ebook img

Atlas of Heart Failure: Cardiac Function and Dysfunction PDF

294 Pages·2002·35.671 MB·English
Save to my drive
Quick download
Download
Most books are stored in the elastic cloud where traffic is expensive. For this reason, we have a limit on daily download.

Preview Atlas of Heart Failure: Cardiac Function and Dysfunction

J-\ T L J-\ S 0 F • at u r e Cardiac Function and Dysfunction THIRD EDITION Editor WILSON S. COLUCCI, MD Professor of Medicine Boston University School of Medicine; Chief Cardiovascular Medicine Boston Medical Center Boston. Massachusetts Series Editor EUGENE BRAUNWALD, MD, MD (HON), SeD (HON) Distinguished Hersey Professor of Medicine Faculty Dean for Academic Programs at Brigham and Women's Hospital and Massachusetts General Hospital Harvard Medical School; Vice President for Academic Programs Partners HealthCare System Boston. Massachusetts Springer Science+B usiness Media, LLC CURRENT MEDICINE, INC. 400 MARKET STREIT, SUITE 700 • PHILADELPHIA, PA 191 06 Developmental Editor ............................................................................. Elise M. Paxson Editorial Assistant ............................................................................. Ann marie D'O rtona Cover Design ....................................................................................... William Whitman Jr. Design and Layout ........................................ Jennifer Knight, John McCullough Illustrators .................................................................... John McCullough, Marie Dean, ................................................................................ Wieslawa Langenfeld, Maureen Looney Assistant Production Manager ...................................................... Penny Weisman Indexing ....................................................................................................................... Holly Lukens Library of Congress Cataloging-in-Publication Data Atlas of heart failure : cardiac function and dysfunction I editor, Wilson S. Colucci. - 3rd ed. p.; em. Includes bibliographical references and index. ISBN 978-1-4615-6492-8 1. Heart failure--Atlases. I. Colucci, Wilson S., 1949- [DNLM: 1. Heart Failure, Congestive--Atlases. 2. Heart--physiology--Atlases. 3. Heart--physiopathology--Atlases. WG 17 A88162 2002] RC685.C53 A85 2002 616.1'29'00222--dc21 2001053786 ISBN 978-1-4615-6492-8 ISBN 978-1-4615-6490-4 (eBook) DOI 10.1007/978-1-4615-6490-4 Although every effort has been made to ensure that drug doses and other information are presented accurately in this publication, the ultimate responsibility rests with the prescribing physician. Neither the publishers nor the authors can be held responsible for errors or for any consequences arising from the use of information contained herein. Products mentioned in this publication should be used in accordance with the prescribing information prepared by the manufacturers. No claims or endorsements are made for any drug or compound presently under investigation. ©Copyright 2002, 1999, 1995 bySpringer Science+ Business Media New York Originally published by Current Medicine, Inc. in 2002 Softcover reprint of the hardcover 3rd edition 2002 All rights reserved. No part of this publi- cation may be reproduced, stored in a retrieval system, or transmitted in any form by any means electronic, mechanical, photocopying, recording, or otherwise, without prior written consent of the publisher. 10 9 8 7 6 5 4 3 For more information please call 1 (800) 427-1796 or (215) 574-2266 or e-mail us at inquiry®phl.cursci.com www.current-science-group.com ii CONTRIBUTORS CARL S. APSTEIN, MD MICHAEL M. GIVERTZ, MD Professor of Medicine and Physiology Assistant Professor of Medicine Boston University School of Medicine; Department of Medicine Attending Cardiologist Harvard Medical School; Boston Medical Center Co-Directo"' Cardiomyopathy and Heart Boston Massachusetts Failure Service Brigham and Women's Hospital ROBERT J. CODY, MD Boston, Massachusetts Professor Department of Internal Medicine JOSHUA M. HARE, MD University of Michigan Health System Associate Professor of Medicine Ann Arbo"' Michigan Department of Medicine/Cardiology johns Hopkins University School of JAY N. COHN, MD Medicine; Cardiovascular Division Associate Directo"' Heart Failure and University of Minnesota Medical School Cardiac Transplantation Minneapolis, Minnesota The johns Hopkins Hospital Baltimore, Maryland WILSON S. COLUCCI, MD Professor of Medicine ARNOLD M. KATZ, MD Boston University School of Medicine; Professor of Medicine (Emeritus) Chie~ Cardiovascular Medicine University of Connecticut School of Boston Medical Center Medicine Boston, Massachusetts Farmington, Connecticut MARK A. CREAGER, MD TODD M. KOELLING, MD Associate Professor of Medicine Assistant Professor Harvard Medical School; Department of Internal Medicine Director, Vascular Center University of Michigan Health System Brigham and Women5 Hospital Ann Arbo"' Michigan Boston, Massachusetts CARL V. LEIER, MD JORGE A. CUSCO, MD Overstreet Professor of Medicine and Department of Cardiovascular Medicine Pharmacology Brigham and Women5 Hospital Division of Cardiology The Ohio State University Medical Center Boston, Massachusetts Columbus, Ohio D. BRADLEY S. DYKE, MD DONNA MANCINI, MD Lecturer Associate Professor Department of Internal Medicine Department of Medicine; University of Michigan Health System Ann Arbor, Michigan Medical Directo"' Cardiac Transplantation Columbia University New York, New York Ill CONTRIBUTORS ANJU NOHRIA, MD DOUGLAS B. SAWYER, MD, PHD Fellow Assistant Professor Cardiovascular Division Department of Medicine Brigham and Women5 Hospital Boston University School of Medicine Boston, Massachusetts Boston, Massachusetts HENRY OOI, MB, MRCPI MARK R. STARLING, MD Fellow Professor of Internal Medicine Department of Cardiology Associate Chie~ Division of Cardiology Boston University School of Medicine; Director, Cardiology Training Program Fellow University of Michigan Health System; Boston University Medical Center Chie~ Cardiovascular Section Boston, Massachusetts Veterans Affairs Medical Center Ann Arbor, Michigan DAVID A. ORSINELLI, MD Associate Professor of Clinical Medicine MAT WILLIAMS, MD Department of Internal Medicine; Department of Surgery The Ohio State University Columbia University Director, Echocardiography Lab New York, New York Ohio State University Hospitals Columbus, Ohio JAMES B. YOUNG, MD, FACC Medical Director MARC A. PFEFFER, MD, PHD Kaufman Center for Heart Failure; Professor of Medicine Head, Section of Heart Failure and Cardiac Harvard Medical School; Transplant Medicine Physician The Cleveland Clinic Foundation Cardiovascular Division Cleveland, Ohio Brigham and Women's Hospital Boston, Massachusetts IV PREFACE Heart failure is a common clinical syndrome and ~-adrenergic blockers, improves clinical that has enormous impact on the prognosis status and reduces mortality. Furthermore, it and lifestyle of patients. appears that the early treatment of patients with In recent years, impressive strides have been left ventricular dysfunction can slow or prevent made toward understanding the pathophysi the progression of disease and the development ology of heart failure at all levels, from mole of heart failure. Several new factors, including cular changes to the integrated circulatory inflammatory cytokines, endothelin, and oxida system. It is now apparent that many forms of tive stress, have been identified that have the primary cardiomyopathy, such as hyper potential to mediate the development of trophic cardiomyopathy and some forms of myocardial failure and have led to promising dilated cardiomyopathy, are genetic in origin, new therapeutic approaches. and rapid progress is being made in identify This edition is divided into three sections. The ing specific molecular defects that cause a first section provides a state-of-the-art review of variety of inherited heart muscle diseases. the mechanisms that regulate normal myocar Likewise, it is now clear that profound sec dial function, beginning with molecular and cel ondary changes occur in previously normal lular events in the cardiomyocyte and progress myocardium in response to abnormal mechani ing to the level of tissue/ organ mechanics and cal stresses and neurohumoral stimuli that result systemic circulatory regulation. In the second from common cardiovascular conditions such as section, pathophysiology is presented in four myocardial infarction, valvular heart disease, chapters that address the etiology of the syn and systemic hypertension. Collectively referred drome, the molecular and cellular basis of to as "remodeling," these secondary changes in myocardial failure, myocardial remodeling, and myocytes, fibroblasts, and other constituents of the critical roles of the circulatory system and the myocardium result in myocyte hypertrophy neurohumoral mechanisms in the pathophysi and apoptosis, alterations in the interstitial ology of heart failure. The third section, which is matrix, chamber enlargement, and abnormalities devoted to the clinical management of patients of systolic and diastolic pump function. These with heart failure, has been expanded with the structural and functional changes determine the addition of three new chapters that address timing and extent of the myocardial dysfunction inhibitors of the renin-angiotensin system, ~- and thereby play a central role in defining the blockers, and diastolic failure, respectively. time course and severity of the clinical syndrome. As understanding of heart failure advances, Advances in understanding the pathophysiolo new approaches to the prevention and treatment gy of heart failure have been paralleled by an of the syndrome will emerge. Conversely, it is impressive expansion in modalities available for likely that lessons learned from prevention and treatment. Only a few years ago, a monograph treatment trials will continue to foster insight into dealing with this syndrome would have focused the mechanisms that determine this syndrome. on therapies directed at the short-term improve The complexity of this intersection of basic and ment of hemodynamic function. Although short clinical information presents a challenge to both term hemodynamic stabilization continues to be the clinician and the investigator but ultimately an important goal of the in-hospital management promises that additional exciting progress will of patients with heart failure, it is increasingly occur in both arenas. We believe that this edition apparent that hemodynamic improvement is of the Atlas of Heart Failure will serve clinicians, only one aspect of successful long-term therapy. investigators, and teachers who are interested in There is now evidence that therapy of heart heart failure by synthesizing and presenting failure with at least two types of neurohormon information that is relevant to all. al antagonists, converting enzyme inhibitors, WilsonS. Colucci, MD v CONTENTS CHAPTER 1 MOLECULAR AND CELLULAR BASIS OF CONTRACTION Arnold M. Katz Structure ..................................................................................................................................... 2 Contraction and Relaxation ........................................................................................................ 6 Cellular Regulation ................................................................................................................... 14 Growth Regulation ................................................................................................................... 17 CHAPTER2 PHYSIOLOGY OF MYOCARDIAL CONTRACTION Mark R. Starling Mechanics of Cardiac Contraction ...........................................................................................2 0 Determinants of Contraction in the Intact Heart.. ..................................................................... 23 Preload .....................................................................................................................................2 5 Contractility ..............................................................................................................................2 8 Afterload ..................................................................................................................................2 9 Myocardial Energetics ..............................................................................................................3 1 Neural Control of Contractility ................................................................................................. 33 CHAPTER3 THE ETIOLOGIC BASIS OF CONGESTIVE HEART FAILURE Joshua M. Hare Etiology and Epidemiology ....................................................................................................... 38 Heart Failure Associated With Coronary Disease .....................................................................3 9 Heart Failure Associated With Valvular Lesions ....................................................................... .41 Idiopathic Dilated Cardiomyopathy ......................................................................................... .43 Inflammatory Diseases of the Myocardium ............................................................................. .44 Secondary Causes of Cardiomyopathy ......................................................................................S O Infiltrative/Restrictive Cardiomyopathies ................................................................................... 58 Hypertrophic Cardiomyopathy ................................................................................................. 60 Right Ventricular Cardiomyopathy ............................................................................................ 61 ICHAPTER4 MOLECULAR AND CELLULAR EVENTS IN MYOCARDIAL HYPERTROPHY AND FAILURE Douglas B. Sawyer and Wilson S. Colucci Ventricular Remodeling ............................................................................................................6 6 Molecular and Cellular Phenotypes .........................................................................................6 7 Calcium Handling and Contractile Protein Expression ............................................................ .70 Cell Death .............................................................. : ................................................................. 73 Cell Replacement .....................................................................................................................7 6 Extracellular Matrix. .................................................................................................................. 77 13-Adrenergic Pathway ..............................................................................................................7 9 Renin-Angiotensin System, Endothelin, and Inflammatory Cytokines ....................................... 80 Oxidative Stress ........................................................................................................................8 3 VI CHAPTER 5 CARDIAC REMODELING AND ITS PREVENTION Marc A. Pfeffer Cardiac Growth and Remodeling .............................................................................................8 8 Early Remodeling After Myocardial Infarction and Infarct Expansion ....................................... 90 Remodeling and Prognosis .......................................................................................................9 2 Progressive Enlargement After Myocardiallnfarction ................................................................ 93 Modification of Remodeling After Myocardial Infarction .......................................................... 95 [CHAPTER 6 NEUROHUMORAL, RENAL, AND VASCULAR ADJUSTMENTS IN HEART FAILURE Anju Nohria, Jorge A. Cusco, and Mark A. Creager Mechanisms in Heart Failure .................................................................................................. 1 04 Sympathetic Nervous System ................................................................................................. 10 4 The Renin-Angiotensin-Aldosterone System ........................................................................... 11 0 The Arginine-Vasopressin System ........................................................................................... 114 Natriuretic Peptides ................................................................................................................1 16 Local Mechanisms ..................................................................................................................1 19 Regional Blood Flow ..............................................................................................................1 24 [CHAPTER 7 ASSESSMENT OF HEART FAILURE James B. Young Overview ............................................................................................................................... 128 Assessing the Patient. ..............................................................................................................1 30 Diagnostic Tests .....................................................................................................................1 39 Designing a Therapeutic Plan ................................................................................................. 142 [CHAPTERS PROGNOSTIC INDICATORS AND ASSESSMENT OF THERAPEUTIC RESPONSES Henry Ooi and Jay N. Cohn Mortality in Patients With Heart Failure .................................................................................. 146 Use of Prognostic Variables .................................................................................................... 149 Assessment of Therapeutic Responses .................................................................................... 1 54 [CHAPTER9 UNSTABLE HEART FAILURE Carl V. Leier and David A. Orsinelli Acute Heart Failure ................................................................................................................1 62 Decompensated Chronic Heart Failure .................................................................................. 171 [CHAPTER 10 DIGITALIS AND DIURETICS D. Bradley S. Dyke and Robert J. Cody Diuretics ................................................................................................................................1 80 Digoxin ..................................................................................................................................1 85 VII CHAPTER 11 ANGIOTENSIN-CONVERTING ENZYME INHIBITION AND ANGIOTENSIN RECEPTOR BLOCKADE Todd M. Koelling and Robert J. Cody Angiotensin-converting Enzyme Inhibitors ............................................................................. 194 Angiotensin Receptor Blockers ...............................................................................................2 04 CHAPTER 12 13-BLOCKERS Michael M. Givertz and Wilson S. Colucci 13 NEW APPROACHES TO THE TREATMENT OF HEART FAILURE Michael M. Givertz and Wilson S. Colucci Neurohormonal Antagonists ...................................................................................................2 24 Inotropic Agents .....................................................................................................................2 31 Resynchronization Therapy ....................................................................................................2 32 Novel Biologic Therapies for Myocardial Recovery ................................................................2 34 CHAPTER 14 CARDIAC TRANSPLANTATION Donna Mancini and Mat Williams Posttransplantation Survival .................................................................................................... 240 Candidate Selection ...............................................................................................................2 40 Donor Selection Criteria .........................................................................................................2 43 Surgical Techniques ................................................................................................................2 44 Allograft Rejection ..................................................................................................................2 46 Quality of Life After Transplantation .......................................................................................2 50 Accelerated Transplantation Atherosclerosis and Retransplantation ........ , ............................... 251 Mechanical-assist Devices ......................................................................................................2 52 CHAPTER 15 DIASTOLIC DYSFUNCTION: PATHOPHYSIOLOGY, CLINICAL FEATURES, AND TREATMENT Carl S. Apstein Normal Diastolic Function .....................................................................................................2 60 Pathophysiology of LV Diastolic Dysfunction .........................................................................2 67 Diastolic Dysfunction with Ischemia, Hypertrophy, and Other Causes ................................... 271 Aging and Diastolic Dysfunction ............................................................................................2 77 Clinical Features, Prognosis, and Treatment ...........................................................................2 82 INDEX ....................................................................................................................................... 1.1 COLOR PLATES ......................................................................................................................C .1 VIII MOLECULAR AND CELLULAR BASIS OF CONTRACTION Arnold M. Katz The ability of the heart to me t th changing demand of the circulation involves three fundamentally different mechanisms [1]. The work of the heart can b regulat d by chang in its ability to empty and fill (or an phy i 1 gy), t utiliz chemical en rgy forth p rformanc of mechanical and o motic work (cell biochemistry), and t replace its constituent parts (gene expression). ach f th control mechanisms operate o era cUff rent time course. A an rgan, the heart adju ts to changing prel ad ( enous return) and aft rload (arterial impedanc ) by length-dependent mechanisms: the Frank-Starling relationship, or Starling' Law of th Heart [2]. These physiologic mechanism , which allow increa d prel ad or after! ad to augment the heart' ability to j ct bl d, provide b at-to-b at adju tment that enable th heart t me t hort-term change in hemodynamics and to equalize the utputs f the two entricle . The econd mechanism relie n biochemical change to m dify the ability of indi idual cardiac myocyt s to contract and to relax, and thu to alter th heart' ability to empty (inotropy) and fill (lusitropy). Most of the cellular mechanisms, which enable the heart to m t uch sustained hemodynamic demands as those caused by exercise and motion, influence the interactions b tween th cardiac contractile proteins by modifying the many membrane ion pumps, ion chann ls, and ion exchanger that regulate the inotropic and lusitr pic prop rtie of the heart [2]. The calcium flux s invol ed in e citation-contraction coupling and r laxation, in tum, ar influenced by a variety of signaling ca cades. These cascades are initiat d by the arrival of an extracellular signal, usually a chemical transmitter or hormone, at the cell surface, and generate a di rse group of intrac llular me engers that modify cardiac function. Th third and most complex of the mechanisms by which the heart adju t the changing demands of th circulati n in olve growth abnormalitie that m dify gene expre sion in the cardiac cells. Th re ulting molecular changes pro ide long-lasting adjustment in re pon e to such timuli as endocrinopathi s (eg, aJtered thyr id function), aging, and chronic hemodynamic o erload. Alth ugh an und rstanding of this third mechanism is till in its infancy, rich and subtle molecular chang caused by growth abn rmalitie in the diseased heart are likely to play an important role in uch c mm n clinical conditi ns a heart failure [3]. ~TRUCTURE Fihrobl.t~l A arcopla. mic r ticulum: ,/ ScHcotubular network,' arcopla_ m1c r t1culum ' ' B 110 hondnon ' ' 1-band -band Z-band ' r-l Thi k fil,lm nt c FIGURE 1-1. Structure of the heart. The heart is composed of both that initiate systole by delivering activator calcium to the myocytes and nonmyoctes. A, Nonmyocytes include connective myofilaments, and calcium pumps that, by removing calcium tissue cells (mainly fibroblasts), vascular smooth muscle cells, from the cytosol, dissociate this activator cation from its binding and endothelial cells. Whereas large cardiac myocytes make up sites on the thin filament. most of the heart's mass, the majority of the cells of the heart Myofilaments contain about 70% of the protein of the cardiac (approximately 70%) are smaller nonmyocytes. The large, myocytes, and most of the membrane surface is found in the mito branched cardiac myocytes, which are enmeshed in a collagen chondria. Other important membranes include the plasma mem network, are separated longitudinally by intercalated disks, brane, which is continuous with the transverse tubular membranes which represent specialized cell-cell junctions. The intercalated (t-tubules) that extend toward the center of the cell and carry depo disks provide strong mechanical connections between adjacent larizing currents into the myocardial cell. cells and contain gap junctions that provide low-resistance C, Each sarcomere, which is delimited by two Z-bands, pathways for electrical conduction. contains one A-band and two half 1-bands. The A-bands are B, Cardiac myocytes that are specialized for contraction contain made up of thick, myosin-containing filaments into which thin myofilaments whose organization in a regular array of thick and filaments interdigitate from the adjacent two half 1-bands. The thin filaments gives rise to the characteristic striated appearance. latter are made up of actin and the regulatory proteins, Also prominent within these cells are two membrane structures: tropomyosin and the troponin complex. Bisecting each Z-band is energy-producing mitochondria and the sarcoplasmic reticulum, a lattice of axial and cross-connecting filaments that includes the which regulates cytosolic Ca2+ concentration. The latter is an overlapping ends of thin filaments from adjacent sarcomeres. intracellular membrane system that contains the calcium channels (Part B adapted from Katz [3].) ATLAS OF HEART FAILURE: CARDIAC FUNCTION AND DYSFUNCTION 2

See more

The list of books you might like

Most books are stored in the elastic cloud where traffic is expensive. For this reason, we have a limit on daily download.