Valvular Heart Disease in Clinical Practice

Transcription

1

2 Valvular Heart Disease in Clinical Practice

3

4 Michael Y. Henein Editor Valvular Heart Disease in Clinical Practice 123

5 Editor Michael Y. Henein Consultant Cardiologist Umea Heart Centre Umea University Sweden ISBN: e-isbn: DOI / British Library Cataloguing in Publication Data A catalogue record for this book is available from the British Library Library of Congress Control Number: c Springer-Verlag London Limited 2009 Apart from any fair dealing for the purposes of research or private study, or criticism or review, as permitted under the Copyright, Designs and Patents Act 1988, this publication may only be reproduced, stored or transmitted, in any form or by any means, with the prior permission in writing of the publishers, or in the case of reprographic reproduction in accordance with the terms of licenses issued by the Copyright Licensing Agency. Enquiries concerning reproduction outside those terms should be sent to the publishers. The use of registered names, trademarks, etc., in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant laws and regulations and therefore free for general use. Product liability: The publisher can give no guarantee for information about drug dosage and application thereof contained in this book. In every individual case the respective user must check its accuracy by consulting other pharmaceutical literature. Printed on acid-free paper Springer Science+Business Media springer.com

6 Preface Over the last three decades, major advances in the management of diseases of the valves have been seen. While cardiac catheterization was in the 1970s, the only means for confirming the diagnosis, Doppler echocardiography has become the corner stone for accurate assessment of valve disease, even in fetuses. Now not only the disease can be identified but also the rate of disease progression (e.g. leaflet calcification and stiffness) can be accurately measured and quantified by echocardiography and multislice/electron beam CT imaging. Surgical treatment of valve disease has also witnessed great advances, having moved from traditional valve replacement to sophisticated repair procedures and the use of extracorporeal pump support in some patients. Robotic valve surgery has also proved a great success, in well selected cases, and is expected to have a fruitful future. Furthermore, in special circumstances, conventional surgical valve excision has now been replaced by percutaneous catheter-based valve replacement for aortic and pulmonary disease. This approach reduces the risk from the surgery itself, avoids general anaesthesia and many potential post-operative complications. This book discusses the practicalities of the diagnosis and treatment of the various aspects of common heart valve diseases, covering most clinical and surgical issues. It is designed to assist clinicians in the management of patients with valve disease and provide them with answers to many of the clinical questions that arise. With the rapid developments in medical technology, the management of valve diseases remains an exciting area for future research, the results of which should be incorporated in a future edition of this book. v

7 vi Preface I would like to take this opportunity to offer my sincere thanks to the other contributors to this book and also to our patients, without whom our knowledge on this and other cardiac diseases would have never matured. Michael Y. Henein London, UK Umeà, Sweden

8 Contents 1 The Mitral Valve Disease... 1 Michael Henein and John Pepper 2 Aortic Valve Disease Michael Henein and Joseph Maalouf 3 Right Heart Valve Disease Michael Henein 4 Pulmonary Valve Disease Michael Henein and Wei Li 5 Stress Echo in Valvular Heart Disease Eugenio Picano 6 Valve Substitutes John Chambers 7 Native and Prosthetic Valve Endocarditis Maurizio Galderisi and Sergio Mondillo Index vii

9

10 Contributors John Chambers, MD Consultant Cardiologist Head of Non-invasive Cardiology St Thomas Hospital, London, UK Maurizio Galderisim, MD Director of Eclo-Lab, Cardioangiology with CCU Federico II University Hospital Naples, Italy Michael Henein, MD Professor and Consultant Cardiologist Umeà University Hospital Heart Centre, Sweden Wei Li, MD Adult Congenital Heart Cardiologist Royal Brompton Hospital London, UK Joseph Maalouf, MD Professor of Medicine Mayo Clinic Rochester, Mennisota USA ix

11 x Contributors Sergio Mondillo, MD Professor and Director of the Postgraduate School of Cardiovascular Diseases of Cardiology University of Siena Siena, Italy John Pepper, MD Professor of Cardiothoracic Surgery Imperial College London Royal Brompton Hospital, UK Eugenio Picano, MD Director Institute of Clinical Physiology of Italian National Research Council Pisa, Italy Michael Rigby, MD Consultant Paediatric Cardiologist Royal Brompton Hospital London, UK Mary Sheppard, MD Consultant Pathologist Royal Brompton Hospital London, UK

12 Chapter 1 The Mitral Valve Disease Michael Henein and John Pepper Common causes of heart valve disease are rheumatic, calcific and less frequently congenital. With the significant decline in the incidence of rheumatic fever in Europe and North America over the last 50 years a parallel shift in the etiology of valve disease occurred with a fall in the incidence of rheumatic valve disease and an increase in the prevalence of degenerative valve pathology. Rheumatic valve disease, however, remains prevalent in the developing countries in Africa, South America and parts of Asia, particularly in areas with limited clinical services. The commonest valve involved with rheumatic pathology is the mitral valve, but this is not exclusive since aortic and tricuspid valves can also be involved [1]. The apparent contemporary increase in the diagnosis of valve disease results from the global increase in age of the population as well as the easy availability and routine use of echocardiography in cardiology clinics. Age affects the valves by making the leaflets thick with fibrous strands and adipose tissue deposition at the closure lines as well as increased calcium deposition. Isolated myxomatous changes may also occur in the valve fibrosa. This complex pathology eventually results in valve dysfunction. In an echocardiographic examination, such effects of age on valve leaflets should be carefully considered, particularly in patients with a suspected diagnosis of endocarditis since leaflet thickening may appear like small M.Y. Henein (ed.), Valvular Heart Disease in Clinical Practice, DOI / , C Springer-Verlag London Limited

13 2 M. Henein, J. Pepper vegetations. They should also be distinguished from other small benign tumors, e.g., fibroelastoma. Medical treatment of mild valve disease is limited, focusing mostly on prophylaxis against endocarditis. In more significant valve disease, medical treatment aims at optimizing the hemodynamics and consequently protecting against ventricular dysfunction. Surgical correction of valve disorder is the main conventional treatment of severe valve disease, particularly in patients with maintained ventricular function. Those with additional irreversible ventricular dysfunction may face significant surgical risk, thus medical therapy might be the best management option for them. In general, valve-related mortality is more prevalent in aortic valve disease than mitral valve disease, largely due to either sudden death from arrhythmia or the frequent development of left ventricular dysfunction that causes congestive heart failure. Other causes of death in valve disease are additional pathologies, e.g. coronary artery disease, endocarditis or arrhythmia. Overall valve surgery is 5 10 times less frequently performed than that for coronary artery disease [1]. Normal Mitral Valve Anatomy and Function Optimum function of the mitral valve depends on the integral function of all its components: leaflets, chordae, annulus and papillary muscles in addition to the left atrium and the left ventricle. A normal mitral valve does not close passively. In addition to the pressure difference between the ventricle and the atrium in systole, the annular contraction and papillary muscle contraction play an important role in the competence of the mitral valve. The anterior mitral valve leaflet represents a continuation of the posterior aortic root wall. The D-shaped annular fibrous ring is located mainly posteriorly, although significant variability exists in different individuals. The normal diameter of the mitral annulus is approximately 3 cm with a circumference of 8 9 cm. The

14 1 The Mitral Valve Disease 3 annulus is not a passive structure, so in addition to its normal movement towards the apex in systole, the contraction of the posterior myocardial muscle shortens its diameter by 25%, making annular dynamics a very important component in the mechanism of mitral valve competence. Left atrial cavity enlargement and shape change result in mitral annular dilatation and hence overall valve dysfunction and incompetence. With progressive increase in left atrial size and development of atrial fibrillation, the lost mechanical atrial activity significantly contributes to mitral valve incompetence and the development of mitral regurgitation. Likewise, atrial fibrillation itself has been shown to contribute to the enlargement of the left atrium and consequently, the development of mitral regurgitation. The two leaflets of the mitral valve meet at the medial and lateral commissures. The U-shaped anterior leaflet area is larger than the posterior leaflet by approximately 3 4 cm 2. The posterior leaflet is, however, wider and shorter than the anterior leaflet by approximately 1.5 cm 2. The posterior leaflet is made up of a number of scallops, commonly three. The two leaflets coapt at the zone of apposition leaving an overlapping segment 5 mm long. The chordal anatomy of the mitral valve is complicated, with around 12 primary chordae rising from each papillary muscle, which divide into secondaries and numerous tertiary branches which attach themselves to the margins of the two leaflets. In addition, a number of basal chordae also attach themselves to the ventricular surface of the two leaflets and to the commissures. The location of the chordae follows that of the papillary muscles antero-laterally and postero-medially. Any rupture or redundancy of the chordae or extra tissue in the leaflets results in mitral regurgitation. The normal mitral valve orifice cross-sectional area is approximately 5.0 cm 2, Figure 1.1 allowing left ventricular filling to occur predominantly in early diastole (approximately two-thirds of stoke volume) at a peak rate of ml/s (Figure 2.1). The remaining one-third of the stroke volume passes through the mitral valve during atrial systole. During diastasis, ventricular volume remains unchanged [2]. With

15 4 M. Henein, J. Pepper FIGURE 1.1. Parasternal 2D long axis view showing anterior (extending from the posterior aortic wall) and posterior (extending from the left atrial posterior wall) mitral valve leaflets. exercise and increase in heart rate, diastasis shortens and the early and late filling components approximate until they summate and become indistinguishable [3]. With age, the filling pattern reverses so that dominant left ventricular filling occurs in late diastole [4] Figure 1.2. Mitral Stenosis Congenital mitral stenosis: It is a relatively rare group of anomalies with considerable variations in the morphological features. Normally included in this diagnosis are cortriatriatum and supra-valvar mitral membrane, which can be identified from the four-chamber and long axis cross-sectional images Figure 1.3. Characteristically, color flow Doppler