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Heart Disease in Women [1 ed.]
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Copyright © 2008. Nova Science Publishers, Incorporated. All rights reserved. Lardner, Benjamin V., and Harrison R. Pennelton. Heart Disease in Women, Nova Science Publishers, Incorporated, 2008. ProQuest Ebook Central,

Copyright © 2008. Nova Science Publishers, Incorporated. All rights reserved. Lardner, Benjamin V., and Harrison R. Pennelton. Heart Disease in Women, Nova Science Publishers, Incorporated, 2008. ProQuest Ebook Central,

HEART DISEASE IN WOMEN

Copyright © 2008. Nova Science Publishers, Incorporated. All rights reserved.

No part of this digital document may be reproduced, stored in a retrieval system or transmitted in any form or by any means. The publisher has taken reasonable care in the preparation of this digital document, but makes no expressed or implied warranty of any kind and assumes no responsibility for any errors or omissions. No liability is assumed for incidental or consequential damages in connection with or arising out of information contained herein. This digital document is sold with the clear understanding that the publisher is not engaged in rendering legal, medical or any other professional services.

Lardner, Benjamin V., and Harrison R. Pennelton. Heart Disease in Women, Nova Science Publishers, Incorporated, 2008. ProQuest Ebook Central,

Copyright © 2008. Nova Science Publishers, Incorporated. All rights reserved. Lardner, Benjamin V., and Harrison R. Pennelton. Heart Disease in Women, Nova Science Publishers, Incorporated, 2008. ProQuest Ebook Central,

HEART DISEASE IN WOMEN

BENJAMIN V. LARDNER AND

HARRISON R. PENNELTON

Copyright © 2008. Nova Science Publishers, Incorporated. All rights reserved.

EDITORS

Nova Science Publishers, Inc. New York

Lardner, Benjamin V., and Harrison R. Pennelton. Heart Disease in Women, Nova Science Publishers, Incorporated, 2008. ProQuest Ebook Central,

Copyright © 2009 by Nova Science Publishers, Inc.

All rights reserved. No part of this book may be reproduced, stored in a retrieval system or transmitted in any form or by any means: electronic, electrostatic, magnetic, tape, mechanical photocopying, recording or otherwise without the written permission of the Publisher. For permission to use material from this book please contact us: Telephone 631-231-7269; Fax 631-231-8175 Web Site: http://www.novapublishers.com NOTICE TO THE READER The Publisher has taken reasonable care in the preparation of this book, but makes no expressed or implied warranty of any kind and assumes no responsibility for any errors or omissions. No liability is assumed for incidental or consequential damages in connection with or arising out of information contained in this book. The Publisher shall not be liable for any special, consequential, or exemplary damages resulting, in whole or in part, from the readers’ use of, or reliance upon, this material. Any parts of this book based on government reports are so indicated and copyright is claimed for those parts to the extent applicable to compilations of such works. Independent verification should be sought for any data, advice or recommendations contained in this book. In addition, no responsibility is assumed by the publisher for any injury and/or damage to persons or property arising from any methods, products, instructions, ideas or otherwise contained in this publication. This publication is designed to provide accurate and authoritative information with regard to the subject matter covered herein. It is sold with the clear understanding that the Publisher is not engaged in rendering legal or any other professional services. If legal or any other expert assistance is required, the services of a competent person should be sought. FROM A DECLARATION OF PARTICIPANTS JOINTLY ADOPTED BY A COMMITTEE OF THE AMERICAN BAR ASSOCIATION AND A COMMITTEE OF PUBLISHERS.

Copyright © 2008. Nova Science Publishers, Incorporated. All rights reserved.

Library of Congress Cataloging-in-Publication Data Heart disease in women / [edited by] Benjamin V. Lardner and Harrison R. Pennelton. p. ; cm. Includes bibliographical references and index. ISBN 978-1-60741-090-4 (E-Book) 1. Heart diseases in women. I. Lardner, Benjamin V. II. Pennelton, Harrison R. [DNLM: 1. Heart Diseases. 2. Women's Health. WG 210 H43475 2009] RC682.H3836 2009 616.1'20082--dc22 2008041207

Published by Nova Science Publishers, Inc.    New York

Lardner, Benjamin V., and Harrison R. Pennelton. Heart Disease in Women, Nova Science Publishers, Incorporated, 2008. ProQuest Ebook Central,

Contents Preface

Copyright © 2008. Nova Science Publishers, Incorporated. All rights reserved.

Chapter I

vii Cardiac Rehabilitation: Secondary Prevention of Cardiovascular Disease in Women Richard Snow, Michelle LaLonde, Cheryl Graffagnino, Kathy Spencer, and Teresa Caulin-Glaser

Chapter II

Effects of Estrogen and its Receptors on Myocardial Infarction Jiang Hong,Chen Jing, He Bo, and Lu Zhi-Bing

Chapter III

Preeclampsia and Risk of Cardiovascular Disease: Epidemiology and Pathophysiology Giovanna Oggè, Simona Cardaropoli and Tullia Todros

1

37

63

Chapter IV

Diabetes and the Risk of Coronary Heart Disease among Women Gang Hu

75

Chapter V

The Impact of Heart Rate as a Cardiovascular Risk Taku Inoue and Kunitoshi Iseki

87

Chapter VI

Women in a World of Men’s Disease: The Case of Female Cardiac Patients Michal Rassin

101

Thromboembolism and Coronary Heart Disease: In Which Aspects are Women Different? Sigrid Nikol and Katharina Middendorf

121

Chapter VII

Chapter VIII Aging Women and Coronary Heart Disease Marek A. Kosmicki and Hanna Szwed Chapter IX

Prognosis of Women with Acute Coronary Syndromes: An Overview Andreja Sinkovic

Lardner, Benjamin V., and Harrison R. Pennelton. Heart Disease in Women, Nova Science Publishers, Incorporated, 2008. ProQuest Ebook Central,

147

209

vi Chapter X

Chapter XI

Contents The Effects of Aging on the Electrophysiological Properties of the Atrial Myocardium in Women with and without Paroxysmal Atrial Fibrillation Osmar Antonio Centurión, Akihiko Shimizu and Shojiro Isomoto Women and Angina Pectoris: Emergency Department and Diagnostic Difficulties in an Undeveloped Community Esed Omerkic and Fahir Barakovic

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Index

Lardner, Benjamin V., and Harrison R. Pennelton. Heart Disease in Women, Nova Science Publishers, Incorporated, 2008. ProQuest Ebook Central,

221

235 245

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Preface Heart disease is an umbrella term for a number of different diseases affecting the heart. As of 2007, it is the leading cause of death in the United States,England, Canada and Wales, killing one person every 34 seconds in the United States alone.Heart disease is synonymous with cardiac disease but not with cardiovascular disease which is any disease of the heart or blood vessels. Among the many types of heart disease are, for example: Angina; Arrhythmia; Congenital heart disease; Coronary artery disease (CAD); Dilated cardiomyopathy; Heart attack (myocardial infarction); Heart failure; Hypertrophic cardiomyopathy; Mitral regurgitation; Mitral valve prolapse; and Pulmonary stenosis. This new book brings together important recent research on heart disease with a focus on women and heart disease. Chapter I - Over the past decade progress has been made toward education and increasing awareness, in both patients and physicians, of the risks of cardiovascular disease in women. There has also been an increase in federally funded initiatives in the area of genderspecific cardiovascular research. However, cardiovascular disease continues to be the primary cause of death among women in the United States. Each year more women than men die of cardiovascular disease. Gender-based differences in the prevalence, risk factors, presentation, treatment, and outcomes of cardiovascular disease remain important areas of active research. A frequently overlooked, yet vitally important, component of treatment for the secondary prevention of cardiovascular disease in women is participation in cardiac rehabilitation. Cardiac rehabilitation programs are comprehensive secondary prevention programs which contain specific core components that aim to optimize cardiac risk reduction, teach and develop healthy behaviors, decrease disability, and promote an active lifestyle for patients with cardiovascular disease. Research has documented the efficacy and effectiveness of cardiac rehabilitation with reductions in mortality and improvements in clinical and behavioral outcomes. Despite this, cardiac rehabilitation is under prescribed and underutilized, especially in women. In this review, the current evidence-based findings, research, and recommendations for cardiac rehabilitation in the treatment of cardiovascular disease in women is addressed with a focus on those areas specific to the needs of women. Persistent gaps in our knowledge regarding the role of cardiac rehabilitation in women with cardiovascular disease are presented as research initiatives for the future. Chapter II - The higher cardiovascular risk in men and post-menopausal women implies a protective action of estrogen. A large number of experimental studies have provided strong

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Benjamin V. Lardner andHarrison R. Pennelton

evidence indicating that estrogen has protective effect in the process of myocardial infarction (MI). Estrogen may prevent deterioration of cardiac function post-MI through improving heart failure of cadiocyte biology and also through mediating arrhythmia. The alternations by estrogen in immune function, apoptosis and endothelial progenitor cells after MI may be the most important mechanisms for cadiocyte survival. For the control of cardiac hypertrophy, estrogen acts as both a potent vasodilator and a direct mediator for cadiocyte. The major mechanisms underlying arrhythmia effect may involve affecting neural remodeling, electrical remodeling and structural remodeling. In this article, we mainly focus on the current mechanisms underlying the estrogen effects after MI through genomic pathway and nongenomic pathway. A further understanding of estrogen and estrogen receptors function and regulation may lead to the development of highly specific prevention and treatment of cardiovascular diseases. Chapter III - Preeclampsia (PE) is a pregnancy-specific syndrome characterised by the appearance of hypertension (systolic blood pressure ≥ 140 mmHg or diastolic blood pressure ≥ 90 mmHg) and proteinuria (≥ 300mg per 24 hours) during the second half of pregnancy (after 20 weeks of gestational age). It may be variously associated with a myriad of other signs and symptoms, such as oedema, visual disturbances, headache, seizures (eclampsia), epigastric pain, HELLP syndrome (haemolysis, liver dysfunction and low platelet count), and it typically resolves after delivery. PE is to be differentiated from other hypertensive disorders in pregnancy, both from a prognostic and a pathophysiological point of view. Under this respect, the NHLBI Working Group on Research on Hypertension During Pregnancy distinguishes PE from: - gestational hypertension: de novo hypertension arising after midpregnancy, in the absence of proteinuria. This category includes women who later satisfy diagnostic criteria for preeclampsia. However, in most cases, proteinuria never occurs, the course is relatively benign, and blood pressure normalizes postpartum; - chronic hypertension: maternal hypertension recognised before pregnancy; it can also be assumed when hypertension is detected before mid-pregnancy and when it fails to normalize 12 weeks after delivery. Women with chronic hypertension are at increased risk to develop superimposed preeclampsia (25% risk) and the outcomes for the mother and infant with preeclampsia superimposed on existing hypertension are worse than with de novo preeclampsia.; - eclampsia is a life-threatening complication of PE characterised by new-onset of seizures in a woman with PE. Such convulsions usually occur after mid-pregnancy, or during delivery, but about one third of eclamptic convulsions occur during the first 48 hours of the postpartum period. The exact incidence of PE is uncertain, but it has been reported to be approximately 58% and to be substantially higher in nulliparous women, and in women with multifetal pregnancies, history of PE in previous pregnancies, family history of PE, chronic hypertension, pregestational diabetes, antiphospholipid antibodies, obesity, age > 40 years. Paradoxically, cigarette smoking reduces the risk. PE is one of the leading causes of maternal mortality in the developing countries and a cause of neonatal morbidity and mortality worldwide. Mortality from PE is largely preventable by delivery that stops the progression of the disease, so that the high rate of

Lardner, Benjamin V., and Harrison R. Pennelton. Heart Disease in Women, Nova Science Publishers, Incorporated, 2008. ProQuest Ebook Central,

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Preface

ix

maternal mortality in developing countries is a marker of low quality of care, rather than disease frequency. Anyway, even in developed countries, PE puts the mother at risk for abruptio placentae, renal failure, pulmonary oedema, stroke and seizures (eclampsia).The reason for neonatal risks depends on the fact that, given the absence of an effective treatment, the only possibility to prevent further deterioration of maternal conditions is delivery, and preterm birth is associated with increased mortality and neurological disabilities. It is estimated that 15% of all preterm births are iatrogenic deliveries for preeclampsia. Moreover, preeclampsia also increases the risk of fetal growth restriction (FGR) that, in turn, is an important cause of neonatal mortality and morbidity and a recognised risk factor for longterm pathologies in adulthood, such as cardiovascular disease and insulin-resistance syndrome. Chapter IV - The number of diabetic patients in the world has been estimated to at least double during the next 30 years. Coronary heart disease is the leading cause of death among patients with type 2 diabetes. The associations of type 2 diabetes and hyperglycemia with the risk of coronary heart disease have been assessed by a number of prospective studies and the results are consistent. Patients with type 2 diabetes have a 2-4 times higher risk of coronary mortality than those without diabetes. Among the middle-aged general population, men have a 2 to 5 times higher risk of coronary heart disease than women. However, women with diabetes will lose their relative protection against coronary heart disease compared with men. In recent years, several studies compared the gender specific impact of diabetes and myocardial infarction at baseline on coronary mortality. These studies found that both diabetes and myocardial infarction at baseline increased coronary mortality. In women, prior myocardial infarction at baseline confers a lower risk on coronary mortality than prior diabetes does. The results of these studies have important implications for clinical practice. For future coronary heart disease risk we need to consider carefully the treatment strategies on individual disease status, particularly type 2 diabetes, in women. Chapter V - An elevated heart rate can indicate a patient’s risk for cardiovascular disease. A large number of population-based studies have demonstrated an association between elevated heart rate and cardiovascular disease as well as all-cause mortality with and without diagnosed cardiovascular disease. Despite accumulating evidence of its significance, elevated heart rate remains neglected as a cardiovascular risk factor. From the preventive point of view, heart rate may be a useful biomeasurement for identifying subjects at risk for hypertension, metabolic syndrome, and cardiovascular events. By identifying subjects with these conditions, targeted and cost-effective cardiovascular disease prevention programs can be planned. Previous findings also suggest that heart rate modulation should be considered in the treatment of cardiovascular disease. There is a linear relationship between heart rate reduction and a reduction in mortality rate. Tachycardia is a strong marker of widespread abnormality of the autonomic control of the circulation. This autonomic nervous system imbalance could explain the association between elevated heart rate and hypertension, metabolic syndrome, and cardiovascular events. Unfortunately, lowering the heart rate is not currently a clinically recognized therapeutic goal. Prospective trials are needed to investigate the heart rate levels that should be considered hazardous and whether treatment of high heart rate can prevent cardiovascular events.

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Chapter VI - The central purpose of the study was to examine differences between women and men, ages 30-50 years, in their responses to heart disease, and to identify the factors influencing them in the fields of health and illness. The study was conducted using a qualitative method. The participants in the study included 30 men and 30 women who suffered from coronary heart disease. The study findings suggest that women delayed seeking treatment and that when they did seek treatment they were not initially diagnosed as suffering from heart disease due to physicians’ perceptions that heart disease is a men’s disease. The recovery period for women was characterized by their quick return to daily home making before their physical condition permitted it. Conversely, the men extended their recovery period and received support from their families. As part of the return to normal life, the men were strict in following the instructions of the health regimen, whereas most of the women ignored it. The women, compared to the men, received less support from their spouses and families, and they noted that social expectations concerning their role were high. Our study concludes that heart disease varies between men and women in the characteristics of its symptoms and in the attitude of medical staff and the public, as well as of patients themselves, towards the disease. The role of the cardiac patient is based on male characteristics and, as a result, men are legitimized and receive social support in all that relates to the disease; consequently, men adhere to the health regimen, whereas women are less inclined to. This study can advance insights on the influence of the gender variable on responses to heart disease, as well as supply information on therapeutic intervention for male and female cardiac patients and the nature of the different measures used for each. Chapter VII - Young women are at a 3-fold higher risk of experiencing venous thromboembolism compared to young men. This risk is further increased by oral contraceptives, smoking, hereditary thrombophilia and/or low socioeconomic status. There are also hints for gender specific differences in the arterial system. Coronary heart disease which is particularly important develops in women 10-15 years later than in men. However, the clinical course in women is often more complicated. In women, thrombophilic predispositions play a more important role before menopause and metabolic risk factors after menopause, compared to men. Thrombus formation needs to be initiated by disturbances of at least one element of the Virchow trias. There is principally no difference between men and women. However, all three elements are influenced by estrogen, resulting in gender specific differences. There is a favourable influence on blood flow by the inhibition of atherogenesis and on the endothelial function by increased NO release, and an unfavourable influence on hemostasis resulting in hypercoagibility. Thus, particularly non-selective hormone replacement therapy for the inhibition of atherogenesis may be questionable due to increased thrombogenicity. The solution may be more selective estrogen receptor modulators. Clinical trials are still needed for both, hormone replacement therapy and the therapy of venous and arterial thromboembolism which has been thus far studied in predominantly male patient cohorts. Chapter VIII - Aging, a natural process in human life, begins at conception, continues with growth and development and finishes with dysfunction of various organs towards the end of life. Coronary heart disease (CHD) is one of the most common cardiovascular diseases, leading to death in women and is responsible for more deaths each year than all other diseases together. The incidence of myocardial infarction (MI) in women, although

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xi

lower than in men, increases dramatically after the menopause. This increase is at least partly due to aging, although men also have a progressive increase in MI with age. The role of the menopause itself is not very clear. The evaluation of chest pain, the main symptom of CHD, is less straightforward in women than in men, because the language used to describe symptoms differs between the sexes. In fact, symptoms in women are slightly different from those in men. Until now, medical data published in literature was based on research done on male patients. However, there are numerous differences in the epidemiology and primary manifestation of CHD in women and men. In addition, the diagnosis of angina pectoris in women is more difficult than in men for several reasons, which are mentioned later in this chapter. The clinical usefulness of some non-invasive tests is lower in women than in men. A number of studies have shown gender-based differences in frequency rates of coronary angiography and revascularization, even among those with acute MI. It should be stressed that women with angina are much more likely than men to have normal coronary arteries on angiography. On the other hand, the risk of complications after coronary angiography in women is higher than in men. This may explain why physicians fail to refer women for subsequent invasive tests. Several case reports included in this paper show the difficulties in diagnosis and treatment of women with CHD. In conclusion, it could be said that difficulties in diagnosis and limited data on the treatment of CHD in women, have led to a situation in which women with CHD often remain under-investigated and under-treated. Chapter IX - Background. Participation of women in studies of acute coronary syndromes, including acute ST-elevation myocardial infarction (MI) as well as unstable angina and/or non-ST-elevation MI is about 30-40% and is remaing constant during last 20 years. It is well known that in ST-elevation MI women, who are older than men and are mostly less agressively treated, experience worse outcome than men. The results of studies of unstable angina and/or non-ST-elevation MI also demonstrated that women are significantly older and with significantly more comorbidities. However, the results of the studies are controvesial, regarding the short- and long term prognosis. Some studies demonstarted significantly increased risk of 30-day and six-month adverse outcomes in women, when compared to men in spite of their similar treatments, but others similar outcomes with similar treatments in spite of older age. Conclusions. In this review article the results of studies, regarding the outcomes of women compared to men in acute coronary syndromes are discussed, especially the use of treatments, including coronary interventions, misuse or errors in medical treatments, as well as future perspectives in women with coronary artery disease in the new millenium. Chapter X - Introduction: The presence of electrophysiological abnormalities of the atrial myocardium with increasing age could explain the differences in the genesis of atrial fibrillation in women with paroxysmal atrial fibrillation (PAF). Aging could influence not only the atrial response to premature atrial depolarizations but also the morphology of atrial electrograms. Material and Methods: Programmed atrial stimulation with single extrastimulus was performed in 102 female patients, 48 of them had normal sinus node function and did not have PAF (Group I), and 54 of them had PAF, idiopathic or associated to other arrhythmias (Group II). Programmed atrial stimulation was performed from the right atrial appendage at

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double diastolic threshold with stimulus duration of 2 ms with a computarized cardiac stimulator. Results: The incidence of induction of repetitive atrial firing (68% vs 36%; p 12 yrs (%) Currently Employed (%) Diabetes (%) Current Smoker (%) Hypertension (%) Obesity (%)

Males (n=1335)

Females (n=471)

p value

63.4 ± 10.8 30.0 87.7 83.5 67.8 47.1 28.4 6.1 71.5 39.5

65.8 ± 12.0 39.5 88.1 54.6 47.8 30.8 27.4 4.3 80.5 40.8

0.0001 0.0001 0.82