsalva; ΔE/A -E, change in E/A -E at A with Valsalva; LIMP, left

932

techom

ventricular index of myocardial performance; P D , pulmonary vein diastolic flow velocity; P S , pulmonary vein systolic flow velocity; PVAR d u r , duration of pulmonary vein atrial flow reversal; TDI, tissue Doppler imaging; VS, peak Valsalva.

a

Data are median (5th and 95th percentile).

From Munagala VK, Jacobsen SJ, Mahoney DW, et al. Association of newer diastolic function parameters with age in healthy subjects: A population -based study. Journal of the American Society of Echocardiography , 2003;16:1049–1056. Used with permission.

27.11 11. Mitral inflow velocities in 117 normal subjects, stratified by phase of respiration Appendix 11: Mitral inflow velocities in 117 normal subjects, stratified by phase of respiration Variable

Inspiration

Expiration

Apnea

Peak E, cm/s

67 ± 14 a

68 ± 15 b

68 ± 15

Peak A, cm/s

48 ± 16

50 ± 16 b

49 ± 15

E/A ratio

1.5 ± 0.6

1.5 ± 0.7

1.7 ± 0.6

DT, ms

195 ± 34

192 ± 33

194 ± 35

83 ± 16

83 ± 16

82 ± 16

IVRT, ms

A, filling wave due to atrial contraction; DT, deceleration time; E, early rapid filling wave; IVRT, isovolumic relaxation time. a

Significantly different ( P