Mayo clinic cardiology

1. Mayo Clinic Cardiology Concise Textbook THIRD EDITION

2. Editors Joseph G. Murphy, MD Margaret A. Lloyd, MD Associate Editors Gregory W. Barsness, MD Arshad Jahangir, MD Garvan C. Kane, MD Lyle J. Olson, MD MAYO CLINIC SCIENTIFIC PRESS AND INFORMA HEALTHCARE USA, INC. Mayo Clinic Cardiology Concise Textbook THIRD EDITION 3. ISBN 0-8493-9057-5 The triple-shield Mayo logo and the words MAYO, MAYO CLINIC, and MAYO CLINIC SCIENTIFIC PRESS are marks of Mayo Foundation for Medical Education and Research. 2007 by Mayo Foundation for Medical Education and Research. All rights reserved. This book is protected by copyright. No part of it may be reproduced, stored in a retrieval system, or transmitted, in any form or by any meanselectronic, mechanical, photocopying, recording, or otherwisewithout the prior written consent of the copyright holder, except for brief quotations embodied in critical articles and reviews. Inquiries should be addressed to Scientific Publications, Plummer 10, Mayo Clinic, 200 First Street SW, Rochester, MN 55905. For order inquiries, contact Taylor & Francis Group, 6000 Broken Sound Parkway NW, Suite #300, Boca Raton, FL 33487. www.taylorandfrancis.com Catalog record is available from the Library of Congress. Care has been taken to confirm the accuracy of the information presented and to describe generally accepted practices. However, the authors, editors, and publisher are not responsible for errors or omissions or for any con- sequences from application of the information in this book and make no warranty, express or implied, with respect to the contents of the publication. This book should not be relied on apart from the advice of a qual- ified health care provider. The authors, editors, and publisher have exerted efforts to ensure that drug selection and dosage set forth in this text are in accordance with cur- rent recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any change in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new or infre- quently employed drug. Some drugs and medical devices presented in this publication have Food and Drug Administration (FDA) clearance for limited use in restrict- ed research settings. It is the responsibility of the health care providers to ascertain the FDA status of each drug or device planned for use in their clinical practice. Printed in Canada 10 9 8 7 6 5 4 3 2 4. DEDICATION This book is dedicated to my parents, my wife Marian, without whose support and encouragement this textbook would not have been possible, and my children Owen, Sinad, and Aidan, as well as Tornados, Spartans, Pink Panthers, and Tommies everywhere. Joseph G. Murphy, MD For my parents, who taught me to love books. Booksellers everywhere, thank you as well. Margaret A. Lloyd, MD v 5. vii FOREWORD It is a distinct honor and pleasure to write this foreword for the third edition of Mayo Clinic Cardiology: Concise Textbook. I have had the pleasure of working on the staff of Mayo Clinics Division of Cardiovascular Diseases for the past 25 years. Although the diagnosis and treatment of cardiovascular diseases and the day-to-day practice of medicine have changed greatly during that time, the Mayo Clinic tradition of clinical excellence in cardiovascular disease has not. The unique strength of the Division is its breadth of clinical expertise across the areas of acute coronary care, electrophysiology, intervention, adult congenital heart disease, valvular heart disease, vascular disease, heart failure, and others. This expertise covers both common conditions in the practice of cardiovascular disease and those that are very uncommon, even in major tertiary referral centers. The breadth of that expertise is reflected in the range of topics covered in this book. The common conditions include ST- segment elevation myocardial infarction, for which Mayo Clinic conducted one of the first clinical trials comparing thrombolytic therapy with acute angioplasty, and chronic mitral insufficiency, to which Mayo Clinic investigators have made multiple major contributions to both diagnosis and the timing and benefit of mitral valve repair. The uncommon conditions include adult congenital heart disease, hypertrophic cardiomyopathy, and pericardial disease, on which the size of our practice has permitted a few of my colleagues to focus their expertise. This book began as an outgrowth of the syllabus for the Mayo Cardiovascular Review Course for Cardiology Boards and Recertification. This highly successful course attracts an annual attendance of more than 700, including cardiology fellows preparing for their initial boards, practicing cardiologists preparing for recertification, and experienced clinicians who simply want to ensure that they are up-to-date on the latest cardiovascular science and care. Readers from any one of these broad categories will find this book very useful. Both the education of cardiology fellows and the practice of cardiovascular medicine are increasingly subject to time constraints. Our fellows complain that 3 or 4 years is simply inadequate to master the rapidly expanding scope of cardiovascular science and practice. Practicing physicians find that their working day grows ever longer, leaving less time for continuing medical education. The strength of this book is its concise presentation of the existing state of cardiovascular practice, as emphasized by its subtitle. There is a growing crisis in the health care system, focused on rapid increases in health care costs and evidence of suboptimal quality. The practice of cardiovascular medicine will be under increasing pressure to shift from the more-care-is-better paradigm that dominated in the past to afocusonimprovingqualityandefficiency.TheDartmouthAtlasofHealthCareidentifiedtheMedicarereferralregioncenteredonRochester,Minnesota, as a high-quality, low-cost region. The principles underlying that efficiency are evident throughout this text. It is hoped that it will assist the reader in his or her personal quest to improve the quality of cardiovascular care in clinical practice. Raymond J. Gibbons, MD Consultant, Division of Cardiovascular Diseases Mayo Clinic Arthur M. & Gladys D. Gray Professor of Medicine Mayo Clinic College of Medicine Rochester, Minnesota 6. PREFACE he cover art of the iceberg heart is meant to symbolize the significant extent of occult cardiovascular disease in our society and the ruthless icy nature of cardiovascular death that curses the sea of humanity. It has been a great honor to oversee the publication of this, the third, edition of Mayo Clinic Cardiology: Concise Textbook (formerly titled Mayo Clinic Cardiology Review). Large textbooks are never the work of one or two individuals but rather the product of a team of dedicated pro- fessionals, as has been the case for this book. This textbook from a single institution was written by a diverse faculty of more than 100 cardiologists from more than 17 countries. This textbook is primarily a teaching and learning textbook of cardiology rather than a reference textbook. In response to welcome feedback from readers of our two previous textbook editions, we have maintained a relatively large typeface to make the textbook easily readable and have avoided the temptation to reduce the font size to increase content. Newer electronic search modalities have made textbook references less timely and we have deleted most chapter references and all multiple-choice questions to save space. This textbook is designed to present the field of cardiology in a reader-friendly format that can be read in about 12 months. Many small cardiology textbooks are bare-bones compilations of facts that do not explain the fundamental concepts of cardiovascular disease, and many large cardiology textbooks are voluminous and describe cardiology in great detail. Mayo Clinic Cardiology: Concise Textbook is designed to be a bridge between these approaches. We sought to present a solid framework of ideas with sufficient depth to make the matter interesting yet concise, aimed specifically toward fellows in training or practicing clinicians wanting to update their knowledge. The book contains 1,400 figures, 483 of which are color photographs to supplement the text. Teaching points and clinical pearls have been added to make the textbook come alive and challenge the reader. The concept for this textbook originated from the first syllabus for the Mayo Cardiovascular Review Course, a function the textbook continues to fulfill. The impetus to produce this textbook owes much to the encouragement of Rick Nishimura, MD, and Steve Ommen, MD, the direc- tors of the Mayo Cardiovascular Review Course now in its 11th year. This third edition is a complete revision of all previous chapters of the textbook and has been expanded at the suggestion of cardiology fellows to now include 40 new chapters, including newer aspects of electrophysiology, interventional cardiology, noninvasive imaging, and randomized clinical trials. The text is intended primarily for cardiology fellows studying for cardiology board certification and practicing cardiologists studying for board recertification. It will also be useful for physicians studying for examinations of the Royal Colleges of Physicians, anesthesiologists, critical care physicians, internists and general physicians with a special interest in cardiology, and coronary care and critical care nurses. WethankallourcolleaguesintheMayoClinicDivisionofCardiovascularDiseasesatRochester,Arizona,andJacksonvillewhogenerouslycon- tributedtothiswork.WealsothankWilliamD.Edwards,MD,forpermissiontouseslidesfromtheMayoCliniccardiologypathologicimagedata- base.LeAnnSteeandRandallJ.Fritz,DVM,atMayoClinic,contributedenormouslythroughtheireditorialguidance.SandyBebermanatInforma Healthcare patiently guided this project through countless tribulations. We thank both Mayo Clinic and the Informa Healthcare production teams: at MayoRoberta Schwartz (production editor), Sharon Wadleigh (scientific publications specialist), Jane Craig and Virginia Dunt (editorial assis- tants), Kenna Atherton and John Hedlund (proofreaders), Karen Barrie (art director), Jonathan Goebel (graphic designer) and Charlene Wibben (ContinuingMedicalEducation);atInformaHealthcareSuzanneLassandro(projecteditor),andRickBeardsley(productionandmanufacturing). We specifically acknowledge colleagues from outside North America who contributed many ideas to this book and who translated previous editions ofthebookintoseveralforeignlanguages.WehaveincludedashortSIconversiontableforcommonlaboratoryvaluestoaidtheirreadingofthebook. We would appreciate comments from our readers about how we might improve this textbook or, specifically, about any errors that you find. Joseph G. Murphy, MD Margaret A. Lloyd, MD Consultant, Division of Cardiovascular Consultant, Division of Cardiovascular Diseases, Diseases, and Chair, Section of Scientific Publications, Mayo Clinic Mayo Clinic Assistant Professor of Medicine Professor of Medicine Mayo Clinic College of Medicine Mayo Clinic College of Medicine Rochester, Minnesota Rochester, Minnesota [email protected] T ix 7. xi SI UNITS AND ALTERNATIVE SCIENTIFIC NAMES SI UNITS Cholesterol (Total Cholesterol, LDL Cholesterol, HDL Cholesterol) 200 mg/dL = 5.2 mmol/L 160 mg/dL = 4.2 mmol/L 130 mg/dL = 3.4 mmol/L 100 mg/dL = 2.6 mmol/L 70 mg/dL = 1.8 mmol/L 40 mg/dL = 1.0 mmol/L Triglycerides 100 mg/dL = 1.1 mmol/L 200 mg/dL = 2.2 mmol/L Glucose 100 mg/dL = 5.5 mmol/L 200 mg/dL = 11.0 mmol/L Creatinine 1 mg/dL = 88.4 mol/L 2 mg/dL = 177 mol/L 3 mg/dL = 265 mol/L ALTERNATIVE SCIENTIFIC NAMES Epinephrine = adrenaline Norepinephrine = noradrenaline Isoproterenol = isoprenaline 8. Michael J. Ackerman, MD, PhD Consultant, Divisions of Cardiovascular Diseases and Pediatric Cardiology and Department of Molecular Pharmacology and Experimental Therapeutics* Associate Professor of Medicine, Pediatrics, and Pharmacology Thomas G. Allison, PhD Consultant, Division of Cardiovascular Diseases* Associate Professor of Medicine Naser M. Ammash, MD Consultant, Division of Cardiovascular Diseases* Associate Professor of Medicine Nandan S. Anavekar, MB, BCh Chief Medical Resident and Instructor in Medicine Christopher P. Appleton, MD Consultant, Division of Cardiovascular Diseases Professor of Medicine Samuel J. Asirvatham, MD Consultant, Division of Cardiovascular Diseases* Associate Professor of Medicine John W. Askew III, MD Fellow in Nuclear Cardiology Luciano Babuin, MD Research Collaborator, Mayo School of Graduate Medical Education Gregory W. Barsness, MD Consultant, Division of Cardiovascular Diseases* Assistant Professor of Medicine Malcolm R. Bell, MD Consultant, Division of Cardiovascular Diseases* Professor of Medicine Patricia J. M. Best, MD Senior Associate Consultant, Division of Cardiovascular Diseases* Assistant Professor of Medicine Joseph L. Blackshear, MD Consultant, Division of Cardiovascular Diseases Professor of Medicine David J. Bradley, MD, PhD Consultant, Division of Cardiovascular Diseases* Assistant Professor of Medicine Peter A. Brady, MD Consultant, Division of Cardiovascular Diseases* Assistant Professor of Medicine Jerome F. Breen, MD Consultant, Department of Radiology* Assistant Professor of Radiology John F. Bresnahan, MD Consultant, Division of Cardiovascular Diseases* Associate Professor of Medicine Frank V. Brozovich, MD, PhD Senior Associate Consultant, Division of Cardiovascular Diseases and Department of Physiology and Biomedical Engineering* Professor of Medicine and of Physiology T. Jared Bunch, MD Fellow in Cardiovascular Diseases and Assistant Professor of Medicine John C. Burnett, Jr, MD Consultant, Division of Cardiovascular Diseases* Professor of Medicine and of Physiology Mark J. Callahan, MD Consultant, Division of Cardiovascular Diseases* Assistant Professor of Medicine Yong-Mei Cha, MD Consultant, Division of Cardiovascular Diseases* Assistant Professor of Medicine Krishnaswamy Chandrasekaran, MD Consultant, Division of Cardiovascular Diseases* Professor of Medicine Panithaya Chareonthaitawee, MD Consultant, Division of Cardiovascular Diseases* Assistant Professor of Medicine Frank C. Chen, MD Fellow in Cardiovascular Diseases Horng H. Chen, MD Consultant, Division of Cardiovascular Diseases* Associate Professor of Medicine Stuart D. Christenson, MD Senior Associate Consultant, Division of Cardiovascular Diseases* Assistant Professor of Medicine Alfredo L. Clavell, MD Consultant, Division of Cardiovascular Diseases* Assistant Professor of Medicine Heidi M. Connolly, MD Consultant, Division of Cardiovascular Diseases* Professor of Medicine CONTRIBUTORS *Mayo Clinic, Rochester, Minnesota. Mayo Clinic College of Medicine, Rochester, Minnesota. Mayo Clinic, Scottsdale, Arizona. Mayo Clinic, Jacksonville, Florida. xiii 9. Leslie T. Cooper, Jr, MD Consultant, Division of Cardiovascular Diseases* Associate Professor of Medicine Richard C. Daly, MD Consultant, Division of Cardiovascular Surgery* Associate Professor of Surgery Brooks S. Edwards, MD Consultant, Division of Cardiovascular Diseases* Professor of Medicine Robert P. Frantz, MD Consultant, Division of Cardiovascular Diseases* Assistant Professor of Medicine Paul A. Friedman, MD Consultant, Division of Cardiovascular Diseases* Professor of Medicine Robert L. Frye, MD Consultant, Division of Cardiovascular Diseases* Professor of Medicine Apoor S. Gami, MD Fellow in Cardiovascular Diseases and Assistant Professor of Medicine Gerald T. Gau, MD Consultant, Division of Cardiovascular Diseases* Professor of Medicine Thomas C. Gerber, MD, PhD Consultant, Division of Cardiovascular Diseases and Department of Radiology Associate Professor of Medicine and of Radiology Bernard J. Gersh, MB, ChB, DPhil Consultant, Division of Cardiovascular Diseases* Professor of Medicine Jason M. Golbin, DO Fellow in Thoracic Diseases and Critical Care Medicine Martha A. Grogan, MD Consultant, Division of Cardiovascular Diseases* Assistant Professor of Medicine Richard J. Gumina, MD Senior Associate Consultant, Division of Cardiovascular Diseases* Stephen C. Hammill, MD Consultant, Division of Cardiovascular Diseases* Professor of Medicine David L. Hayes, MD Chair, Division of Cardiovascular Diseases* Professor of Medicine Sharonne N. Hayes, MD Consultant, Division of Cardiovascular Diseases* Associate Professor of Medicine Anthony A. Hilliard, MD Fellow in Cardiovascular Diseases Michael J. Hogan, MD, MBA Consultant, Division of Regional and International Medicine Assistant Professor of Medicine David R. Holmes, Jr, MD Consultant, Division of Cardiovascular Diseases* Professor of Medicine Allan S. Jaffe, MD Consultant, Division of Cardiovascular Diseases* Professor of Medicine Arshad Jahangir, MD Consultant, Division of Cardiovascular Diseases* Associate Professor of Medicine Traci L. Jurrens, MD Fellow in Cardiovascular Diseases Ravi Kanagala, MD Senior Associate Consultant, Division of Cardiovascular Diseases* Assistant Professor of Medicine Garvan C. Kane, MD Fellow in Cardiovascular Diseases and Instructor in Medicine Birgit Kantor, MD, PhD Senior Associate Consultant, Division of Cardiovascular Diseases* Assistant Professor of Medicine Tomas Kara, MD, PhD Research Fellow in Hypertension and Assistant Professor of Medicine Bijoy K. Khandheria, MD Chair, Division of Cardiovascular Diseases Professor of Medicine Stephen L. Kopecky, MD Consultant, Division of Cardiovascular Diseases* Professor of Medicine Iftikhar J. Kullo, MD Consultant, Division of Cardiovascular Diseases* Associate Professor of Medicine Sudhir S. Kushwaha, MD Consultant, Division of Cardiovascular Diseases* Associate Professor of Medicine Andr C. Lapeyre III, MD Consultant, Division of Cardiovascular Diseases* Assistant Professor of Medicine Hon-Chi Lee, MD, PhD Consultant, Division of Cardiovascular Diseases* Professor of Medicine *Mayo Clinic, Rochester, Minnesota. Mayo Clinic College of Medicine, Rochester, Minnesota. Mayo Clinic, Scottsdale, Arizona. Mayo Clinic, Jacksonville, Florida. xiv 10. Amir Lerman, MD Consultant, Division of Cardiovascular Diseases* Professor of Medicine Margaret A. Lloyd, MD Consultant, Division of Cardiovascular Diseases* Assistant Professor of Medicine Francisco Lopez-Jimenez, MD, MS Consultant, Division of Cardiovascular Diseases* Assistant Professor of Medicine Verghese Mathew, MD Consultant, Division of Cardiovascular Diseases* Associate Professor of Medicine Robert D. McBane, MD Consultant, Division of Cardiovascular Diseases* Associate Professor of Medicine Marian T. McEvoy, MD Consultant, Division of Dermatology* Associate Professor of Dermatology Michael D. McGoon, MD Consultant, Division of Cardiovascular Diseases* Professor of Medicine Shaji C. Menon, MD Fellow in Pediatric Cardiology Fletcher A. Miller, Jr, MD Consultant, Division of Cardiovascular Diseases* Professor of Medicine Todd D. Miller, MD Consultant, Division of Cardiovascular Diseases* Professor of Medicine Wayne L. Miller, MD, PhD Consultant, Division of Cardiovascular Diseases* Associate Professor of Medicine Andrew G. Moore, MD Consultant, Division of Cardiovascular Diseases* Instructor in Medicine Thomas M. Munger, MD Consultant, Division of Cardiovascular Diseases* Assistant Professor of Medicine Joseph G. Murphy, MD Consultant, Division of Cardiovascular Diseases* Professor of Medicine Ajay Nehra, MD Consultant, Department of Urology* Professor of Urology Rick A. Nishimura, MD Consultant, Division of Cardiovascular Diseases* Professor of Medicine Jae K. Oh, MD Consultant, Division of Cardiovascular Diseases* Professor of Medicine Lyle J. Olson, MD Consultant, Division of Cardiovascular Diseases* Professor of Medicine Steve Ommen, MD Consultant, Division of Cardiovascular Diseases* Associate Professor of Medicine Oyere K. Onuma, BS Research Trainee, Division of Cardiovascular Diseases* Thomas A. Orszulak, MD Consultant, Division of Cardiovascular Surgery* Professor of Surgery Michael J. Osborn, MD Consultant, Division of Cardiovascular Diseases* Associate Professor of Medicine Narith N. Ou, PharmD Pharmacist* Lance J. Oyen, PharmD Pharmacist* Assistant Professor of Pharmacy Douglas L. Packer, MD Consultant, Division of Cardiovascular Diseases* Professor of Medicine John G. Park, MD Consultant, Division of Pulmonary and Critical Care Medicine* Assistant Professor of Medicine Robin Patel, MD Consultant, Division of Infectious Diseases* Associate Professor of Microbiology and Professor of Medicine Patricia A. Pellikka, MD Consultant, Division of Cardiovascular Diseases* Professor of Medicine Sabrina D. Phillips, MD Senior Associate Consultant, Division of Cardiovascular Diseases* Assistant Professor of Medicine Co-burn J. Porter, MD Consultant, Division of Pediatric Cardiology* Professor of Pediatrics Udaya B. S. Prakash, MD Consultant, Division of Pulmonary and Critical Care Medicine* Professor of Medicine,*Mayo Clinic, Rochester, Minnesota. Mayo Clinic College of Medicine, Rochester, Minnesota. Mayo Clinic, Scottsdale, Arizona. Mayo Clinic, Jacksonville, Florida. xv 11. Abhiram Prasad, MD Consultant, Division of Cardiovascular Diseases* Assistant Professor of Medicine Sarinya Puwanant, MD Research Fellow in Cardiovascular Diseases Robert F. Rea, MD Consultant, Division of Cardiovascular Diseases* Associate Professor of Medicine Margaret M. Redfield, MD Consultant, Division of Cardiovascular Diseases* Professor of Medicine Guy S. Reeder, MD Consultant, Division of Cardiovascular Diseases* Professor of Medicine Charanjit S. Rihal, MD Consultant, Division of Cardiovascular Diseases* Professor of Medicine Richard J. Rodeheffer, MD Consultant, Division of Cardiovascular Diseases* Professor of Medicine Brian P. Shapiro, MD Fellow in Cardiovascular Diseases Win-Kuang Shen, MD Consultant, Division of Cardiovascular Diseases* Professor of Medicine Raymond C. Shields, MD Consultant, Division of Cardiovascular Diseases* Instructor in Medicine Clarence Shub, MD Consultant, Division of Cardiovascular Diseases* Professor of Medicine Justo Sierra Johnson, MD, MS Research Fellow in Cardiovascular Diseases Robert D. Simari, MD Consultant, Division of Cardiovascular Diseases* Professor of Medicine Lawrence J. Sinak, MD Consultant, Division of Cardiovascular Diseases* Assistant Professor of Medicine Virend K. Somers, MD, PhD Consultant, Division of Cardiovascular Diseases* Professor of Medicine Peter C. Spittell, MD Consultant, Division of Cardiovascular Diseases* Assistant Professor of Medicine James M. Steckelberg, MD Chair, Division of Infectious Diseases* Professor of Medicine Thoralf M. Sundt III, MD Consultant, Division of Cardiovascular Surgery* Professor of Surgery Imran S. Syed, MD Fellow in Cardiovascular Diseases Deepak R. Talreja, MD Fellow in Cardiovascular Diseases and Instructor in Medicine Zelalem Temesgen, MD Consultant, Division of Infectious Diseases* Associate Professor of Medicine Andre Terzic, MD Consultant, Department of Molecular Pharmacology* Professor of Medicine and of Pharmacology Randal J. Thomas, MD, MS Consultant, Division of Cardiovascular Diseases* Assistant Professor of Medicine Henry H. Ting, MD Consultant, Division of Cardiovascular Diseases* Assistant Professor of Medicine Cindy W. Tom, MD Research Fellow in Cardiovascular Diseases Laurence C. Torsher, MD Consultant, Division of Anesthesia* Assistant Professor of Anesthesiology Teresa S. M. Tsang, MD Consultant, Division of Cardiovascular Diseases* Professor of Medicine Eric M. Walser, MD Senior Associate Consultant, Department of Radiology Professor of Radiology Carole A. Warnes, MD Consultant, Division of Cardiovascular Diseases* Professor of Medicine Paul W. Wennberg, MD Consultant, Division of Cardiovascular Diseases* Assistant Professor of Medicine Robert Wolk, MD, PhD Research Collaborator in Cardiovascular Diseases* R. Scott Wright, MD Consultant, Division of Cardiovascular Diseases* Professor of Medicine Waldemar E. Wysokinski, MD Consultant, Division of Cardiovascular Diseases* Assistant Professor of Medicine Leonid V. Zingman, MD Research Associate, Division of Cardiovascular Diseases* Assistant Professor of Medicine and Instructor in Pharmacology *Mayo Clinic, Rochester, Minnesota. Mayo Clinic College of Medicine, Rochester, Minnesota. Mayo Clinic, Scottsdale, Arizona. Mayo Clinic, Jacksonville, Florida. xvi 12. FUNDAMENTALS OF CARDIOVASCULAR DISEASE . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1 1. Cardiovascular Examination . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .3 Clarence Shub, MD 2. Applied Anatomy of the Heart and Great Vessels . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .27 Joseph G. Murphy, MD, R. Scott Wright, MD 3. Evidence-Based Medicine and Statistics in Cardiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .55 Apoor S. Gami, MD, Charanjit S. Rihal, MD 4. Noncardiac Surgery in Patients With Heart Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .61 Traci L. Jurrens, MD, Clarence Shub, MD 5. Essential Molecular Biology of Cardiovascular Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .73 Cindy W. Tom, MD, Robert D. Simari, MD 6. Medical Ethics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .95 John G. Park, MD 7. Restrictions on Drivers and Aircraft Pilots With Cardiac Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . .103 Stephen L. Kopecky, MD NONINVASIVE IMAGING . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .115 8. Principles of Echocardiography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .117 Teresa S. M. Tsang, MD 9. Stress Echocardiography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .143 Patricia A. Pellikka, MD 10. Transesophageal Echocardiography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .151 Sarinya Puwanant, MD, Lawrence J. Sinak, MD, Krishnaswamy Chandrasekaran, MD 11. Nuclear Imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .161 John W. Askew III, MD, Todd D. Miller, MD 12. Positron Emission Tomography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .173 Panithaya Chareonthaitawee, MD 13. Cardiovascular Computed Tomography and Magnetic Resonance Imaging . . . . . . . . . . . . . . . . . . .185 Thomas C. Gerber, MD, PhD, Eric M. Walser, MD 14. Cardiac Radiography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .205 Jerome F. Breen, MD, Mark J. Callahan, MD 15. Atlas of Radiographs of Congenital Heart Defects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .223 Sabrina D. Phillips, MD, Joseph G. Murphy, MD 16. Cardiopulmonary Exercise Testing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .231 Thomas G. Allison, PhD 17. Stress Test Selection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .241 Stuart D. Christenson MD xvii TABLE OF CONTENTS 13. ELECTROPHYSIOLOGY . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .247 18. Electrocardiographic Diagnoses: Criteria and Definitions of Abnormalities . . . . . . . . . . . . . . . . . . .249 Stephen C. Hammill, MD 19. Cardiac Cellular Electrophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .295 Hon-Chi Lee, MD, PhD 20. Normal and Abnormal Cardiac Electrophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .309 Douglas L. Packer, MD 21. Indications for Electrophysiologic Testing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .321 Michael J. Osborn, MD 22. Cardiac Channelopathies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .335 T. Jared Bunch, MD, Michael J. Ackerman, MD, PhD 23. Pediatric Arrhythmias . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .345 Co-burn J. Porter, MD 24. Atrial Fibrillation: Pathogenesis, Diagnosis, and Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .351 Paul A. Friedman, MD 25. Atrial Fibrillation: Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .363 David J. Bradley, MD, PhD 26. Atrial Flutter . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .371 Yong-Mei Cha, MD 27. Supraventricular Tachycardia: Diagnosis and Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .379 Samuel J. Asirvatham, MD 28. Ventricular Tachycardia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .389 Thomas M. Munger, MD 29. Arrhythmias in Congenital Heart Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .405 Peter A. Brady, MD 30. Arrhythmias During Pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .415 Peter A. Brady, MD 31. Heritable Cardiomyopathies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .425 Shaji C. Menon, MD, Steve R. Ommen, MD, Michael J. Ackerman, MD, PhD 32. Syncope: Diagnosis and Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .443 Win-Kuang Shen, MD 33. Pacemakers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .455 David L. Hayes, MD, Margaret A. Lloyd, MD 34. Cardiac Resynchronization Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .467 David L. Hayes, MD 35. Technical Aspects of Implantable Cardioverter-Defibrillators . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .473 Robert F. Rea, MD 36. Implantable Cardioverter-Defibrillator Trials and Prevention of Sudden Cardiac Death . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .481 Margaret A. Lloyd, MD, Bernard J. Gersh, MB, ChB, DPhil 37. Sudden Cardiac Death . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .493 Ravi Kanagala, MD xviii 14. 38. Heart Disease in Athletes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .507 Stephen C. Hammill, MD 39. Atlas of Electrophysiology Tracings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .509 Douglas L. Packer, MD VALVULAR HEART DISEASE . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .521 40. Valvular Stenosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .523 Rick A. Nishimura, MD 41. Valvular Regurgitation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .535 Rick A. Nishimura, MD 42. Rheumatic Heart Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .549 Andrew G. Moore, MD 43. Carcinoid and Drug-Related Heart Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .555 Heidi M. Connolly, MD, Patricia A. Pellikka, MD 44. Prosthetic Heart Valves . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .563 Martha A. Grogan, MD, Fletcher A. Miller, Jr, MD 45. Surgery for Cardiac Valve Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .575 Thomas A. Orszulak, MD AORTA AND PERIPHERAL VASCULAR DISEASE . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .583 46. Peripheral Vascular Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .585 Peter C. Spittell, MD 47. Cerebrovascular Disease and Carotid Stenting . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .595 Peter C. Spittell, MD, David R. Holmes, Jr, MD 48. The Aorta . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .601 Peter C. Spittell, MD 49. Renovascular Disease and Renal Artery Stenting . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .613 Verghese Mathew, MD 50. Pathophysiology of Arterial Thrombosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .625 Robert D. McBane, MD, Waldemar E. Wysokinski, MD 51. Treatment and Prevention of Arterial Thrombosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .635 Robert D. McBane, MD, Waldemar E. Wysokinski, MD 52. Venous and Lymphatic Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .655 Raymond C. Shields, MD 53. Vasculitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .663 Paul W. Wennberg, MD 54. Marfan Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .673 Naser M. Ammash, MD, Heidi M. Connolly, MD xix 15. CORONARY ARTERY DISEASE RISK FACTORS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .685 55. Coronary Heart Disease Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .687 Thomas G. Allison, PhD 56. Metabolic Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .695 Thomas G. Allison, PhD 57. Pathogenesis of Atherosclerosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .699 Joseph L. Blackshear, MD, Birgit Kantor, MD, PhD 58. Dyslipidemia and Classical Factors for Atherosclerosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .715 Francisco Lopez-Jimenez, MD, MS, Justo Sierra Johnson, MD, MS, Virend K. Somers, MD, PhD, Gerald T. Gau, MD 59. Novel Risk Markers for Atherosclerosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .725 Iftikhar J. Kullo, MD 60. Diabetes Mellitus and Coronary Artery Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .735 Robert L. Frye, MD, David R. Holmes, Jr, MD 61. Hypertension . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .741 Michael J. Hogan, MD, MBA 62. Heart Disease in Women . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .751 Patricia J. M. Best, MD, Sharonne N. Hayes, MD 63. Heart Disease in the Elderly . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .761 Imran S. Syed, MD, Joseph G. Murphy, MD, R. Scott Wright, MD 64. Erectile Dysfunction and Heart Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .767 Bijoy K. Khandheria, MD, Ajay Nehra, MD MYOCARDIAL INFARCTION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .771 65. Cardiac Biomarkers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .773 Brian P. Shapiro, MD, Luciano Babuin, MD, Allan S. Jaffe, MD 66. Acute Coronary Syndromes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .781 Anthony A. Hilliard, MD, Stephen L. Kopecky, MD 67. Chronic Stable Angina . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .795 Frank C. Chen, MD, Frank V. Brozovich, MD, PhD 68. Right Ventricular Infarction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .807 Richard J. Gumina, MD, R. Scott Wright, MD, Joseph G. Murphy, MD 69. Adjunctive Therapy in Acute Myocardial Infarction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .813 R. Scott Wright, MD, Imran S. Syed, MD, Joseph G. Murphy, MD 70. Complications of Acute Myocardial Infarction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .827 Joseph G. Murphy, MD, John F. Bresnahan, MD, Margaret A. Lloyd, MD, Guy S. Reeder, MD 71. Reperfusion Strategy for ST-Elevation Myocardial Infarction: Fibrinolysis Versus Percutaneous Coronary Intervention . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .843 Henry H. Ting, MD 72. Fibrinolytic Trials in Acute Myocardial Infarction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .855 Patricia J. M. Best, MD, Bernard J. Gersh, MB, ChB, DPhil, Joseph G. Murphy, MD xx 16. 73. Risk Stratification After Myocardial Infarction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .869 Randal J. Thomas, MD, MS 74. Cardiac Rehabilitation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .875 Thomas G. Allison, PhD 75. Coronary Artery Bypass Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .883 Thoralf M. Sundt III, MD DISEASES OF THE HEART, PERICARDIUM, AND PULMONARY CIRCULATION . . . . . . . . . . . . . . . .891 76. Pericardial Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .893 Jae K. Oh, MD 77. Pulmonary Embolism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .913 Jason M. Golbin, DO, Udaya B. S. Prakash, MD 78. Pulmonary Hypertension . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .929 Michael D. McGoon, MD 79. Pregnancy and the Heart . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .951 Heidi M. Connolly, MD 80. Adult Congenital Heart Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .965 Carole A. Warnes, MD 81. HIV Infection and the Heart . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .977 Joseph G. Murphy, MD, Zelalem Temesgen, MD 82. Infective Endocarditis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .983 Robin Patel, MD, Joseph G. Murphy, MD, James M. Steckelberg, MD 83. Systemic Disease and the Heart . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1017 Marian T. McEvoy, MD, Joseph G. Murphy, MD 84. Cardiac Tumors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1027 Joseph G. Murphy, MD, R. Scott Wright, MD 85. Sleep Apnea and Cardiac Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1035 Tomas Kara, MD, PhD, Robert Wolk, MD, PhD, Virend K. Somers, MD, PhD 86. Cardiovascular Trauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1043 Joseph G. Murphy, MD, R. Scott Wright, MD 87. Acute Brain Injury and the Heart . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1049 Nandan S. Anavekar, MB, BCh, Sarinya Puwanant, MD, Krishnaswamy Chandrasekaran, MD 88. Noncardiac Anesthesia in Patients With Cardiovascular Disease . . . . . . . . . . . . . . . . . . . . . . . . . . .1057 Laurence C. Torsher, MD CARDIOMYOPATHY AND HEART FAILURE . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1069 89. Cardiovascular Reflexes and Hormones . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1071 Alfredo L. Clavell, MD, John C. Burnett, Jr, MD 90. Systolic Heart Function . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1077 Wayne L. Miller, MD, PhD, Lyle J. Olson, MD 91. Diastolic Heart Function . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1087 Christopher P. Appleton, MD xxi 17. 92. Heart Failure: Diagnosis and Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1101 Richard J. Rodeheffer, MD, Margaret M. Redfield, MD 93. Pharmacologic Therapy of Systolic Ventricular Dysfunction and Heart Failure . . . . . . . . . . . . . . .1113 Richard J. Rodeheffer, MD, Margaret M. Redfield, MD 94. Myocarditis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1125 Leslie T. Cooper, Jr, MD, Oyere K. Onuma, BS 95. Dilated Cardiomyopathy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1139 Horng H. Chen, MD 96. Restrictive Cardiomyopathy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1145 Sudhir S. Kushwaha, MD 97. Hypertrophic Cardiomyopathy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1153 Steve Ommen, MD 98. Right Ventricular Failure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1167 Robert P. Frantz, MD 99. Congestive Heart Failure: Surgical Therapy and Permanent Mechanical Support . . . . . . . . . . . . .1173 Richard C. Daly, MD, Brooks S. Edwards, MD 100. Cardiac Transplantation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1179 Brooks S. Edwards, MD, Richard C. Daly, MD CARDIAC PHARMACOLOGY . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1187 101. Principles of Pharmacokinetics and Pharmacodynamics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1189 Arshad Jahangir, MD, Leonid V. Zingman, MD, Andre Terzic, MD, PhD 102. Antiarrhythmic Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1205 Peter A. Brady, MD 103. Modulators of the Renin-Angiotensin System . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1223 Garvan C. Kane, MD, Peter A. Brady, MD 104. Principles of Diuretic Usage . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1231 Garvan C. Kane, MD, Joseph G. Murphy, MD 105. Digoxin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1233 Arshad Jahangir, MD 106. Principles of Inotropic Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1245 Garvan C. Kane, MD, Joseph G. Murphy, MD, Arshad Jahangir, MD 107. Nitrate Therapies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1249 Garvan C. Kane, MD, Peter A. Brady, MD 108. Calcium Channel Blockers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1253 Arshad Jahangir, MD 109. -Adrenoceptor Blockers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1265 Arshad Jahangir, MD 110. Antiplatelet Agents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1283 Garvan C. Kane, MD, Yong-Mei Cha, MD, Joseph G. Murphy, MD 111. Cardiac Drug Adverse Effects and Interactions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1291 Narith N. Ou, PharmD, Lance J. Oyen, PharmD, Arshad Jahangir, MD xxii 18. 112. Lipid-Lowering Medications and Lipid-Lowering Clinical Trials . . . . . . . . . . . . . . . . . . . . . . . . . . .1309 Joseph G. Murphy, MD, R. Scott Wright, MD INVASIVE AND INTERVENTIONAL CARDIOLOGY . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1325 113. Endothelial Dysfunction and Cardiovascular Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1327 Brian P. Shapiro, MD, Amir Lerman, MD 114. Coronary Artery Physiology and Intracoronary Ultrasonography . . . . . . . . . . . . . . . . . . . . . . . . . .1343 Abhiram Prasad, MD 115. Coronary Anatomy and Angiographic Views . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1357 Andr C. Lapeyre III, MD 116. Principles of Interventional Cardiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1369 Gregory W. Barsness, MD, Joseph G. Murphy, MD 117. High-Risk Percutaneous Coronary Interventions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1381 Gregory W. Barsness, MD 118. Invasive Hemodynamics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1393 Rick A. Nishimura, MD 119. Contrast-Induced Nephropathy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1407 Patricia J. M. Best, MD, Charanjit S. Rihal, MD 120. Diagnostic Coronary Angiography and Ventriculography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1413 Joseph G. Murphy, MD 121. Catheter Closure of Intracardiac Shunts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1441 Guy S. Reeder, MD 122. Atlas of Hemodynamic Tracings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1451 Deepak R. Talreja, MD, Rick A. Nishimura, MD, Joseph G. Murphy, MD 123. Endomyocardial Biopsy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1481 Joseph G. Murphy, MD, Robert P. Frantz, MD, Leslie T. Cooper, Jr, MD 124. Coronary Stents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1489 Joseph G. Murphy, MD, Gregory W. Barsness, MD 125. Cardiac Emergencies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1503 Arshad Jahangir, MD, Joseph G. Murphy, MD 126. Cardiogenic Shock . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1515 Malcolm R. Bell, MD APPENDIX . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1525 Preparing for Cardiology Examinations Joseph G. Murphy, MD, Margaret A. Lloyd, MD CREDIT LINES . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1541 INDEX . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1553 xxiii 19. S E C T I O N I Fundamentals of Cardiovascular Disease Transected Aorta: Motor Vehicle Accident 20. GENERAL APPEARANCE The physical examination, including the general appearance of the patient, is an extremely important component of cardiology examinations. Almost every question has physical examination findings that provide critical clues to the answer in the stem of the question. Important clues to a cardiac diagnosis can be obtained from inspection of the patient (Table 1). BLOOD PRESSURE Blood pressure should always be determined in both arms and in the legs if there is any suspicion of coarctation of the aorta.A difference in systolic blood pressure between both arms of more than 10 mm Hg is abnormal (Table 2). ABNORMALITIES ON PALPATION OF THE PRECORDIUM The patient should be examined in both the supine and the left lateral decubitus position. Examining the apical impulse by the posterior approach with the patient in the sitting position may at times be the best method to appreciate subtle abnormalities of precordial motion.The normal apical impulse occurs during early systole with an outward motion imparted to the chest wall. During mid and late systole, the left ventricle (LV) is diminishing in volume and the apical impulse moves away from the chest wall.Thus,outward precordial apical motion occurring in late systole is abnormal. Remember that point of maximal impulse is not synony- mous with apical impulse. Palpation of the Apex Constrictive pericarditis or tricuspid regurgitation produces a subtle systolic precordial retraction. The apical impulse of LV enlargement is usually widened or diffuse (>3 cm in diameter), can be palpated in two interspaces, and is displaced leftward. A subtle presystolic ventricular rapid filling wave (A wave) frequently associated with LV hypertrophymay be better visualized than palpated by observing the motion of the stethoscope applied lightly on the chest wall,with appropriate timing during simultaneous auscultation. Likewise, a palpable A wave can be detected in this manner.The apical impulse of LV hypertrophy without dilatation is sustained and localized but should not be displaced. Causes of a palpable A wave (presystolic impulse) include the following: 1. Aortic stenosis 2. Hypertrophic obstructive cardiomyopathy 3. Systemic hypertension 3 CARDIOVASCULAR EXAMINATION Clarence Shub, MD 1 21. 4 Section I Fundamentals of Cardiovascular Disease Table 1. Clinical Clues to Specific Cardiac Abnormalities Detectable From the General Examination Condition Appearance Associated cardiac abnormalities Marfan syndrome Tall Aortic root dilatation Long extremities Mitral valve prolapse Acromegaly Large stature Cardiac hypertrophy Coarse facial features Spade hands Turner syndrome Web neck Aortic coarctation Hypertelorism Pulmonary stenosis Short stature Pickwickian syndrome Severe obesity Pulmonary hypertension Somnolence Friedreich ataxia Lurching gait Hypertrophic cardiomyopathy Hammertoe Pes cavus Duchenne type muscular dystrophy Pseudohypertrophy of calves Cardiomyopathy Ankylosing spondylitis Straight back syndrome Aortic regurgitation Stiff (poker) spine Heart block (rare) Jaundice Yellow skin or sclera Right-sided congestive heart failure Prosthetic valve dysfunction (hemolysis) Sickle cell anemia Cutaneous ulcers Pulmonary hypertension Painful crises Secondary cardiomyopathy Lentigines (LEOPARD syndrome*) Brown skin macules that do Hypertrophic obstructive cardio- not increase with sunlight myopathy Pulmonary stenosis Hereditary hemorrhagic telangiectasia Small capillary hemangiomas Pulmonary arteriovenous fistula (Osler-Weber-Rendu disease) on face or mouth, with or without cyanosis Pheochromocytoma Pale, diaphoretic skin Catecholamine-induced secondary Neurofibromatosiscaf-au- dilated cardiomyopathy lait spots Lupus Butterfly rash on face Verrucous endocarditis Raynaud phenomenonhands Myocarditis Livedo reticularis Pericarditis Sarcoidosis Cutaneous nodules Secondary cardiomyopathy Erythema nodosum Heart block Tuberous sclerosis Angiofibromas (face; adenoma Rhabdomyoma sebaceum) Myxedema Coarse, dry skin Pericardial effusion Thinning of lateral eyebrows Left ventricular dysfunction Hoarseness of voice Right-to-left intracardiac shunt Cyanosis and clubbing of distal Any of the lesions that cause extremities Eisenmenger syndrome Differential cyanosis and Reversed shunt through patent duc- clubbing tus arteriosus 22. The apical impulse of LV hypertrophy without dilatation is sustained and localized. It should not be displaced but may be accompanied by a palpable presystolic outward movement,the A wave. Outward precordial apical motion occurring in late systole is abnormal. Multiple abnormal outward precordial movements may occur: presystolic, systolic, or late systolic rebound and an A wave in late diastole. Palpation of the Lower Sternal Area Precordial motion in the lower sternal area usually reflects right ventricular (RV) motion.RV hypertrophy due to systolic overload (such as in pulmonary stenosis) causes a sustained outward lift. Diastolic overload (such as in atrial septal defect [ASD]) causes a vigorous nonsustained motion. In severe mitral regurgitation, the left atrium expands in systole but is limited in its posterior motion by the spine.The RV may then be pushed forward, and the parasternal region is lifted indirectly. Significant overlap of sites of maximal pulsation occurs in LV and RV overload states. For example, in RV overload, the abnormal impulse can overlap with the LV in the apical sternal region (between the apex and the left lower sternal border). An LV apical aneurysm may produce a delayed outward motion and cause a rockingmotion. Palpation of the Left Upper Sternal Area Abnormal pulsations at the left upper sternal border (pulmonic area) can be due to a dilated pulmonary artery (e.g., poststenotic dilatation in pulmonary valve stenosis, idiopathic dilatation of the pulmonary artery, or increased pulmonary flow related to ASD or pul- Chapter 1 Cardiovascular Examination 5 Table 1. (continued) Condition Appearance Associated cardiac abnormalities Holt-Oram syndrome Rudimentary or absent thumb Atrial septal defect Down syndrome Mental retardation Endocardial cushion defect Simian crease of palm Characteristic facies Scleroderma Tight, shiny skin of fingers Pulmonary hypertension with contraction Myocardial, pericardial, or endocar- Characteristic taut mouth dial disease and facies Rheumatoid arthritis Typical hand deformity Myocardial, pericardial, or endo- Subcutaneous nodules cardial disease (often subclinical) Thoracic bony abnormality Pectus excavatum Pseudocardiomegaly Straight back syndrome Mitral valve prolapse Carcinoid syndrome Reddish cyanosis of face Right-sided cardiac valve stenosis or Periodic flushing regurgitation *LEOPARD syndrome: lentigines, electrocardiographic changes, ocular hypertelorism, pulmonary stenosis, abnormal genitalia, retardation of growth, deafness. Table 2. Causes of Blood Pressure Discrepancy Between Arms or Between Arms and Legs Arterial occlusion or stenosis of any cause Dissecting aortic aneurysm Coarctation of the aorta Patent ductus arteriosus Supravalvular aortic stenosis Thoracic outlet syndrome 23. monary hypertension). Pulsations of increased blood flow are dynamic and quick, whereas pulsations due to pressure overload cause a sustained impulse. If the apical impulse is not palpable and the patient is hemodynamically unstable, consider cardiac tamponade as the first diagnosis. Palpation of the Right Upper Sternal Area Abnormal pulsations at the right upper sternal border (aortic area) should suggest an aortic aneurysm. An enlarged left lobe of the liver associated with severe tricuspid regurgitation may be appreciated in the epigas- trium,and the epigastric site may be the location of the maximal cardiac impulse in patients with emphysema or an enlarged RV. RV hypertrophy due to systolic overload causes a sustained outward lift. Diastolic overload (as in ASD) causes a vigorous nonsustained motion. In severe mitral regurgitation,the left atrium expands in systole but is limited in its posterior motion by the spine.The RV may then be pushed forward, and the parasternal region is liftedindirectly. Significant overlap of sites of maximal pulsation occurs in LV and RV overload states. Pulsations of increased blood flow are dynamic and quick, whereas pulsations due to pressure overload cause a sustained impulse. JUGULAR VEINS Abnormal waveforms in the jugular veins reflect abnormal hemodynamics of the right side of the heart. In the presence of normal sinus rhythm, there are two positive or outward moving waves (a and v) and two visible negative or inward moving waves (x and y) (Fig. 1).The x descent is sometimes referred to as the systolic collapse. Ordinarily, the c wave is not readily visible.The a wave can be identified by simultaneous auscultation of the heart and inspection of the jugular veins.The a wave occurs at about the time of the first heart sound (S1).The x descent follows.The v wave,a slower,more undulating wave, occurs near the second heart sound (S2).The y descent follows.The a wave is normally larger than the v wave, and the x descent is more marked than the y descent (Tables 3 and 4). Normal jugular venous pressure decreases with inspiration and increases with expiration.Veins that fill at inspiration (Kussmaul sign), however, are a clue to constrictive pericarditis, pulmonary embolism, or RV infarction (Table 5). Jugular veins that fill at inspiration (Kussmaul sign) are a clue to constrictive pericarditis, pulmonary embolism,or RV infarction. Hepatojugular (Abdominojugular) Reflux Sign The neck veins distend with steady (>10 seconds) upper abdominal compression while the patient continues to breathe normally without straining. Straining may cause a false-positive hepatojugularreflux sign. The neck veins may collapse or remain distended. Jugular venous pressure that remains increased and then falls abruptly (4 cm H2O) indicates an abnormal response. It may occur in LV failure with secondary pulmonary hypertension.In patients with chronic congestive heart failure,a positive hepatojugular reflux sign (with or without increased jugular venous pressure), a third heart sound (S3), and radiographic pulmonary vascular redistribution are independent predictors of increased pulmonary capillary wedge pressure.The 6 Section I Fundamentals of Cardiovascular Disease Fig. 1. Normal jugular venous pulse. The jugular v wave is built up during systole, and its height reflects the rate of filling and the elasticity of the right atrium. Between the bottom of the y descent (y trough) and the begin- ning of the a wave is the period of relatively slow filling of the atrioventricle or diastasis period. The wave built up during diastasis is the h wave. The h wave height also reflects the stiffness of the right atrium. S1, first heart sound; S2, second heart sound. 24. abdominojugular maneuver can also be useful for elicit- ing venous pulsations if they are difficult to visualize. A positive hepatojugular(abdominojugular) reflux sign may be found in LV failure with secondary pulmonary hypertension. If the jugular veins are engorged but not pulsatile, consider superior vena caval obstruction. ARTERIAL PULSE Abnormalities of the Carotid Pulse Hyperdynamic Carotid Pulse A vigorous, hyperdynamic carotid pulse is consistent with aortic regurgitation. It may also occur in other states of high cardiac output or be caused by the wide pulse pressure associated with atherosclerosis,especially in the elderly. Dicrotic and Bisferiens Pulses A dicrotic carotid pulse occurs in myocardial failure, especially in association with hypotension, decreased cardiac output, and increased peripheral resistance. Dicrotic and bisferious are the Greek and Latin terms, respectively, for twice beating, but in cardiology they are not equivalent. The second impulse occurs in early diastole with the dicrotic pulse and in late systole with the bisferiens pulse.The bisferiens pulse usually occurs in combined aortic regurgitation and aortic stenosis, but occasionally it occurs in pure aortic regurgitation. Aortic Stenosis Pulsus parvus (soft or weak) classically occurs in aortic stenosis but can also result from severe stenosis of any cardiac valve or can occur with low cardiac output of Chapter 1 Cardiovascular Examination 7 Table 3. Timing of Jugular Venous Pulse Waves a waveprecedes the carotid arterial pulse and is simultaneous with S4, just before S1 x descentbetween S1 and S2 v wavejust after S2 y descentafter the v wave in early diastole Table 4. Abnormal Jugular Venous Pulse Waves Increased a wave 1. Tricuspid stenosis 2. Decreased right ventricular compliance due to right ventricular hypertrophy in severe pulmonary hypertension Pulmonary stenosis Pulmonary vascular disease 3. Severe left ventricular hypertrophy due to pressure by the hypertrophied septum on right ventricular filling (Bernheim effect) Hypertrophic obstructive cardiomyopathy Rapid x descent Cardiac tamponade Increased v wave Tricuspid regurgitation Atrial septal defect Rapid y descent (Friedreich sign) Constrictive pericarditis Table 5. Differentiation of Internal Jugular Vein Pulse and Carotid Pulse Jugular vein pulse Carotid pulse Double peak when in Single peak sinus rhythm Obliterated by gentle Unaffected by pressure gentle pressure Changes with position Unaffected by and inspiration position or inspiration any cause. Severe aortic stenosis also produces a slowly increasing delayed pulse (pulsus tardus). Because of the effects of aging on the carotid arteries, the typical findings of pulsus parvus and pulsus tardus may be less apparent or absent in the elderly, even with severe degrees of aortic stenosis. Hypertrophic Obstructive Cardiomyopathy In hypertrophic obstructive cardiomyopathy, the ventricular obstruction begins in mid systole, increases as 25. contraction proceeds, and decreases in late systole.The initial carotid impulse is brisk.The pulse may be bifid as well (Table 6). Inequality of the carotid pulses can be due to carotid atherosclerosis,especially in elderly patients.In a young patient, consider supravalvular aortic stenosis. (The right side then should have the stronger pulse.) Aortic dissection and thoracic outlet syndrome may also produce inequality of arterial pulses. A pulsating cervi- cal mass,usually on the right,may be caused by athero- sclerotic bucklingof the right common carotid artery and give the false impression of a carotid aneurysm. Transmitted Murmurs Transmitted murmurs of aortic origin,most often due to aortic stenosis (less often due to coarctation, patent ductus arteriosus, pulmonary stenosis, and ventricular septal defect), decrease in intensity as the stethoscope ascends the neck,whereas a carotid bruit is usually louder higher in the neck and decreases in intensity as the stethoscope is inched proximally toward the chest.Both conditions may coexist,especially in elderly patients.An abrupt change in the acoustic characteristics (pitch) of the bruit as the stethoscope is inched upward may be a clue to the presence of combined lesions. Pulsus Paradoxus Paradoxical pulse is an exaggeration of the normal (10 mm) inspiratory decline in arterial pressure. It occurs classically in cardiac tamponade but occasionally with other restrictive cardiac abnormalities, severe congestive heart failure, pulmonary embolism, or chronic obstructive pulmonary disease (Table 7). Pulsus Alternans Pulsus alternans (alternation of stronger and weaker beats) rarely occurs in healthy subjects and then is transient after a premature ventricular contraction.It usually is associated with severe myocardial failure and is frequently accompanied by an S3,both of which impart an ominous prognosis.Pulsus alternans may be affected by alterations in venous return and may disappear as congestive heart failure progresses. Electrical alternans (alternating variation in the height of the QRS complex) is unrelated to pulsus alternans (Table 8). A dicrotic carotid pulse occurs in myocardial failure, often in association with hypotension, decreased cardiac output,and increased peripheral resistance. Pulsus parvus (soft or weak) classically occurs in aortic stenosis but can also result from severe stenosis of any cardiac valve or can occur with severely low cardiac output of any cause. Because of the effects of aging on the carotid arteries, the typical findings of pulsus parvus and 8 Section I Fundamentals of Cardiovascular Disease Table 6. Causes of a Double-Impulse Carotid Arterial Pulse Dicrotic pulse (systolic + diastolic impulse) Cardiomyopathy Left ventricular failure Bisferiens pulse (two systolic impulses) Aortic regurgitation Combined aortic valve stenosis and regurgitation (dominant regurgitation) Bifid pulse (two systolic impulses with inter- vening pulse collapse) Hypertrophic cardiomyopathy Table 7. Causes of Pulsus Paradoxus Constrictive pericarditis Pericardial tamponade Severe emphysema Severe asthma Severe heart failure Pulmonary embolism Morbid obesity Table 8. Pulsus and Electrical Alternans Pulsus alternans Severe heart failure Electrical alternans Pericardial tamponade Large pericardial effusions 26. pulsus tardus may be less apparent or absent in the elderly,even with severe degrees of aortic stenosis. Inequality of the carotid pulses can be due to carotid atherosclerosis, especially in elderly patients. In a young patient, consider supravalvular aortic stenosis. (The right side then should have the stronger pulse.) Transmitted murmurs of aortic origin, most often due to aortic stenosis (less often due to coarctation, patent ductus arteriosus, pulmonary stenosis, or ventricular septal defect), decrease in intensity as the stethoscope ascends the neck,whereas a carotid bruit is usually louder higher in the neck and decreases in intensity as the stethoscope is inched proximally toward the chest. Paradoxical pulse occurs classically in cardiac tamponade but occasionally with other restrictive cardiac abnormalities, severe congestive heart failure, pulmonary embolism, or chronic obstructive pulmonary disease. Pulsus alternans usually is associated with severe myocardial failure and is frequently accompanied by an S3,both of which impart an ominous prognosis. Abnormalities of the Femoral Pulse In hypertension, simultaneous palpation of radial and femoral pulses may reveal a delay or relative weakening of the femoral pulses, suggesting aortic coarctation. The finding of a femoral (or carotid) bruit in an adult suggests diffuse atherosclerosis. Fibromuscular dyspla- sia is less common and occurs in younger patients. HEART SOUNDS First Heart Sound Only the mitral (M1) and tricuspid (T1) components of S1 are normally audible. M1 occurs before T1 and is the loudest component. Wide splitting of S1 occurs with right bundle branch block and Ebstein anomaly. Factors Influencing the Intensity of S1 PR Interval The PR interval varies inversely with the loudness of S1with a long PR interval, the S1 is soft; conversely, with a short PR interval,the S1 is loud. Mitral Valve Disease Mitral stenosis produces a loud S1 if the valve is pliable. When the valve becomes calcified and immobile, the intensity of S1 decreases.The S1 may also be soft in severe aortic regurgitation (related to early closure of the mitral valve) caused by LV filling from the aorta. The Rate of Increase of Systolic Pressure Within the LV A loud S1 can be produced by hypercontractile states, such as fever,exercise,thyrotoxicosis,and pheochromocytoma.Conversely,a soft S1 can occur in LV failure. If S1 seems louder at the lower left sternal border than at the apex (implying a loud T1), suspect ASD or tricuspid stenosis. Atrial fibrillation produces a variable S1 intensity. (The intensity is inversely related to the previous RR cycle length; a longer cycle length produces a softer S1.) A variable S1 intensity during a wide complex, regular tachycardia suggests atrioventricular dissociation and ventricular tachycardia.The marked delay of T1 in Ebstein anomaly is related to the late billowing effect of the deformed (sail-like) anterior leaflet of the tricuspid valve as it closes in systole.Table 9 lists causes of an abnormal S1. If S1 seems to be louder at the base than at the apex, suspect an ejection sound masquerading as S1. If the S1 is louder at the lower left sternal border than at the apex (implying a loud T1), suspect ASD or tricuspid stenosis. Chapter 1 Cardiovascular Examination 9 Table 9. Abnormalities of S1 and Their Causes Loud S1 Short PR interval Mitral stenosis Left atrial myxoma Hypercontractile states Soft S1 Long PR interval Depressed left ventricular function Early closure of mitral valve in acute severe aortic incompetence Ruptured mitral valve leaflet or chordae Left bundle branch block 27. A variable S1 intensity during a wide complex, regular tachycardia suggests atrioventricular dissociation and ventricular tachycardia. The marked delay of T1 in Ebstein anomaly is related to the late billowing effect of the deformed (sail- like) anterior leaflet of the tricuspid valve as it closes in systole. Systolic Ejection Clicks (or Sounds) The ejection click (sound) follows S1 closely and can be confused with a widely split S1 or, occasionally, with an early nonejection click. Clicks can originate from the left or right side of the heart. The three possible mechanisms for production of the clicks are as follows: 1. Intrinsic abnormality of the aortic or pulmonary valve,such as congenital bicuspid aortic valve 2. Pulsatile distention of a dilated great artery, as occurs in increased flow states such as truncus arteriosus (aortic click) or ASD (pulmonary click) or in idiopathic dilatation of the pulmonary artery 3. Increased pressure in the great vessel, such as in aortic or pulmonary hypertension Because an aortic click is not usually heard with uncomplicated coarctation, its presence should suggest associated bicuspid aortic valve. In the latter condition, the click diminishes in intensity, becomes buriedin the systolic murmur, and ultimately disappears as the valve becomes heavily calcified and immobile later in the course of the disease.Although a click implies cusp mobility, its presence does not necessarily exclude severe stenosis. A click would be expected to be absent in subvalvular stenosis.The timing of the pulmonary click in relationship to S1 (reflecting the isovolumic contraction period of the RV) is associated with hemodynamic severity in valvular pulmonary stenosis.With higher systolic gradient and lower pulmonary artery systolic pressure, the isovolumic contraction period shortens and thus the earlier the click occurs in relationship to S1. A pulmonary click can occur in idiopathic dilatation of the pulmonary artery, and this condition may be a masquerader of ASD, especially in young adults.The pulmonary click due to valvular pulmonary stenosis is the only right-sided heart sound that decreases with inspiration. Most other right-sided auscultatory events either increase in intensity with inspiration (most commonly) or show minimal change.The pulmonary click is best heard along the upper left sternal border, but if it is loud enough or if the RV is markedly dilated,it may be heard throughout the precordium.The aortic click radiates to the aortic area and the apex and does not change with respiration.The causes of ejection clicks are listed in Table 10. The presence, absence, or loudness of the ejection click does not correlate with the degree of valvular stenosis. An aortic click is not heard with uncomplicated coarctation; its presence should suggest associated bicuspid aortic valve. A click is absent in subvalvular or supravalvular aortic stenosis or hypertrophic obstructive cardiomyopathy. A pulmonary click can occur in idiopathic dilatation of the pulmonary artery, a condition that may mimic ASD,especially in young adults. The pulmonary click is best heard along the upper left sternal border.The aortic click radiates to the aortic area and the apex and does not change with respiration. Mid-to-Late Nonejection Clicks (Systolic Clicks) Nonejection clicks are most commonly due to mitral valve prolapse. Rarely, nonejection clicks can be caused by papillary muscle dysfunction, rheumatic mitral valve disease, or hypertrophic obstructive cardiomyopathy. 10 Section I Fundamentals of Cardiovascular Disease Table 10. Causes of Ejection Clicks Aortic click Congenital valvular aortic stenosis Congenital bicuspid aortic valve Truncus arteriosus Aortic incompetence Aortic root dilatation or aneurysm Pulmonary click Pulmonary valve stenosis Atrial septal defect Chronic pulmonary hypertension Tetralogy of Fallot with pulmonary valve stenosis (absent if there is only infundibular stenosis) Idiopathic dilated pulmonary artery 28. Other rare causes of nonejection clicks (that can masquerade as mitral prolapse) include ventricular or atrial septal aneurysms, ventricular free wall aneurysms, and ventricular and atrial mobile tumors, such as myxoma. A nonejection click not due to mitral valve prolapse does not have the typical responses to bedside maneuvers found with mitral valve prolapse,as outlined below. Mitral Valve Prolapse Maneuvers that decrease LV volume,such as standing or the Valsalva maneuver,move the click earlier in the cardiac cycle.Conversely,maneuvers that increase LV volume,such as assuming the supine position and elevating the legs,move the click later in the cardiac cycle.With a decrease in LV volume, a systolic murmur, if present, would become longer. Interventions that increase systemic blood pressure make the murmur louder. Miscellaneous causes of nonejection clicks (that can masquerade as mitral prolapse) include ventricular or atrial septal aneurysms, ventricular free wall aneurysms, and ventricular and atrial mobile tumors, such as myxoma. Maneuvers that decrease LV volume, such as standing or the Valsalva maneuver, move the click earlier in the cardiac cycle. Conversely, maneuvers that increase LV volume, such as assuming the supine position and elevating the legs, move the click later in the cardiac cycle. Second Heart Sound S2 is often best heard along the upper and middle left sternal border.Splitting of S2 (Fig.2) is best heard during normal breathing with the subject in the sitting position. Chapter 1 Cardiovascular Examination 11 SPLITTING? NORMAL NARROW FIXED WIDE FIXED REVERSED Normal Pulm HT RBBB PS ASD PDA (L to R shunt) LBBB AS IHD S2 + OS S2 + S3 S2 + pericardial knock S2 + tumor plop A2 > P2 Normal P2 > A2 Pulm HT (any) cause AS Pseudo: VSD & L to R shunt A2 vs P2? Fig. 2. Branching logic tree for second heart sound (S2) splitting. A2, aortic closure sound; AS, aortic stenosis; ASD, atrial septal defect; HT, hypertension; IHD, ischemic heart disease; LBBB, left bundle branch block; L to R, left-to- right; OS, opening snap; P2, pulmonic closure sound; PDA, patent ductus arteriosus; PS, pulmonary stenosis; Pulm HT, pulmonary hypertension; RBBB, right bundle branch block; S3, third heart sound; VSD, ventricular septal defect. 29. Determinants of S2 include the following: 1. Ventricularactivation(bundlebranchblockdelays closureoftheventriclesrespectivesemilunarvalve) 2. Ejection time 3. Valve gradient (increased gradient with low pressure in the great vessel delays closure) 4. Elastic recoil of the great artery (decreased elastic recoil delays closure,such as in idiopathic dilatation of the pulmonary artery) Splitting of S2 Wide but physiologic splitting of S2 (Fig. 3) may be due to the following: 1. Delayed electrical activation of the RV,such as in right bundle branch block or premature ventric- ularcontractionoriginatingintheLV(whichcon- ducts with a right bundle branch block pattern) 2. Delay of RV contraction,such as in increased RV stroke volume and RV failure 3. Pulmonary stenosis (prolonged ejection time) In ASD, there is only minimal respiratory variation in S2 splitting.This is referred to as fixed splitting. Fixed splitting should be verified with the patient in the sitting or standing position because healthy subjects occasionally appear to have fixed splitting in the supine position.When the degree of splitting is unusu- ally wide, especially when the pulmonary component of the second heart sound (P2) is diminished, suspect concomitant pulmonary stenosis. Indeed, this condition is the cause of the most widely split S2 that can be recorded. Wide, fixed splitting, although considered typical of ASD, occurs in only 70% of patients with ASD. However, persistent expiratory splitting is audible in most. Normal respiratory variation of the S2 occurs in up to 8% of patients with ASD. With Eisenmenger physiology,the left-to-right shunting decreases and the degree of splitting narrows. A pulmonary systolic ejection murmur (increased flow) is common in patients with ASD, and with a significant left-to-right shunt, a diastolic tricuspid flow murmur can be heard as well. As with aortic stenosis,as pulmonary stenosis increases in severity, P2 decreases in intensity, and ultimately S2 becomes single. The wide splitting of S2 in mitral regurgitation and ventricular septal defect is related to early aortic valve closure (in ventricular septal defect, P2 is delayed as well), which, in turn, is due to decreased LV ejection time, but the loud pansystolic regurgitant murmur often obscures the wide splitting of S2 so that the S2 appears to be single. Partial anomalous pulmonary venous connection may occur alone or in combination with ASD (most often of the sinus venosus type). Wide splitting of S2 occurs in both conditions, but it usually shows normal respiratory variation in isolated partial anomalous pulmonary venous connection. 12 Section I Fundamentals of Cardiovascular Disease Fig. 3. Diagrammatic representation of normal and abnormal patterns in the respiratory variation of the second heart sound. The heights of the bars are propor- tional to the sound intensity. A, aortic component; AS, aortic stenosis; ASD, atrial septal defect; Exp., expiration; Insp., inspiration; MI, mitral incompetence; P, pulmonary component; PS, pulmonary stenosis; VSD, ventricular septal defect. 30. Pulmonary hypertension may cause wide splitting of S2, although the intensity of P2 is usually increased and widely transmitted throughout the precordium. Fixed splitting should be verified with the patient in the sitting or standing position because healthy subjects occasionally appear to have fixed splitting in the supine position. Wide, fixed splitting, although considered typical of ASD,occurs in only 70% of patients with ASD. Wide splitting of S2 occurs in both partial anomalous pulmonary venous connection and ASD, but it usually shows normal respiratory variation in isolated partial anomalous pulmonary venous connection. Pulmonary hypertension may cause wide splitting of S2, although the intensity of P2 is usually increased and widely transmitted throughout the precordium. Paradoxical (Reversed) Splitting of S2 Paradoxical splitting of S2 is usually caused by conditions that delay aortic closure. Examples include the following: 1. Electrical delay of LV contraction, such as left bundle branch block (most commonly) 2. Mechanical delay of LV ejection, such as aortic stenosis and hypertrophic obstructive cardiomyopathy 3. Severe LV systolic failure of any cause 4. Patent ductus arteriosus,aortic regurgitation,and systemic hypertension are other rare causes of paradoxic splitting Paradoxical splitting of S2 (that is, with normal QRS duration) may be an important bedside clue to significant LV dysfunction. In severe aortic stenosis, the paradoxical splitting is only rarely recognized because the late systolic ejection murmur obscures S2. However, when paradoxical splitting of S2 is found in association with aortic stenosis, usually in young adults (assuming left bundle branch block is absent), severe aortic obstruction is suggested. Similarly, paradoxical splitting in hypertrophic obstructive cardiomyopathy implies a significant resting LV outflow tract gradient. Transient paradoxical splitting of S2 can occur with myocardial ischemia, such as during an episode of angina, either alone or in combination with an apical systolic murmur of mitral regurgitation (papillary muscle dysfunction) or prominent fourth heart sound (S4). When paradoxical splitting of S2 is found in association with aortic stenosis, usually in young adults (assuming left bundle branch block is absent), severe aortic obstruction is suggested. Similarly, paradoxical splitting in hypertrophic obstructive cardiomyopathy implies a significant resting LV outflow tract gradient. Transient paradoxical splitting of S2 can occur with myocardial ischemia, such as during an episode of angina,either alone or in combination with an apical systolic murmur of mitral regurgitation (papillary muscle dysfunction) or a prominent S4. Intensity of S2 Loud S2 Ordinarily,the intensity of the aortic component of the second heart sound (A2) exceeds that of the P2. In adults, a P2 that is louder than A2, especially if P2 is transmitted to the apex, implies either pulmonary hypertension or marked RV dilatation, such that the RV now occupies the apical zone.The latter may occur in ASD (approximately 50% of patients). Hearing two components of the S2 at the apex is abnormal in adults, because ordinarily only A2 is heard at the apex.Thus, when both components of S2 are heard at the apex in adults,suspect ASD or pulmonary hypertension. Soft S2 Decreased intensity of A2 or P2, which may cause a single S2, reflects stiffening and decreased mobility of the aortic or pulmonary valve (aortic stenosis or pulmonary stenosis, respectively). A single S2 may also be heard in older patients and the following cases: 1. With only one functioning semilunar valve,such asinpersistenttruncusarteriosus,pulmonaryatre- sia,or tetralogy of Fallot 2. When one component of S2 is enveloped in a long systolic murmur,such as in ventricular septal defect 3. With abnormal relationships of great vessels,such as in transposition of the great arteries When both components of S2 are heard at the apex in adults, implying an increased pulmonary component of S2, suspect ASD or pulmonary hypertension. Chapter 1 Cardiovascular Examination 13 31. Opening Snap A high-pitched snapping sound related to mitral or tricuspid valve opening, when present, is abnormal and is referred to as an opening snap (OS).This may arise from either a doming stenotic mitral valve or tricuspid valve, more commonly the former.The intensity of an OS correlates with valve mobility.Rarely,an OS occurs in the absence of atrioventricular valve stenosis in conditions associated with increased flow through the valve,such as significant mitral regurgitation. In mitral stenosis, the presence of an OS, often accompanied by a loud S1, implies a pliable mitral valve.The OS is often well transmitted to the left sternal border and even to the aortic area. In mitral stenosis,the absence of an OS implies the following: 1. Severe valvular immobility and calcification (note thatanOScanstillbeheardinsomeofthesecases) 2. Mitral regurgitation is the predominant lesion Significant mitral stenosis may be present in the absence of an OS if the mitral valve leaflets are fixed and immobile. S2-OS Interval The S2mitral OS interval reflects the isovolumic relaxation period of the LV.With increased severity of mitral stenosis and greater increase in left atrial pressures, the S2-OS interval becomes shorter and may be confused with a split S2.The S2-OS interval should not vary with respiration.The S2-OS interval widens on standing, whereas the split S2 either does not change or narrows. Mild mitral stenosis is associated with an S2-OS interval of more than 90 ms,and severe mitral stenosis with an interval of less than 70 ms. However, the S2-OS interval is an unreliable predictor of the severity of mitral stenosis. Other factors that increase left atrial pressures, such as mitral regurgitation or LV failure, can also affect this interval. When the S2-OS interval is more than 110 to 120 ms, the OS may be confused with an LV S3. In comparison, the LV S3 is usually low-pitched and is localized to the apex. A tricuspid valve OS caused by tricuspid stenosis can be recognized by its location along the left sternal border and its increase with inspiration.In normal sinus rhythm, a prominent A wave can be seen in the jugular venous pulse,along with slowing of the Y descent. An LV S3, which implies that rapid LV filling can occur,is rare in pure mitral stenosis.Also,an RV S3 can occur in mitral stenosis with severe secondary pulmonary hypertension and RV failure. An RV S3 is found along the left sternal border and increases with inspiration. A tumor plop due to an atrial myxoma has the same early diastolic timing as an OS and can be confused with it. In mitral stenosis, the presence of an OS, often accompanied by a loud S1, implies a pliable mitral valve that is not heavily calcified. (In such cases, the patient may be a candidate for mitral commissuroto- my or balloon valvuloplasty rather than mitral valve replacement.) In general, mild mitral stenosis is associated with an S2-OS interval >90 ms, and severe mitral stenosis with an interval 100 pg/mL b d a+b=722 a+b+c+d=1,538 Values for b and d are calculated by use of simple algebra. The following are derived using the for- mulas in Table 2: Sensitivity = 650/722 = 90% Specificity = 596/816 = 73% PPV = 650/870 = 75% NPV = 596/668 = 89% +LR = 0.9/0.27 = 3.3 LR = 0.1/0.73 = 0.14 See text for abbreviations. 78. The American College of Cardiology and the American Heart Association (ACC/AHA) have pub- lished guidelines for the perioperative evaluation and management of patients with heart disease who are to have noncardiac operations.The guidelines recom- mend a conservative approach. Expensive testing, invasive strategies, and revascularization are rarely, if ever,warranted just to get the patient through an operation.Rather, the indications for extensive perioperative testing or revascularization are generally similar to those in a nonoperative setting. Testing or revascularization is not indicated just to get the patient through an operation. EFFECT OF CORONARY ARTERY DISEASE The risk of a perioperative myocardial infarction in patients without clinical evidence of heart disease is approximately 0.15%. In patients with clinical heart disease,the risk of a perioperative myocardial infarction can be stratified according to the cardiovascular profile of the patient (major, intermediate, minor, or no clinical predictors of increased risk) and according to the cardiac stress of the operation (high,medium,or low stress or risk). Patients without clinical evidence of heart disease are at low risk (about 0.15%) of perioperative myocardial infarction. The mortality rate in association with perioperative myocardial infarction is significantly higher than that with an infarct unrelated to an operation. Previously, the risk of perioperative myocardial infarction was less well recognized and the antemortem diagnosis was more difficult.Increased awareness of the problem,better patient selection, improved anesthetic and operative techniques, improved perioperative monitoring and management, and improved diagnostic techniques (including the newer biomarkers such as serum tro- ponin) have all contributed to a significant reduction in mortality from perioperative myocardial infarction. The risk of perioperative reinfarction is increased in the first 6 month

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