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(BQ) Part 1 book Harrison''s cardiovascular medicine presents the following contents: Introduction to cardiovascular disorders, diagnosis of cardiovascular disorders, heart rhythm disturbances, disorders of the heart. 2nd Edition HARRISON’S TM Cardiovascular Medicine Derived from Harrison’s Principles of Internal Medicine, 18th Edition Editors Dan L Longo, md Professor of Medicine, Harvard Medical School; Senior Physician, Brigham and Women’s Hospital; Deputy Editor, New England Journal of Medicine, Boston, Massachusetts Dennis L Kasper, md William Ellery Channing Professor of Medicine, Professor of Microbiology and Molecular Genetics, Harvard Medical School; Director, Channing Laboratory, Department of Medicine, Brigham and Women’s Hospital, Boston, Massachusetts J Larry Jameson, md, PhD Robert G Dunlop Professor of Medicine; Dean, University of Pennsylvania School of Medicine; Executive Vice-President of the University of Pennsylvania for the Health System, Philadelphia, Pennsylvania Anthony S Fauci, md Chief, Laboratory of Immunoregulation; Director, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland Stephen L Hauser, md Robert A Fishman Distinguished Professor and Chairman, Department of Neurology, University of California, San Francisco, San Francisco, California Joseph Loscalzo, md, PhD Hersey Professor of the Theory and Practice of Medicine, Harvard Medical School; Chairman, Department of Medicine; Physician-in-Chief, Brigham and Women’s Hospital, Boston, Massachusetts 2nd Edition HARRISON’S TM Cardiovascular Medicine Editor Joseph Loscalzo, MD, PhD Hersey Professor of the Theory and Practice of Medicine, Harvard Medical School; Chairman, Department of Medicine; Physician-in-Chief, Brigham and Women’s Hospital, Boston, Massachusetts New York   Chicago   San Francisco   Lisbon   London   Madrid   Mexico City Milan   New Delhi   San Juan   Seoul   Singapore   Sydney   Toronto Copyright © 2013 by McGraw-Hill Education, LLC All rights reserved Except as permitted under the United States Copyright Act of 1976, no part of this publication may be reproduced or distributed in any form or by any means, or stored in a database or retrieval system, without the prior written permission of the publisher ISBN: 978-0-07-181499-7 MHID: 0-07-181499-X The material in this eBook also appears in the print version of this title: ISBN: 978-0-07-181498-0, MHID: 0-07-181498-1 All trademarks are trademarks of their respective owners Rather than put a trademark symbol after every occurrence of a trademarked name, we use names in an editorial fashion only, and to the benefit of the trademark owner, with no intention of infringement of the trademark Where such designations appear in this book, they have been printed with initial caps McGraw-Hill Education eBooks are available at special quantity discounts to use as premiums and sales promotions, or for use in corporate training programs To contact a representative please e-mail us at bulksales@mcgraw-hill.com Dr Fauci’s work as an editor and author was performed outside the scope of his employment as a U.S government employee This work represents his personal and professional views and not necessarily those of the U.S government This book was set in Bembo by Cenveo® Publisher Services The editors were James F Shanahan and Kim J Davis The production supervisor was Catherine H Saggese Project management was provided by Tania Andrabi, Cenveo Publisher Services The cover design was by Thomas DePierro Cover illustration, the coronary vessels of the heart, © MedicalRF.com/Corbis TERMS OF USE This is a copyrighted work and McGraw-Hill Education, LLC and its licensors reserve all rights in and to the work Use of this work is subject to these terms Except as permitted under the Copyright Act of 1976 and the right to store and retrieve one copy of the work, you may not decompile, disassemble, reverse engineer, reproduce, modify, create derivative works based upon, transmit, distribute, disseminate, sell, publish or sublicense the work or any part of it without McGraw-Hill Education’s prior consent You may use the work for your own noncommercial and personal use; any other use of the work is strictly prohibited Your right to use the work may be terminated if you fail to comply with these terms THE WORK IS PROVIDED “AS IS.” McGRAW-HILL EDUCATION AND ITS LICENSORS MAKE NO GUARANTEES OR WARRANTIES AS TO THE ACCURACY, ADEQUACY OR COMPLETENESS OF OR RESULTS TO BE OBTAINED FROM USING THE WORK, INCLUDING ANY INFORMATION THAT CAN BE ACCESSED THROUGH THE WORK VIA HYPERLINK OR OTHERWISE, AND EXPRESSLY DISCLAIM ANY WARRANTY, EXPRESS OR IMPLIED, INCLUDING BUT NOT LIMITED TO IMPLIED WARRANTIES OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE McGraw-Hill Education and its licensors not warrant or guarantee that the functions contained in the work will meet your requirements or that its operation will be uninterrupted or error free Neither McGraw-Hill Education nor its licensors shall be liable to you or anyone else for any inaccuracy, error or omission, regardless of cause, in the work or for any damages resulting therefrom McGraw-Hill Education has no responsibility for the content of any information accessed through the work Under no circumstances shall McGraw-Hill Education and/or its licensors be liable for any indirect, incidental, special, punitive, consequential or similar damages that result from the use of or inability to use the work, even if any of them has been advised of the possibility of such damages This limitation of liability shall apply to any claim or cause whatsoever whether such claim or cause arises in contract, tort or otherwise Contents Contributors vii Preface ix 13 Diagnostic Cardiac Catheterization and Coronary Angiography 117 Jane A Leopold, David P Faxon SECTION I SECTION III Introduction to Cardiovascular Disorders Heart Rhythm Disturbances 14 Principles of Electrophysiology 128 David D Spragg, Gordon F Tomaselli   Basic Biology of the Cardiovascular System Joseph Loscalzo, Peter Libby, Jonathan Epstein 15 The Bradyarrhythmias 137 David D Spragg, Gordon F Tomaselli   Epidemiology of Cardiovascular Disease 20 Thomas A Gaziano, J Michael Gaziano 16 The Tachyarrhythmias 151 Francis Marchlinski   Approach to the Patient with Possible Cardiovascular Disease 28 Joseph Loscalzo SECTION IV Disorders of the heart SECTION II Diagnosis of Cardiovascular Disorders 17 Heart Failure and Cor Pulmonale 182 Douglas L Mann, Murali Chakinala   Chest Discomfort 34 Thomas H Lee 18 Cardiac Transplantation and Prolonged Assisted Circulation 201 Sharon A Hunt, Hari R Mallidi   Dyspnea 42 Richard M Schwartzstein 19 Congenital Heart Disease in the Adult 207 John S Child, Jamil Aboulhosn   Hypoxia and Cyanosis 49 Joseph Loscalzo 20 Valvular Heart Disease 219 Patrick O’Gara, Joseph Loscalzo   Edema 54 Eugene Braunwald, Joseph Loscalzo 21 Cardiomyopathy and Myocarditis 248 Lynne Warner Stevenson, Joseph Loscalzo   Palpitations 61 Joseph Loscalzo 22 Pericardial Disease 273 Eugene Braunwald   Physical Examination of the Cardiovascular System 63 Patrick T O’Gara, Joseph Loscalzo 23 Tumors and Trauma of the Heart 284 Eric H Awtry, Wilson S Colucci 10 Approach to the Patient with a Heart Murmur 76 Patrick T O’Gara, Joseph Loscalzo 24 Cardiac Manifestations of Systemic Disease 289 Eric H Awtry, Wilson S Colucci 11 Electrocardiography 89 Ary L Goldberger 25 Infective Endocarditis 294 Adolf W Karchmer 12 Noninvasive Cardiac Imaging: Echocardiography, Nuclear Cardiology, and MRI/CT Imaging 101 Rick A Nishimura, Panithaya Chareonthaitawee, Matthew Martinez 26 Acute Rheumatic Fever 309 Jonathan R Carapetis 27 Chagas’ Disease 316 Louis V Kirchhoff, Anis Rassi, Jr v Contents vi 28 Cardiogenic Shock and Pulmonary Edema 320 Judith S Hochman, David H Ingbar 38 Diseases of the Aorta 467 Mark A Creager, Joseph Loscalzo 29 Cardiovascular Collapse, Cardiac Arrest, and Sudden Cardiac Death 328 Robert J Myerburg, Agustin Castellanos 39 Vascular Diseases of the Extremities 476 Mark A Creager, Joseph Loscalzo SECTION V Disorders of the vasculature 30 The Pathogenesis, Prevention, and Treatment of Atherosclerosis 340 Peter Libby 31 Disorders of Lipoprotein Metabolism 353 Daniel J Rader, Helen H Hobbs 32 The Metabolic Syndrome 377 Robert H Eckel 33 Ischemic Heart Disease 385 Elliott M Antman, Andrew P Selwyn, Joseph Loscalzo 34 Unstable Angina and Non-ST-Segment Elevation Myocardial Infarction 407 Christopher P Cannon, Eugene Braunwald 40 Pulmonary Hypertension 490 Stuart Rich SECTION VI Cardiovascular Atlases 41 Atlas of Electrocardiography 500 Ary L Goldberger 42 Atlas of Noninvasive Cardiac Imaging 517 Rick A Nishimura, Panithaya Chareonthaitawee, Matthew Martinez 43 Atlas of Cardiac Arrhythmias 526 Ary L Goldberger 44 Atlas of Percutaneous Revascularization 539 Jane A Leopold, Deepak L Bhatt, David P Faxon 35 ST-Segment Elevation Myocardial Infarction 415 Elliott M Antman, Joseph Loscalzo Appendix Laboratory Values of Clinical Importance 549 Alexander Kratz, Michael A Pesce, Robert C Basner, Andrew J Einstein 36 Percutaneous Coronary Interventions and Other Interventional Procedures 434 David P Faxon, Deepak L Bhatt Review and Self-Assessment 575 Charles Wiener, Cynthia D Brown, Anna R Hemnes 37 Hypertensive Vascular Disease 443 Theodore A Kotchen Index 615 CONTRIBUTORS Numbers in brackets refer to the chapter(s) written or cowritten by the contributor UCLA Adult Noninvasive Cardiodiagnostics Laboratory, Ronald Reagan-UCLA Medical Center, Los Angeles, California [19] Jamil Aboulhosn, MD Assistant Professor, Departments of Medicine and Pediatrics, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California [19] Wilson S Colucci, MD Thomas J Ryan Professor of Medicine, Boston University School of Medicine; Chief of Cardiovascular Medicine, Boston Medical Center, Boston, Massachusetts [23, 24] Elliott M Antman, MD Professor of Medicine, Harvard Medical School; Brigham and Women’s Hospital, Boston, Massachusetts [33, 35] Mark A Creager, MD Professor of Medicine, Harvard Medical School; Simon C Fireman Scholar in Cardiovascular Medicine; Director, Vascular Center, Brigham and Women’s Hospital, Boston, Massachusetts [38, 39] Eric H Awtry, MD Assistant Professor of Medicine, Boston University School of Medicine; Inpatient Clinical Director, Section of Cardiology, Boston Medical Center, Boston, Massachusetts [23, 24] Robert H Eckel, MD Professor of Medicine, Division of Endocrinology, Metabolism and Diabetes, Division of Cardiology; Professor of Physiology and Biophysics, Charles A Boettcher, II Chair in Atherosclerosis, University of Colorado School of Medicine, Anschutz Medical Campus, Director Lipid Clinic, University of Colorado Hospital, Aurora, Colorado [32] Robert C Basner, MD Professor of Clinical Medicine, Division of Pulmonary, Allergy, and Critical Care Medicine, Columbia University College of Physicians and Surgeons, New York, New York [Appendix] Deepak L Bhatt, MD, MPH Associate Professor of Medicine, Harvard Medical School; Chief of Cardiology, VA Boston Healthcare System; Director, Integrated Interventional Cardiovascular Program, Brigham and Women’s Hospital and VA Boston Healthcare System; Senior Investigator, TIMI Study Group, Boston, Massachusetts [36, 44] Andrew J Einstein, MD, PhD Assistant Professor of Clinical Medicine, Columbia University College of Physicians and Surgeons; Department of Medicine, Division of Cardiology, Department of Radiology, Columbia University Medical Center and New York-Presbyterian Hospital, New York, New York [Appendix] Eugene Braunwald, MD, MA (Hon), ScD (Hon) FRCP Distinguished Hersey Professor of Medicine, Harvard Medical School; Founding Chairman, TIMI Study Group, Brigham and Women’s Hospital, Boston, Massachusetts [7, 22, 34] Jonathan A Epstein, MD, DTMH William Wikoff Smith Professor of Medicine; Chairman, Department of Cell and Developmental Biology; Scientific Director, Cardiovascular Institute, University of Pennsylvania, Philadelphia, Pennsylvania [1] Cynthia D Brown, MD Assistant Professor of Medicine, Division of Pulmonary and Critical Care Medicine, University of Virginia, Charlottesville, Virginia [Review and Self-Assessment] David P Faxon, MD Senior Lecturer, Harvard Medical School; Vice Chair of Medicine for Strategic Planning, Department of Medicine, Brigham and Women’s Hospital, Boston, Massachusetts [13, 36, 44] Christopher P Cannon, MD Associate Professor of Medicine, Harvard Medical School; Senior Investigator, TIMI Study Group, Brigham and Women’s Hospital, Boston, Massachusetts [34] J Michael Gaziano, MD, MPH Professor of Medicine, Harvard Medical School; Chief, Division of Aging, Brigham and Women’s Hospital; Director, Massachusetts Veterans Epidemiology Center, Boston VA Healthcare System, Boston, Massachusetts [2] Jonathan Carapetis, PhD, MBBS, FRACP, FAFPHM Director, Menzies School of Health Research, Charles Darwin University, Darwin, Australia [26] Agustin Castellanos, MD Professor of Medicine, and Director, Clinical Electrophysiology, Division of Cardiology, University of Miami Miller School of Medicine, Miami, Florida [29] Thomas A Gaziano, MD, MSc Assistant Professor, Harvard Medical School; Assistant Professor, Health Policy and Management, Center for Health Decision Sciences, Harvard School of Public Health; Associate Physician in Cardiovascular Medicine, Department of Cardiology, Brigham and Women’s Hospital, Boston, Massachusetts [2] Murali Chakinala, MD Associate Professor of Medicine, Division of Pulmonary and Critical Care Medicine, Washington University School of Medicine, St Louis, Missouri [17] Panithaya Chareonthaitawee, MD Associate Professor of Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota [12, 42] Ary L Goldberger, MD Professor of Medicine, Harvard Medical School; Wyss Institute for Biologically Inspired Engineering, Harvard University; Beth Israel Deaconess Medical Center, Boston, Massachusetts [11, 41, 43] John S Child, MD, FACC, FAHA, FASE Streisand Professor of Medicine and Cardiology, Geffen School of Medicine, University of California, Los Angeles (UCLA); Director, Ahmanson-UCLA Adult Congenital Heart Disease Center; Director, Anna R Hemnes, MD Assistant Professor, Division of Allergy, Pulmonary, and Critical Care Medicine, Vanderbilt University Medical Center, Nashville, Tennessee [Review and Self-Assessment] vii viii Contributors Helen H Hobbs, MD Professor of Internal Medicine and Molecular Genetics, University of Texas Southwestern Medical Center, Dallas, Texas; Investigator, Howard Hughes Medical Institute, Chevy Chase, Maryland [31] Judith S Hochman, MD Harold Snyder Family Professor of Cardiology; Clinical Chief, Leon Charney Division of Cardiology; Co-Director, NYU-HHC Clinical and Translational Science Institute; Director, Cardiovascular Clinical Research Center, New York University School of Medicine, New York, New York [28] Sharon A Hunt, MD, FACC Professor, Division of Cardiovascular Medicine, Stanford University, Palo Alto, California [18] David H Ingbar, MD Professor of Medicine, Pediatrics, and Physiology; Director, Pulmonary Allergy, Critical Care and Sleep Division, University of Minnesota School of Medicine, Minneapolis, Minnesota [28] Adolf W Karchmer, MD Professor of Medicine, Harvard Medical School; Division of Infectious Diseases, Beth Israel Deaconess Medical Center, Boston, Massachusetts [25] Louis V Kirchhoff, MD, MPH Professor of Internal Medicine (Infectious Diseases) and Epidemiology, Department of Internal Medicine, The University of Iowa, Iowa City, Iowa [27] Theodore A Kotchen, MD Professor Emeritus, Department of Medicine; Associate Dean for Clinical Research, Medical College of Wisconsin, Milwaukee, Wisconsin [37] Alexander Kratz, MD, PhD, MPH Associate Professor of Pathology and Cell Biology, Columbia University College of Physicians and Surgeons; Director, Core Laboratory, Columbia University Medical Center, New York, New York [Appendix] Thomas H Lee, MD, MSc Professor of Medicine, Harvard Medical School; Network President, Partners Healthcare System, Boston, Massachusetts [4] Jane A Leopold, MD Associate Professor of Medicine, Harvard Medical School; Brigham and Women’s Hospital, Boston, Massachusetts [13, 44] Peter Libby, MD Mallinckrodt Professor of Medicine, Harvard Medical School; Chief, Cardiovascular Medicine, Brigham and Women’s Hospital, Boston, Massachusetts [1, 30] Joseph Loscalzo, MD, PhD Hersey Professor of the Theory and Practice of Medicine, Harvard Medical School; Chairman, Department of Medicine; Physician-in-Chief, Brigham and Women’s Hospital, Boston, Massachusetts [1, 3, 6–10, 20, 21, 33, 35, 38, 39] Hari R Mallidi, MD Assistant Professor of Cardiothoracic Surgery; Director of Mechanical Circulatory Support, Stanford University Medical Center, Stanford, California [18] Douglas L Mann, MD Lewin Chair and Chief, Cardiovascular Division; Professor of Medicine, Cell Biology and Physiology, Washington University School of Medicine, St Louis, Missouri [17] Francis Marchlinski, MD Professor of Medicine; Director, Cardiac Electrophysiology, University of Pennsylvania Health System, Philadelphia, Pennsylvania [16] Matthew Martinez, MD Lehigh Valley Physician Group, Lehigh Valley Heart Specialists, Allentown, Pennsylvania [12, 42] Robert J Myerburg, MD Professor, Departments of Medicine and Physiology, Division of Cardiology; AHA Chair in Cardiovascular Research, University of Miami Miller School of Medicine, Miami, Florida [29] Rick A Nishimura, MD, FACC, FACP Judd and Mary Morris Leighton Professor of Cardiovascular Diseases; Professor of Medicine; Consultant, Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota [12, 42] Patrick T O’Gara, MD Professor of Medicine, Harvard Medical School; Director, Clinical Cardiology, Brigham and Women’s Hospital, Boston, Massachusetts [9, 10, 20] Michael A Pesce, PhD Professor Emeritus of Pathology and Cell Biology, Columbia University College of Physicians and Surgeons; Columbia University Medical Center, New York, New York [Appendix] Daniel J Rader, MD Cooper-McClure Professor of Medicine and Pharmacology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania [31] Anis Rassi, Jr., MD, PhD, FACC, FACP, FAHA Scientific Director, Anis Rassi Hospital, Goiânia, Brazil [27] Stuart Rich, MD Professor of Medicine, Department of Medicine, Section of Cardiology, University of Chicago, Chicago, Illinois [40] Richard M Schwartzstein, MD Ellen and Melvin Gordon Professor of Medicine and Medical Education; Associate Chief, Division of Pulmonary, Critical Care, and Sleep Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts [5] Andrew P Selwyn, MD, MBCHB Professor of Medicine, Harvard Medical School; Brigham and Women’s Hospital, Boston, Massachusetts [33] David D Spragg, MD Assistant Professor of Medicine, Johns Hopkins University, Baltimore, Maryland [14, 15] Lynne Warner Stevenson, MD Professor of Medicine, Harvard Medical School; Director, Heart Failure Program, Brigham and Women’s Hospital, Boston, Massachusetts [21] Gordon F Tomaselli, MD Michel Mirowski, MD Professor of Cardiology; Professor of Medicine and Cellular and Molecular Medicine; Chief, Division of Cardiology, Johns Hopkins University, Baltimore, Maryland [14, 15] Charles M Wiener, MD Dean/CEO Perdana University Graduate School of Medicine, Selangor, Malaysia; Professor of Medicine and Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland [Review and Self-Assessment] PREFACE it As knowledge about these complex systems expands, the opportunity for identifying unique therapeutic targets increases, holding great promise for definitive interventions in the future Regenerative medicine is another area of cardiovascular medicine that is rapidly achieving translation Recognition that the adult human heart can repair itself, albeit sparingly with typical injury, and that cardiac precursor (stem) cells reside within the myocardium to this can be expanded, and can be used to repair if not regenerate a normal heart is an exciting advance in the field These concepts represent a completely novel paradigm that will revolutionize the future of the subspecialty In view of the importance of cardiovascular medicine to the field of internal medicine, and the rapidity with which the scientific basis for the discipline is advancing, Harrison’s Cardiovascular Medicine was developed The purpose of this sectional is to provide the readers with a succinct overview of the field of cardiovascular medicine To achieve this goal, Harrison’s Cardiovascular Medicine comprises the key cardiovascular chapters contained in the eighteenth edition of Harrison’s Principles of Internal Medicine, contributed by leading experts in the field This sectional is designed not only for physicians-in-training on cardiology rotations, but also for practicing clinicians, other health care professionals, and medical students who seek to enrich and update their knowledge of this rapidly changing field The editors trust that this book will increase both the readers’ knowledge of the field, and their appreciation for its importance The first section of the book, “Introduction to Cardiovascular Disorders,” provides a systems overview, beginning with the basic biology of the cardiovascular system, followed by epidemiology of cardiovascular disease, and approach to the patient The integration of pathophysiology with clinical management is a hallmark of Harrison’s, and can be found throughout each of the subsequent disease-oriented chapters The book is divided into six main sections that reflect the scope of cardiovascular medicine: (I) Introduction to the Cardiovascular System; (II) Diagnosis of Cardiovascular Disorders; (III) Heart Rhythm Disturbances; (IV) Disorders of the Heart; (V) Disorders of the Vasculature; and (VI) Cardiovascular Atlases Our access to information through web-based journals and databases is remarkably efficient Although these sources of information are invaluable, the daunting body of data creates an even greater need for synthesis by experts in the field Thus, the preparation of these chapters is a special craft that requires the ability to distill Harrison’s Principles of Internal Medicine has been a respected information source for more than 60 years Over time, the traditional textbook has evolved to meet the needs of internists, family physicians, nurses, and other health care providers The growing list of Harrison’s products now includes Harrison’s for the iPad, Harrison’s Manual of Medicine, and Harrison’s Online This book, Harrison’s Cardiovascular Medicine, now in its second edition, is a compilation of chapters related to cardiovascular disorders Our readers consistently note the sophistication of the material in the specialty sections of Harrison’s Our goal was to bring this information to our audience in a more compact and usable form Because the topic is more focused, it is possible to enhance the presentation of the material by enlarging the text and the tables We have also included a Review and Self-Assessment section that includes questions and answers to provoke reflection and to provide additional teaching points Cardiovascular disease is the leading cause of death in the United States, and is rapidly becoming a major cause of death in the developing world Advances in the therapy and prevention of cardiovascular diseases have clearly improved the lives of patients with these common, potentially devastating disorders; yet, the disease prevalence and the risk factor burden for disease (especially obesity in the United States and smoking worldwide) continue to increase globally Cardiovascular medicine is, therefore, of crucial importance to the field of internal medicine Cardiovascular medicine is a large and growing subspecialty, and comprises a number of specific subfields, including coronary heart disease, congenital heart disease, valvular heart disease, cardiovascular imaging, electrophysiology, and interventional cardiology Many of these areas involve novel technologies that facilitate diagnosis and therapy The highly specialized nature of these disciplines within cardiology and the increasing specialization of cardiologists argue for the importance of a broad view of cardiovascular medicine by the internist in helping to guide the patient through illness and the decisions that arise in the course of its treatment The scientific underpinnings of cardiovascular medicine have also been evolving rapidly The molecular pathogenesis and genetic basis for many diseases are now known and, with this knowledge, diagnostics and therapeutics are becoming increasingly individualized Cardiovascular diseases are largely complex phenotypes, and this structural and physiological complexity recapitulates the complex molecular and genetic systems that underlie ix 324 Left heart catheterization and coronary angiography Measurement of LV pressure and definition of the coronary anatomy provide useful information and are indicated in most patients with CS complicating MI Cardiac catheterization should be performed when there is a plan and capability for immediate coronary intervention (see later) or when a definitive diagnosis has not been made by other tests Treatment Acute Myocardial Infarction SECTION IV Disorders of the Heart General Measures  (Fig 28-2) In addition to the usual treatment of acute MI (Chap 35), initial therapy is aimed at maintaining adequate systemic and coronary perfusion by raising systemic BP with vasopressors and adjusting volume status to a level that ensures optimum LV filling pressure There is interpatient variability, but the values that generally are associated with adequate perfusion are systolic BP ∼90 mmHg or mean BP >60 mmHg and PCWP >20 mmHg Hypoxemia and acidosis must be corrected; most patients require ventilatory support with either endotracheal intubation or noninvasive ventilation to correct these abnormalities and reduce the work of breathing (see “Pulmonary Edema,” later) Negative inotropic agents should be discontinued, and the doses of renally cleared medications adjusted Hyperglycemia should be controlled with insulin Bradyarrhythmias may require transvenous pacing Recurrent ventricular tachycardia or rapid atrial fibrillation may require immediate treatment (Chap 16) Vasopressors  Various IV drugs may be used to augment BP and cardiac output in patients with CS All have important disadvantages, and none has been shown to change the outcome in patients with established shock Norepinephrine is a potent vasoconstrictor and inotropic stimulant that is useful for patients with CS As first line of therapy norepinephrine was associated with fewer adverse events, including arrhythmias, compared to a dopamine randomized trial of patients with several eteologies of circulatory shock Although it did not significantly improve survival compared to dopamine, its relative safety suggests that norepinephrine is reasonable as initial vasopressor therapy Norepinephrine should be started at a dose of to μg/min and titrated upward as necessary If systemic perfusion or systolic pressure cannot be maintained at >90 mmHg with a dose of 15 μg/ min, it is unlikely that a further increase will be beneficial Dopamine has varying hemodynamic effects based on the dose; at low doses (≤2 μg/kg per min), it dilates the renal vascular bed, although its outcome benefits at this low dose have not been demonstrated conclusively; at moderate doses (2–10 μg/kg per min), it has positive chronotropic and inotropic effects as a consequence of β-adrenergic receptor stimulation At higher doses, a vasoconstrictor effect results from α-receptor stimulation It is started at an infusion rate of 2–5 μg/kg per min, and the dose is increased every 2–5 to a maximum of 20–50 μg/kg per Dobutamine is a synthetic sympathomimetic amine with positive inotropic action and minimal positive chronotropic activity at low doses (2.5 μg/kg per min) but moderate chronotropic activity at higher doses Although the usual dose is up to 10 μg/kg per min, its vasodilating activity precludes its use when a vasoconstrictor effect is required Aortic Counterpulsation  In CS, mechanical assistance with an intraaortic balloon pumping (IABP) system capable of augmenting both arterial diastolic pressure and cardiac output is helpful in rapidly stabilizing patients A sausage-shaped balloon is introduced percutaneously into the aorta via the femoral artery; the balloon is automatically inflated during early diastole, augmenting coronary blood flow The balloon collapses in early systole, reducing the afterload against which the LV ejects IABP improves hemodynamic status temporarily in most patients In contrast to vasopressors and inotropic agents, myocardial O2 consumption is reduced, ameliorating ischemia IABP is useful as a stabilizing measure in patients with CS before and during cardiac catheterization and percutaneous coronary intervention (PCI) or before urgent surgery IABP is contraindicated if aortic regurgitation is present or aortic dissection is suspected Ventricular assist devices may be considered for eligible young patients with refractory shock as a bridge to cardiac transplantation (Chap 18) The rapid establishment of blood flow in the infarct-related artery is essential in the management of CS and forms the centerpiece of management The randomized SHOCK Trial demonstrated that 132 lives were saved per 1000 patients treated with early revascularization with PCI or coronary artery bypass graft (CABG) compared with initial medical therapy including IABP with fibrinolytics followed by delayed revascularization The benefit is seen across the risk strata and is sustained up to 11 years after an MI Early revascularization with PCI or CABG is a class I recommendation for patients age 35 years of age [1 per 500-1,000] 0.001%/Year High coronary risk profile 30 Post-MI low EF, VT 40 50 60 Age [Years] SCD accounts for approximately one-half the total number of cardiovascular deaths As shown in Fig 29-1B, the very high-risk subgroups provide more focused populations (“percent per year”) for predicting cardiac arrest or SCD, but the representation of such subgroups within the overall population burden of SCD, indicated by the absolute number of events (“events per year”), is relatively small The requirements for achieving a major population impact are effective prevention of underlying diseases and/or new epidemiologic probes that will allow better resolution of specific high-risk subgroups within the large general populations Strategies for predicting and preventing SCD are classified as primary and secondary Primary prevention, as defined in various implantable defibrillator trials, refers to the attempt to identify individual patients at specific Percent 10 0,0 200,0 300,0 00 00 00 Patients (n) which they are derived are presented Approximately 50% of all cardiac deaths are sudden and unexpected The incidence triangle on the left (“Percent / Year”) indicates the approximate percentage of sudden and nonsudden deaths in each of the population subgroups indicated, ranging from the lowest percentage in unselected adult populations (0.1–2% per year) to the highest percentage in patients with VT or VF during convalescence after an MI (approximately 50% per year) The triangle on the right indicates the total number of events per year in each of these groups to reflect incidence in context with the size of the population subgroups The highest risk categories identify the smallest number of total annual events, and the lowest incidence category accounts for the largest number of events per year EF, ejection fraction; VT, ventricular tachycardia; VF, ventricular fibrillation; MI, myocardial infarction (After RJ Myerburg et al: Circulation 85:2, 1992.) risk for SCD and institute preventive strategies Secondary prevention refers to measures taken to prevent recurrent cardiac arrest or death in individuals who have survived a previous cardiac arrest A third category consists of interventions intended to abort sudden cardiac arrests, thus avoiding their progression to death This focuses primarily on out-of-hospital response strategies The primary prevention strategies currently used depend on the magnitude of risk among the various population subgroups Because the annual incidence of SCD among the unselected adult population is limited to 1–2 per 1000 population per year (Fig 29-1) and >30% of all SCDs due to coronary artery disease occur as the first clinical manifestation of the disease (Fig 29-2A), the only currently practical strategies are profiling for risk of developing CHD and risk factor control (Fig 29-2B) The most powerful long-term risk factors include age, cigarette smoking, elevated serum cholesterol, diabetes mellitus, elevated blood pressure, LV hypertrophy, and nonspecific electrocardiographic abnormalities Markers of inflammation (e.g., levels of Cardiovascular Collapse, Cardiac Arrest, and Sudden Cardiac Death Prediction and Prevention of Cardiac Arrest and Sudden Cardiac Death 10 15 20 25 30 CHAPTER 29 Figure 29-1  Panel A demonstrates age-related risk for SCD For the general population age 35 years and older, SCD risk is 0.1–0.2% per year (1 per 500–1000 population) Among the general population of adolescents and adults younger than age 30 years, the overall risk of SCD is per 100,000 population, or 0.001% per year The risk of SCD increases dramatically beyond age 35 years The greatest rate of increase is between 40 and 65 years (vertical axis is discontinuous) Among patients older than 30 years of age, with advanced structural heart disease and markers of high risk for cardiac arrest, the event rate may exceed 25% per year, and age-related risk attenuates (Modified from Myerburg and Castellanos 2008, with permission of publisher.) Panel B demonstrates the incidence of SCD in population subgroups and the relation of total number of events per year to incidence figures Approximations of subgroup incidence figures and the related population pool from B 332 Proportion of Sudden Deaths (%) 100 A 50 40 30 20 10 5-10% Arrhythmic risk markers 7DUJHW ‡$6+'ULVNIDFWRUV ‡$QDWRPLFVFUHHQLQJ ‡&OLQLFDOPDUNHUV ‡7UDQVLHQWULVNSUHGLFWRUV SECTION IV B 7-15% Hemodynamic risk markers ≤20% Acute M.I.; unstable AP ≥30% First clinical event ~33% Known disease; low power or non-specific markers ‡,QGLYLGXDOULVNSUHGLFWRUV ([DPSOHV ‡)UDPLQJKDPULVNLQGH[ ‡&7LPDJLQJ ‡()DQJLRJUDSK\ *RDO ‡3UHGLFWHYROXWLRQRIGLVHDVH ‡,GHQWLI\&$' ‡'HILQHH[WHQWRIGLVHDVH ‡$0(36 ‡+LVWRU\RIKHDUWIDLOXUH ‡(3DQGKHPRG\QDPLFYDULDWLRQV ‡$XWRQRPLFIOXFWXDWLRQV ‡3UHGLFWRUVRILVFKHPLD ‡)DPLOLDOJHQHWLFSURILOHV ‡,GHQWLI\DUUK\WKPLDPDUNHUV ‡'HILQHKLJKULVNVXEJURXSV ‡&OLQLFDOPDUNHUVRILQVWDELOLW\ ‡4XDQWLI\DXWRQRPLFWULJJHUV ‡3UHGLFWXQVWDEOHSODTXHV ‡3UHGLFWVSHFLILF6&'ULVN  EHIRUHGLVHDVHH[SUHVVLRQ 6HQVLWLYLW\ ‡9HU\ORZ ‡0RGHUDWHIRUDQDWRP\ ‡+LJKIRUH[WHQWRIGLVHDVH  YDULDEOHIRUVSHFLILFLW\RIULVN ‡/RZWRLQWHUPHGLDWHIRUVFUHHQLQJ ‡+LJKIRUVSHFLILFJURXSV ‡3ULPDU\SUHGLFWLYHYDOXHXQNQRZQ ‡8QFHUWDLQVRPHPHDVXUHVXVHIXO " ‡8QNQRZQSRWHQWLDOO\KLJK ‡+LJKSRWHQWLDOIRUIXWXUHSURILOLQJ Disorders of the Heart Figure 29-2  Population subsets, risk predictors, and distribution of sudden cardiac deaths (SCDs) according to clinical circumstances A The population subset with high-risk arrhythmia markers in conjunction with low ejection fraction is a group at high risk of SCD but accounts for 95% Continuous electrocardiographic (ECG) recordings fortuitously obtained at the onset of a cardiac arrest commonly demonstrate changes in cardiac electrical activity during the minutes or hours before the event There is a tendency for the heart rate to increase and for advanced grades of PVCs to evolve Most cardiac arrests that are caused by VF begin with a run of nonsustained or sustained VT, which then degenerates into VF The probability of achieving successful resuscitation from cardiac arrest is related to the interval from onset of loss of circulation to institution of resuscitative efforts, the setting in which the event occurs, the mechanism (VF, VT, PEA, asystole), and the clinical status of the patient before the cardiac arrest Return of circulation and survival rates as a result of defibrillation decrease almost linearly from the first minute to 10 After min, survival rates are no better than 25–30% in out-of-hospital settings Those settings in which it is possible to institute prompt cardiopulmonary resuscitation (CPR) followed by prompt defibrillation provide a better chance of a successful outcome However, the CHAPTER 29 Among patients in the acute, convalescent, and chronic phases of myocardial infarction (Chap 35), subgroups at high absolute risk of SCD can be identified During the acute phase, the potential risk of cardiac arrest from onset through the first 48 h may be as high as 15%, emphasizing the importance for patients to respond promptly to the onset of symptoms Those who survive acute-phase VF, however, are not at continuing risk for recurrent cardiac arrest indexed to that event During the convalescent phase after MI (3 days to ∼6 weeks), an episode of sustained ventricular tachycardia (VT) or VF, which is usually associated with a large infarct, predicts a natural history mortality risk of >25% at 12 months At least one-half of the deaths are sudden Aggressive intervention techniques may reduce this incidence After passage into the chronic phase of MI, the longer-term risk for total mortality and SCD mortality is predicted by a number of factors (Fig 29-2B) The most important for both SCD and nonsudden death is the extent of myocardial damage sustained as a result of the acute MI This is measured by the magnitude of reduction of the ejection fraction (EF) and/ or the occurrence of heart failure Various studies have demonstrated that ventricular arrhythmias identified by ambulatory monitoring contribute significantly to this risk, especially in patients with an EF
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