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For technical assistance: email expertconsult.help@elsevier.com call 1-800-401-9962 (inside the US) call +1-314-447-8200 (outside the US) Use of the current edition of the electronic version of this book (eBook) is subject to the terms of the nontransferable, limited license granted on expertconsult.inkling.com Access to the eBook is limited to the first individual who redeems the PIN, located on the inside cover of this book, at expertconsult.inkling.com and may not be transferred to another party by resale, lending or other means Better Together Designed as companions to the bestselling Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine, the Braunwald suite includes titles covering everything from valvular heart disease to lipidology to hypertension, ensuring you’re equipped with all the cardiology resources you need for effective care Visit us.elsevierhealth.com/BraunwaldFamily to shop the entire collection today! The family that keeps families together NEW! NEW! EXPLORE the entire Braunwald family of resources! Heart Failure: A Companion to Braunwald’s Heart Disease, 3rd Edition Mann & Felker 978-1-4557-7237-7 Stay current with recent developments in the field, improved patient management strategies, and new drug therapies and implantable devices that will make a difference in your patients’ lives Diabetes in Cardiovascular Disease: A Companion to Braunwald’s Heart Disease McGuire 978-1-4557-5418-2 This interdisciplinary resource bridges the gap between the cardiology and endocrinology communities of scientists and care providers, and highlights the emerging scientific and clinical topics that are relevant for cardiologists, diabetologists/endocrinologists, and the extended diabetes care team Cardiovascular Intervention: Clinical Lipidology: Bhatt 978-0-323-26219-4 Ballantyne 978-0-323-28786-9 A Companion to Braunwald’s Heart Disease This reference contains focused chapters on how to utilize cutting-edge interventional technologies, with an emphasis on the latest protocols and standards of care Valvular Heart Disease: A Companion to Braunwald’s Heart Disease, 4th Edition Otto & Bonow 978-1-4557-4860-0 Give your patients the most accurate diagnoses, the best possible heart disease treatment options, and the expert care they deserve with this indispensable resource for your everyday practice Vascular Medicine: Hypertension: Creager, Beckman, & Loscalzo 978-1-4377-2930-6 Black & Elliott 978-1-4377-2766-1 A Companion to Braunwald’s Heart Disease, 2nd Edition Make the most of today’s innovative medical therapies, advances in vascular imaging, and new drugs to improve your patients’ cardiovascular health Acute Coronary Syndromes: A Companion to Braunwald’s Heart Disease, 2nd Edition Theroux 978-1-4160-4927-2 Dr Pierre Theroux and his team of expert contributors present advances in diagnostic and imaging techniques, such as biomarkers, nuclear cardiology, echocardiography, and multislice CT; secondary prevention; and new antiplatelet, anti-ischemic, and gene therapies A Companion to Braunwald’s Heart Disease, 2nd Edition This respected cardiology reference covers everything you need to know to effectively manage the chronic problems of your hypertensive patients Preventive Cardiology: A Companion to Braunwald’s Heart Disease Blumenthal, Foody & Wong 978-1-4377-1366-4 Address the prevention and risk stratification of cardiovascular disease so that you can delay the onset of disease and moderate the effects and complications Shop online at us.elsevierhealth.com/BraunwaldFamily A Companion to Braunwald’s Heart Disease, 2nd Edition From basic science to pathogenesis of atherothrombotic disease, this reference offers unparalleled coverage and expert guidance on lipidology in a straightforward, accessible, and user-friendly style Cardiovascular Therapeutics : A Companion to Braunwald’s Heart Disease, 4th Edition Antman 978-1-4557-0101-8 Manage cardiovascular problems more effectively with this comprehensive resource, which addresses pharmacological, interventional, and surgical management approaches for each type of cardiovascular disease Clinical Arrhythmology and Electrophysiology: A Companion to Braunwald’s Heart Disease, 2nd Edition Issa, Miller, & Zipes 978-1-4557-1274-8 With its unique, singular focus on the clinical aspect of cardiac arrhythmias, this title makes it easy to apply today’s most up-to-date guidelines for diagnosis and treatment Mechanical Circulatory Support: A Companion to Braunwald’s Heart Disease Kormos & Miller 978-1-4160-6001-7 Access the clinically relevant information you need to effectively use this therapy to treat and manage end-stage cardiovascular disease BRAUNWALD’S HEART DISEASE REVIEW AND ASSESSMENT This page intentionally left blank BRAUNWALD’S HEART DISEASE REVIEW AND ASSESSMENT 10TH EDITION Leonard S Lilly, MD Professor of Medicine Harvard Medical School Chief, Brigham and Women’s/Faulkner Cardiology Brigham and Women’s Hospital Boston, Massachusetts 1600 John F Kennedy Blvd Ste 1800 Philadelphia, PA 19103-2899 BRAUNWALD’S HEART DISEASE REVIEW AND ASSESSMENT, TENTH EDITION  ISBN: 978-0-323-34134-9 Copyright © 2016 by Elsevier, Inc All rights reserved No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher Details on how to seek permission, and further information about the Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency can be found at our website: www.elsevier.com/permissions This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein) Notices Knowledge and best practice in this field are constantly changing As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility With respect to any drug or pharmaceutical products identified, readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors assume any liability for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein Previous editions copyrighted 2012, 2008, 2006, 2001, 1997, 1992, and 1989 Library of Congress Cataloging-in-Publication Data Braunwald’s heart disease : review and assessment / [edited by] Leonard S Lilly.—Tenth edition    p ; cm   title: Heart disease review and assessment   “Study guide designed to accompany the tenth edition of Braunwald’s heart disease: a textbook of cardiovascular medicine, edited by Dr Douglas Mann, Dr Douglas Zipes, Dr Peter Libby, and Dr Robert Bonow”—Preface   Includes bibliographical references   ISBN 978-0-323-34134-9 (pbk : alk paper)   I.  Lilly, Leonard S., editor.  II.  Braunwald’s heart disease Tenth edition Guide to (work):  III.  Title: Heart disease review and assessment   [DNLM:  1.  Heart Diseases—Examination Questions.  WG 18.2]   RC669.2   616.1′20076—dc23    2015004713 Content Strategist: Dolores Meloni Content Development Specialist: Jennifer Ehlers Publishing Services Manager: Catherine Jackson Senior Project Manager: Rachel E McMullen Design Direction: Xiaopei Chen Printed in the United States of America Last digit is the print number:  9  8  7  6  5  4  3  2  Contributors Marc P Bonaca, MD Cardiovascular Division Brigham and Women’s Hospital Boston, Massachusetts Sections IV and V Fidencio Saldaña, MD Cardiovascular Division Brigham and Women’s Hospital Boston, Massachusetts Section IV Akshay Desai, MD Cardiovascular Division Brigham and Women’s Hospital Boston, Massachusetts Section II Victor Soukoulis, MD, PhD Division of Cardiovascular Medicine University of Virginia Charlottesville, Virginia Section I Neal K Lakdawala, MD Cardiovascular Division Brigham and Women’s Hospital Boston, Massachusetts Section III Garrick Stewart, MD Cardiovascular Division Brigham and Women’s Hospital Boston, Massachusetts Section II Bradley A Maron, MD Cardiovascular Division Brigham and Women’s Hospital; Department of Cardiology Boston VA Healthcare System Boston, Massachusetts Section IV Neil Wimmer, MD Cardiovascular Division Brigham and Women’s Hospital Boston Massachusetts Section III Amy Miller, MD, PhD Cardiovascular Division Brigham and Women’s Hospital Boston, Massachusetts Section I vii This page intentionally left blank 287 BIBLIOGRAPHY ANSWER TO QUESTION 651 C (Braunwald, pp 1905-1906; Fig 87-19) This patient presents with an acute subarachnoid hemorrhage and a markedly abnormal ECG Electrocardiographic abnormalities are present in approximately 70% of patients with subarachnoid hemorrhage and can include ST-segment elevation or depression, deep symmetric T wave inversions as in this patient, and a prolonged QT interval that can lead to torsades de pointes.1 The mechanism of cardiac and electrocardiographic abnormalities in acute brain injury likely relates to autonomic nervous system dysfunction and excessive myocardial catecholamine release.2 In this setting, myocardial damage can occur with release of cardiac biomarkers, without primary acute coronary plaque rupture or thrombus formation The magnitude of peak troponin elevation, but not the degree of electrocardiographic abnormality, is predictive of an adverse cardiac outcome Beta-blockers appear useful in minimizing myocardial damage and controlling arrhythmias in patients with subarachnoid hemorrhage REFERENCES Naidech AM, Kreiter KT, Janjua N, et al: Cardiac troponin elevation, cardiovascular morbidity, and outcome after subarachnoid hemorrhage Circulation 112:2851, 2005 Samuels MA: The brain-heart connection Circulation 116:77, 2007 ANSWER TO QUESTION 652 D (Braunwald, pp 1789-1791) It is generally safe and appropriate to continue most chronically administered cardiac medications up to the day of surgery and to resume them as soon as possible after the operation This is true of beta-blockers in patients with underlying coronary artery disease (or other indications for chronic beta-blocker use) and continuing such therapy perioperatively is a class I American College of Cardiology/American Heart Association guideline recommendation.1 However, there has been controversy about the role of initiating preoperative beta-blocker therapy for the purpose of risk reduction, as summarized in a recent systemic review.2 Conclusions from randomized clinical trials have varied, in part related to methodologic differences in the studies The evidence to date suggests that beta-blockers reduce the perioperative risk of cardiac events (ischemia, atrial fibrillation, need for coronary interventions), but can be associated with bradycardia, hypotension, and stroke, particularly if high doses or longacting preparations are initiated shortly before surgery.3 If initiation of preoperative beta-blocker therapy is planned, it should be started at least 2-7 days before surgery, to assess tolerability and safety, and to allow titration of the dosage if appropriate Thus, current guidelines consider the initiation of a beta-blocker without dose titration immediately before surgery (especially high-dose or long-acting forms) as potentially harmful, and should be avoided (class III indication).1 Although nitrates reduce intraoperative ischemia, cardiac outcomes are not affected Statins have anti-inflammatory and plaque-stabilizing properties, and studies in patients undergoing vascular surgery have demonstrated reduced cardiac event rates in patients on such therapy perioperatively.4 REFERENCES Fleisher LA, Fleischmann KE, Auerbach AD, et al: 2014 ACC/AHA guideline on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines Circulation 130:e278, 2014 Wijeysundera DN, Duncan D, Nkonde-Price C, et al: Perioperative beta blockade in noncardiac surgery: a systematic review for the 2014 ACC/AHA guideline on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines J Am Coll Cardiol 64:2406, 2014 Devereaux PJ, Yang H, Yusuf S, et al: Effects of extended-release metoprolol succinate in patients undergoing non-cardiac surgery (POISE trial): a randomised controlled trial Lancet 371:1839, 2008 Durazzo AE, Machado FS, Ikeoka DT, et al: Reduction in cardiovascular events after vascular surgery with atorvastatin: a randomized trial J Vasc Surg 39:967, 2004 ANSWER TO QUESTION 653 C (Braunwald, pp 1712-1713) Assessment of the heart’s normal aging process is difficult because of the high prevalence of cardiovascular disease in older individuals Studies in which coronary artery disease and other common cardiovascular conditions have been carefully excluded have revealed several pertinent findings First, there is moderate hypertrophy of left ventricular (LV) myocardial cells, probably in response to increased arterial stiffness and loss of cardiac myocyte number with age Although myocardial cells are unable to proliferate, they can increase in size as an adaptive response Despite alterations in contractile proteins leading to reductions in the velocity of contraction and lengthening of contraction and relaxation times, peak contractile force production is maintained at normal levels, and there appear to be no changes in cardiac output, stroke volume, or ejection fraction at rest with normal aging However, there are changes in beta-adrenoceptor–mediated inotropic and chronotropic cardiovascular responses with aging that result from generalized desensitization Thus, the maximal heart rate during exercise and other cardiovascular responses to exercises are blunted Among the cellular and molecular changes that occur with aging, endothelial production of nitric oxide (NO) decreases, likely reflecting a combination of decreased endothelial cell mass (increased cell senescence and apoptosis) and increased NO utilization because of elevated vascular superoxide anion production in older subjects BIBLIOGRAPHY Lakatta E, Wang M, Najjar S: Arterial aging and subclinical arterial disease are fundamentally intertwined at macroscopic and molecular levels Med Clin North Am 93:583, 2009 O’Rourke M, Hashimoto J: Mechanical factors in arterial aging: a clinical perspective J Am Coll Cardiol 50:1, 2007 Cardiovascular Disease in Special Populations; Cardiovascular Disease and Disorders of Other Organs Canto JG, Rogers WJ, Goldberg RJ, et al: Association of age and sex with myocardial infarction symptom presentation and in-hospital mortality JAMA 307:813, 2012 288 ANSWER TO QUESTION 654 CHAPTERS 76 TO 89 V D (Braunwald, p 1213) Deep sternal wound infection is among the most serious complications of cardiac surgery Approximately 1.4% of patients undergoing median sternotomy experience this adverse outcome Such patients present approximately weeks after surgery with fever, leukocytosis, bacteremia, discharge, and erythema at the wound site Risk factors for the development of mediastinal infection include a prolonged cardiopulmonary bypass time, excessive bleeding necessitating reexploration for hemostatic control, the use of both internal mammary arteries, and older age Atrial fibrillation is also a predictor of mediastinitis in patients undergoing coronary artery bypass grafting.1 Obesity is the most important risk factor for sternal dehiscence, whether or not infection is present The incidence of postoperative deep sternal wound infection appears to be decreasing.2 A significant contribution to this reduction is that the rate among diabetics has fallen from about 3.2% to about 1.0% over the past decade, possibly related to the introduction of perioperative intravenous insulin About half of deep sternal wound infections are caused by Staphylococcus species, whereas gram-negative organisms account for about 40% Confirmation of a sternal wound infection often requires surgical exploration and removal of material for Gram stain and culture Imaging techniques, including computed tomography or magnetic resonance imaging are helpful Intravenous antibiotics, with possible débridement and irrigation, may be required for prolonged periods Early diagnosis and initiation of treatment enhance the prognosis Mediastinal infections not seem to change patency rates of the bypass grafts themselves pulmonary veno-occlusive disease or impending left ventricular failure When oral calcium channel blockers are used to treat PAH, high doses are required to achieve full clinical benefit (e.g., amlodipine 20 to 30 mg/day, nifedipine 180 to 240 mg/ day, or diltiazem 720 to 960 mg/day) BIBLIOGRAPHY Galiè N, Corris PA, Frost A, et al: Updated treatment algorithm of pulmonary arterial hypertension J Am Coll Cardiol 62:D60, 2013 ANSWER TO QUESTION 656 C (Braunwald, pp 1912-1914, Fig 88-8) ANSWER TO QUESTION 655 Risk factors for contrast-induced acute kidney injury (CIAKI) include chronic renal insufficiency, diabetic nephropathy, intravascular volume depletion, renal artery stenosis, and concurrent use of agents that alter renal hemodynamics (e.g., angiotensin-converting enzyme inhibitors) The smallest possible volume of contrast agent should be used in patients with renal insufficiency, because the risk of nephrotoxicity is related to the amount injected At present, the intervention that has been demonstrated to consistently reduce the incidence of this complication in patients at risk is intravenous normal saline hydration before and after the procedure A randomized trial of IV isotonic sodium bicarbonate in elective coronary procedures showed no difference in post-procedure CI-AKI compared with IV saline, such that either could be used for hydration Several other agents have been evaluated for prevention of CI-AKI, including mannitol, calcium channel antagonists, dopamine, and atrial natriuretic peptide; however, none has been shown to reduce the risk of renal complications.1 It has been hypothesized that lower ionic strength contrast agents should reduce the incidence of contrast nephropathy Although that has not been demonstrated in patients with normal baseline renal function, the risk of contrast-induced nephropathy is reduced in patients with baseline renal insufficiency (with or without diabetes) if nonionic low-osmolar contrast medium is used Several small studies had suggested that oral administration of N-acetylcysteine, an antioxidant, can reduce the risk of CI-AKI; however, a large randomized trial did not confirm this benefit.2 C (Braunwald, p 1689) REFERENCES REFERENCES Elenbaas TW, Soliman Hamad MA, Schönberger JP, et al: Preoperative atrial fibrillation and elevated C-reactive protein levels as predictors of mediastinitis after coronary artery bypass grafting Ann Thorac Surg 89:704, 2010 Matros E, Aranki SF, Bayer LR, et al: Reduction in incidence of deep sternal wound infections: random or real? J Thorac Cardiovasc Surg 139:680, 2010 Cardiac catheterization plays an important role in patients with suspected pulmonary arterial hypertension (PAH), to confirm the diagnosis, establish the severity of disease, and determine prognosis Patients with PAH demonstrate a normal or low pulmonary capillary wedge pressure (PCWP), distinguishing PAH from pulmonary venous hypertension A vasodilator challenge during catheterization allows assessment of pulmonary vasoreactivity and helps to guide therapy Such a challenge can be accomplished with intravenous adenosine, intravenous epoprostenol, or inhaled nitric oxide A favorable acute effect of these vasodilators (i.e., >10 mm Hg decrease in mean PAP and/or >33% decrease in pulmonary vascular resistance) without adverse effects (e.g., a decline in cardiac output or systemic blood pressure, or a rise in PCWP) is predictive of a favorable response to oral calcium channel blockers An increase in PCWP during vasodilator testing would be consistent with James MT, Samuel SM, Manning MA, et al: Contrast-induced acute kidney injury and risk of adverse clinical outcomes after coronary angiography: a systematic review and meta-analysis Circ Cardiovasc Interv 6:37, 2013 ACT Investigators: Acetylcysteine for prevention of renal outcomes in patients undergoing coronary and peripheral vascular angiography: main results from the randomized Acetylcysteine for Contrastinduced nephropathy Trial (ACT) Circulation 124:11, 2011 ANSWER TO QUESTION 657 A (Braunwald, pp 1802-1803; Table 81-4) The major cardiovascular changes that occur in hypothyroidism include a reduction in cardiac contractility, an increase in systemic vascular resistance, and a slowing of the heart rate The decreased cardiac contractility and 289 BIBLIOGRAPHY Klein I: The cardiovascular system in hypothyroidism In Braverman LE, Cooper DS, editors: Werner & Ingbar’s the thyroid: a fundamental and clinical text, ed 10, Philadelphia, 2012, Lippincott, Williams & Wilkins, pp 575 Rodondi N, Bauer DC, Cappola AR: Subclinical thyroid dysfunction, cardiac function, and the risk of heart failure The Cardiovascular Health study J Am Coll Cardiol 52:1152, 2008 ANSWER TO QUESTION 658 C (Braunwald, pp 1282-1287, 1308; see also Answer to Question 67) Marfan syndrome, caused by mutations in the fibrillin gene (FBN1), is associated with significant morbidity and mortality from cardiovascular causes The most life-threatening complication is aortic dissection Patients with Marfan syndrome are predisposed to this complication because of aortic cystic medial degeneration, and such dissections usually commence just above the coronary ostia and may extend into the entire length of the aorta Beta-blockers limit aortic shear stress and are an important component of prevention Prospective studies have confirmed a slowing of aortic dilatation and reduced risk of dissection in patients treated with atenolol or propranolol For hypertensive patients, an angiotensin receptor blocker should also be considered, based on animal studies showing a beneficial effect at slowing progression of aortic enlargement, presumably through effects on TGF-β signaling The dimension of the proximal aorta can be followed serially by transthoracic echocardiography, computed tomography, or magnetic resonance imaging Prophylactic aortic root replacement is recommended in Marfan syndrome patients once the diameter approaches 5 cm to prevent dissection and progressive aortic regurgitation.1 Some groups recommend replacement even earlier, when the diameter is in the 4.5- to 5.0-cm range Aortic dissection is an unfortunate potential complication of pregnancy in Marfan syndrome, occurring most commonly between the third trimester and the first month postpartum The risk of dissection in this setting is related to the size of the aortic root and appears to be low in patients with root diameters of ≤4 cm.2 Progressive valvular impairments are also common in patients with Marfan syndrome The risk of severe aortic regurgitation increases as the diameter of the aortic root enlarges Mitral valve prolapse, associated with elongated and redundant leaflets, is detected in 60% to 80% of patients by echocardiography.3 Progression to severe mitral regurgitation occurs in up to 25% of patients REFERENCES Hiratzka LF, Bakris GL, Beckman JA, et al: 2010 guidelines for the diagnosis and management of patients with thoracic aortic disease: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, American Association for Thoracic Surgery, American College of Radiology, American Stroke Association, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of Thoracic Surgeons, and Society for Vascular Medicine Circulation 121:e266, 2010 Goland S, Elkayam U: Cardiovascular problems in pregnant women with Marfan syndrome Circulation 119:619, 2009 Weyman AE, Scherrer-Crosbie M: Marfan syndrome and mitral valve prolapse J Clin Invest 114:1543, 2004 ANSWER TO QUESTION 659 B (Braunwald, p 1824) This patient has heparin-induced thrombocytopenia (HIT), of which there are two forms Type I HIT is the common, milder form that likely results from non–immune-mediated heparin-induced aggregation of platelets Platelet counts usually drop within days of therapy but rarely fall below 100,000/µL, and patients not often develop bleeding complications In the majority of such cases, heparin can be continued and the platelet count will improve Type II HIT, which has developed in the patient presented in this question, is the more dangerous form It produces more severe thrombocytopenia, with levels often 4 METS of activity) without stopping or experiencing anginal symptoms, most surgical procedures will be well tolerated and no additional preoperative cardiac testing is typically necessary Conversely, a patient who develops shortness of breath or chest discomfort with only minor exertion is at high risk for postoperative cardiac events and warrants additional cardiac testing, especially if more than a minor surgical procedure is planned Historically, the cardiac risk of noncardiac surgery in patients with prior myocardial infarction (MI) has related inversely to the length of time that has passed since the acute coronary event Studies from the 1970s concluded that purely elective surgery should be delayed for months after an MI to ensure that cardiovascular risk had returned to baseline In those studies, the risk of reinfarction or death was approximately 30% when patients were operated on within months of an MI, but only 5% when months had elapsed before the operation Later studies, in the era of careful perioperative monitoring, demonstrated much lower cardiac complication rates: about a 6% risk of reinfarction for operations performed within months of an MI and a 2% risk for operations performed within to months These historic risks are less relevant today in the era of early revascularization (mechanical or fibrinolytic) and aggressive postevent pharmacologic therapy for acute coronary syndromes (ACS) Current guidelines suggest that the highest risk of elective surgery for such patients is limited to the first 30 days after an ACS, as disrupted coronary plaque and myocardium heal BIBLIOGRAPHY Fleisher LA, Fleischmann KE, Auerbach AD, et  al: 2014 ACC/AHA guideline on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines Circulation 130:e278, 2014 Gupta PK, Gupta H, Sundaram A, et al: Development and validation of a risk calculator for prediction of cardiac risk after surgery Circulation 124:381, 2011 ANSWER TO QUESTION 669 C (Braunwald, pp 1762-1763; see also Answer to Question 636) The presentation of this patient is most consistent with peripartum cardiomyopathy This disorder is a form of dilated cardiomyopathy that manifests in the last trimester of pregnancy or in the early postpartum period.1 The etiology is unknown, and there are no diagnostic tests to confirm the diagnosis Its incidence is higher in women >the age of 30, in twin pregnancies, in multiparous women, and in African Americans The prognosis of this disorder is favorable compared with other forms of dilated cardiomyopathy, with 50% to 60% of patients showing marked improvement or complete recovery within months postpartum The remainder either stabilizes with reduced cardiac function or declines progressively, eventually requiring cardiac transplantation The predictors for a poor outcome include older age, higher parity, severe left ventricular dilatation, and onset of symptoms later after delivery There is a high risk of relapse of peripartum cardiomyopathy in subsequent pregnancies, and that risk appears to be greatest in women who have persistently impaired cardiac function 293 REFERENCE ANSWERS TO QUESTIONS 670 TO 674 670–E, 671–D, 672–B, 673–C, 674–A (Braunwald, pp 1846-1847, 1855, 1856, 1858) The spondyloarthropathies, including ankylosing spondylitis, Reiter syndrome, and psoriatic arthritis, have a predilection for arthritis of the sacroiliac and lumbosacral joints These diseases are associated with the histocompatibility antigen HLA-B27 and occur predominantly in men Ankylosing spondylitis is the most common of these syndromes to involve the heart and classically causes dilatation of the aortic valve ring with fibrous thickening and inflammation.1 The aorta in ankylosing spondylitis is histologically similar to that in syphilitic aortitis, including adventitial scarring, intimal proliferation, and narrowing of the vasa vasorum Aortic regurgitation results from thickening of the valvular cusps and dilatation of the aortic root.2 Conduction system disorders, due to fibrous infiltration in the atrioventricular node and the bundle of His, may be seen in ankylosing spondylitis as well Reiter syndrome is a form of nonpurulent, reactive arthritis that may follow enteric or urogenital infections It is frequently associated with uveitis/conjunctivitis and nongonococcal urethritis The cardiac complications of Reiter syndrome are similar to those of ankylosing spondylitis Cardiac abnormalities in patients with systemic sclerosis/ scleroderma often relate to systemic or pulmonary hypertension, but may also include myocardial fibrosis and contraction band necrosis, causing diastolic and/or systolic ventricular function Symptomatic pericarditis occurs in 7% to 20% of patients Conduction defects and thickening of the mitral and aortic valves may also occur.3 Giant cell arteritis predominantly causes inflammation of the aorta, its major branches, and coronary arteries Weakening of the vessels may lead to dilatation, aneurysm formation, and valvular insufficiency The vascular pathology often reveals granuloma formation Behỗet syndrome is a multisystem disorder highlighted by recurrent oral and genital ulcers and uveitis The ulcers are often painful and necrotic, and eye involvement occasionally progresses to blindness The etiology of the disease is unclear but appears to involve endothelial activation as a mediator of vascular inflammation Venous and arterial thrombosis may occur, as well as aneurysm formation of the large vessels Diffuse aortitis in Behỗet syndrome can lead to aortic root dilatation and valvular insufficiency.4 REFERENCES Bodnar N, Kerekes G, Seres I, et al: Assessment of subclinical vascular disease associated with ankylosing spondylitis J Rheumatol 38:723, 2011 Huffer LL, Furgerson JL: Aortic root dilatation with sinus of Valsalva and coronary artery aneurysms associated with ankylosing spondylitis Tex Heart Inst J 33:70, 2006 Steen V: The heart in systemic sclerosis Curr Rheumatol Rep 6:137, 2004 Tsui KL, Lee KW, Chan WK, et al: Behcet’s aortitis and aortic regurgitation: a report of two cases J Am Soc Echocardiogr 17:83, 2004 ANSWERS TO QUESTIONS 675 TO 678 675–C, 676–B, 677–D, 678–A (Braunwald, pp 688, 692, 961, 1821, 1824) Numerous cardiac medications can cause adverse effects For example, heparin can result in thrombocytopenia by two main mechanisms as described in the Answer to Question 659 A positive direct Coombs test is seen in up to 10% of patients who receive alpha-methyldopa, an antihypertensive that is sometimes used in pregnancy In these patients, IgG antibody is directed against the Rh complex of red cells Hemolysis may be severe but improves within several weeks after cessation of the medication The most common side effects of ticagrelor, a platelet P2Y12 receptor inhibitor, are bleeding, dyspnea (~15% of patients in the PLATO trial1), and ventricular pauses, which are typically asymptomatic Dyspnea, when present, usually occurs soon after initiating therapy and is self-limited The mechanism is unknown Procainamide may cause a syndrome resembling systemic lupus erythematosus (SLE) Symptoms consist of polyarthralgias, pleuritis, and photosensitive rashes Unlike conventional SLE, nephritis and central nervous system complications are very rare Patients with drug-induced lupus are antinuclear antibody (ANA) positive with antibodies to histones but rarely display hypocomplementemia or antibodies to DNA Discontinuation of procainamide typically results in improvement of symptoms within a few days to weeks However, ANA levels may remain elevated for years REFERENCE Storey RF, Becher RC, Harrington RA, et al: Characterization of dyspnoea in PLATO study patients treated with ticagrelor or clopidogrel and its association with clinical outcomes Eur Heart J 32:2945, 2011 ANSWERS TO QUESTIONS 679 TO 683 679–C, 680–A, 681–B, 682–B, 683–C (Braunwald, pp 1846-1849; see also Answers to Question 632 and Question 633) Takayasu arteritis, also termed pulseless disease, is of unknown etiology and is characterized by marked fibrous and degenerative scarring of the elastic fibers of the vascular media It most commonly involves the aorta and carotid arteries The disease is 10 times more common in women than in men, and in most patients onset occurs during the teen years.1 Patients typically present with malaise, weight loss, night sweats, arthralgias, pleuritic pain, anorexia, and fatigue Regardless of whether a patient goes through this initial phase, after a latent period symptoms and signs referable to the obliterative and inflammatory changes in affected blood vessels begin to appear These include diminished or absent pulses with claudication (upper extremities > lower extremities), hypertension (related to renal artery stenosis or increased vessel rigidity), and aortic root aneurysms with aortic regurgitation Common laboratory abnormalities include elevated sedimentation rate, low-grade leukocytosis, and normocytic anemia Treatment includes glucocorticoid therapy Patients Cardiovascular Disease in Special Populations; Cardiovascular Disease and Disorders of Other Organs Blauwet LA, Cooper LT: Diagnosis and management of peripartum cardiomyopathy Heart 97:1070, 2011 294 with refractory symptoms may respond to the addition of CHAPTERS 76 TO 89 V cyclophosphamide Recent studies have shown beneficial effects of tumor necrosis factor antagonists.2 Giant cell arteritis (GCA; also termed temporal arteritis) is a disease of unknown etiology characterized by granulomatous inflammation of large- to medium-caliber arteries with a special predilection for the vessels of the head and neck.3 It arises primarily in elderly people with a female predominance Clinically, the triad of severe headache, fever, and marked malaise characterizes the illness The headaches are often severe and are typically localized over involved temporal arteries Claudication of the jaw muscles during chewing is present in up to two thirds of patients Involvement of the ophthalmic artery leads to visual symptoms and may result in irreversible blindness The syndrome of polymyalgia rheumatica, consisting of diffuse muscular aching and stiffness, occurs in about 40% of patients with giant cell arteritis In a minority of cases, involvement of the aorta or its major branches may lead to symptoms and signs similar to those of Takayasu arteritis, although renal artery involvement is rare in GCA Patients with giant cell arteritis appear ill and are almost always febrile Affected vessels feel abnormal to palpation and are tender, allowing experienced examiners to make the diagnosis of temporal arteritis at the bedside by identifying an indurated, beaded, tender temporal artery Laboratory tests often reveal a very high sedimentation rate, normochromic, normocytic anemia, and elevated acutephase reactants Biopsy of an involved temporal artery confirms the diagnosis Management of giant cell arteritis includes early intervention with high-dose steroid therapy (60 to 80  mg of prednisone per day) followed by a gradual taper to a maintenance dose, which is typically continued for to years Early administration of steroid therapy is crucial to the prevention of involvement of the ophthalmic arteries and possible blindness REFERENCES Keenan NG, Mason JC, Maceira A, et al: Integrated cardiac and vascular assessment in Takayasu arteritis by cardiovascular magnetic resonance Arthritis Rheum 60:3501, 2009 Mason JC: Takayasu arteritis—advances in diagnosis and management Nat Rev Rheumatol 6:406, 2010 Weyand CM, Goronzy JJ: Medium and large vessel vasculitis N Engl J Med 349:160, 2003 ANSWERS TO QUESTIONS 684 TO 688 684–C, 685–A, 686–B, 687–D, 688–E (Braunwald, pp 1613-1617; Table 69-1) Several chemotherapeutic agents have potential cardiovascular toxicities The anthracyclines (e.g., doxorubicin, daunorubicin, and idarubicin) may cause acute cardiac effects (including atrial and ventricular arrhythmias and pericardial effusion) or more chronic impairment (dilated cardiomyopathy with congestive heart failure) As described in the Answer to Question 544, heart failure due to anthracycline therapy is dose related and develops more frequently when concurrent risk factors are present, including prior heart disease, radiation therapy exposure to the heart, and use of other cardiotoxic chemotherapeutic agents (e.g., trastuzumab, paclitaxel) Patients receiving 5-fluorouracil may experience acute chest pain and myocardial infarction during or immediately after infusion The mechanism of this adverse effect is unknown Cyclophosphamide and ifosfamide are alkylating agents that can cause an acute hemorrhagic myoperi­ carditis Interleukins, which are potent modulators of the immune system, are associated with capillary leak syndrome, hypotension, noncardiogenic pulmonary edema, and nephrotoxicity Sunitinib is a tyrosine kinase inhibitor that targets vascular endothelial cell growth factor receptors and is used to inhibit progression of renal cell carcinoma and gastrointestinal stromal tumors Hypertension is a common side effect, with marked elevation in blood pressure in 8% to 20% of patients BIBLIOGRAPHY Lal H, Kolaja KL, Force T: Cancer genetics and the cardiotoxicity of the therapeutics J Am Coll Cardiol 61:267, 2013 Senkus E, Jassem J: Cardiovascular effects of systemic cancer treatment Cancer Treat Rev 37:300, 2011 ANSWERS TO QUESTIONS 689 TO 693 689–C, 690–D, 691–E, 692–A, 693–B (Braunwald, pp 1795-1804) Endocrine disorders often have cardiovascular manifestations Excess thyroid hormone levels result in tachycardia, palpitations, and hypertension, often with a widened pulse pressure.1 Cardiac examination reveals a hyperdynamic impulse with an accentuated S1 Systolic murmurs are common, and a Means-Lerman scratch, a grating systolic sound at the upper left sternal border, may be auscultated during expiration The cardiovascular manifestations of hypothyroidism include bradycardia, diastolic hypertension with a narrowed pulse pressure, cardiomegaly with a reduced ejection fraction, and pericardial effusion, which only rarely results in tamponade physiology.1 Cushing syndrome is associated with accelerated atherosclerosis, likely related to hypertension and hyperglycemia in this condition Carney complex is a genetic syndrome that includes Cushing syndrome, cardiac myxomas, and pigmented dermal lesions This autosomal dominant syndrome arises most commonly from mutations in the PRKAR1A gene, which encodes a regulatory subunit of protein kinase A.2 Hyperaldosteronism is associated with excess aldosterone production from an adrenal or extra-adrenal source Hypertension, hypokalemia, and metabolic alkalosis are common findings.3 Many of the cardiac findings are nonspecific and are a consequence of the metabolic and electrolyte abnormalities For example, U waves and ventricular arrhythmias result from associated hypokalemia Parathyroid hormone has direct inotropic and chronotropic effects on the heart, likely due to increased myocyte calcium entry.4 Hypercalcemia associated with hyper­ parathyroidism may result in excess calcium deposition in the heart, hypertension, and shortening of the QT interval REFERENCES Klein I, Danzi S: Thyroid disease and the heart Circulation 116:1725, 2007 295 ANSWERS TO QUESTIONS 694 TO 697 694–B, 695–C, 696–D, 697–A (Braunwald, pp 1830-1832) Tissue-type plasminogen activator (tPA), the major physiologic activator of plasminogen, is both synthesized naturally by endothelial cells and produced commercially by recombinant DNA technology for the purpose of therapeutic fibrinolysis The protein is synthesized in a single-chain form, which is subsequently converted to a two-chain form by proteolytic cleavage of a single plasmin-sensitive site Both the single-chain and the two-chain forms have endogenous proteolytic activity The alpha chain of tPA is derived from the amino-terminal portion of single-chain tPA and contains a pair of finger-like structures referred to as “kringle” domains Lysine binding sites located on these domains confer binding specifically for fibrin As a result, tPA is a relatively fibrin-specific activator that converts plasminogen to plasmin two or three times more efficiently in the presence of fibrin The protease domain of tPA contains a proteolytic site responsible for this conversion This portion is homologous with other serine proteases, such as urokinase and trypsin Urokinase is a two-chain serine protease that is synthesized in both renal tubular epithelial cells and endothelial cells While urokinase converts plasminogen to plasmin by hydrolyzing the same bond as that acted on by tPA, the proteolytic activity of urokinase is not enhanced by the presence of fibrin Therefore, urokinase may activate circulating plasminogen as effectively as plasminogen absorbed onto fibrin thrombi Streptokinase is a single polypeptide chain of 414 amino acids that is produced by a strain of hemolytic streptococci Streptokinase does not cause thrombolysis by intrinsic enzymatic activity Instead, it activates the fibrinolytic system by combining with plasminogen to form a plasminogen activator complex that is then capable of converting plasminogen to plasmin Plasmin then degrades fibrin and other procoagulant proteins Many individuals have circulating antibodies to streptokinase as a result of previous streptococcal infections Therefore, a large dose of streptokinase is administered to neutralize these antibodies Antistreptococcal antibodies may remain high up to months after administration Tenecteplase is a genetically engineered mutant form of tPA that displays a prolonged half-life and increased fibrin specificity Unlike tPA, which requires a continuous infusion, tenecteplase is injected as a single intravenous bolus, which facilitates administration ANSWERS TO QUESTIONS 698 TO 702 698–A, 699–B, 700–D, 701–C, 702–A (Braunwald, pp 1822-1826) Unfractionated heparin (UFH) is a naturally occurring compound that acts in vivo by combining with antithrombin (an inhibitor of thrombin and factors X, IX, and XI) The conformational change that occurs in antithrombin allows for an accelerated interaction with the activated clotting factors, limiting thrombin generation and fibrin formation Commercial heparin is extracted from porcine intestinal mucosa and bovine lung and does not inactivate clot-bound thrombin or factor VII Heparin is not absorbed by the gastrointestinal tract and is therefore administered in intravenous or subcutaneous forms The bioavailability of subcutaneous injections of UFH is only 30% The activated partial thromboplastin time (aPTT) test is used to determine the inhibitory effect of UFH For acute thrombosis or embolism, intravenous heparin is administered with a goal aPTT of 1.5 to times the control value Subcutaneous UFH is often used for patients who require a lower level of anticoagulation Heparin therapy’s major complication is bleeding There is up to a 30% incidence of heparin-induced thrombocytopenia that may be associated with thromboembolic events and often resolves with discontinuation of the drug (see Answer to Question 659) In addition, heparin may cause osteoporosis, elevated liver enzymes, increased vascular permeability, alopecia, and hypoaldosteronism (and associated hyperkalemia) Low-molecular-weight heparin (LMWH) also produces an anticoagulant effect by binding to antithrombin However, in distinction to UFH, LMWH preferentially inhibits factor Xa more than thrombin LMWH formulations bind less with platelet factor 4, plasma proteins, and endothelial cells, and therefore have >90% bioavailability when administered by subcutaneous injection Other advantages of LMWH include a prolonged half-life and predictable anticoagulant responses (Table 5-6) Patients receiving LMWH not require serial laboratory monitoring to monitor the anticoagulant effect, except those with renal failure, extreme obesity, or pregnancy Heparin-induced thrombocytopenia can occur with LMWH but is less common than with UFH BIBLIOGRAPHY Garcia DA, Baglin TP, Weitz JL, et al: Parenteral anticoagulants: Antithrombotic Therapy and Prevention of Thrombosis, ed 9: American College of Chest Physicians Evidence-based Clinical Practie Guidelines Chest 141:e24S, 2012 TABLE 5-6  Advantages of Low-Molecular-Weight Heparin and Fondaparinux over Heparin ADVANTAGE CONSEQUENCE Better bioavailability and longer half-life after subcutaneous injection Can be given subcutaneously once or twice daily for both prophylaxis and treatment Dose-independent clearance Simplified dosing Predictable anticoagulant response Monitoring of coagulation is unnecessary in most patients BIBLIOGRAPHY Lower risk for HIT Longstaff C, William S, Thelwell C: Fibrin binding and the regulation of plasminogen activators during thrombolytic therapy Cardiovasc Hematol Agents Med Chem 6:212, 2008 Safer than heparin for short- or long-term administration Lower risk for osteoporosis Safer than heparin for long-term administration Cardiovascular Disease in Special Populations; Cardiovascular Disease and Disorders of Other Organs Vezzosi D, Vignaux O, Dupin N, et al: Carney complex: clinical and genetic 2010 update Ann Endocrinol 6:486, 2010 Stowasser M: Primary aldosteronism in 2011: towards a better understanding of causation and consequences Nat Rev Endocrinol 8:70, 2011 Andersson P, Rydberg E, Willenheimer R: Primary hyperparathyroidism and heart disease: a review Eur Heart J 25:1776, 2004 296 ANSWERS TO QUESTIONS 703 TO 706 CHAPTERS 76 TO 89 V 703–D, 704–B, 705–A, 706–C (Braunwald, pp 1844-1845, 1846-1847, 1853, 1854, 1856, 1858-1859; see also Answers to Questions 670 to 674) Rheumatologic disorders often involve the cardiovascular system and can result in pericardial, myocardial, valvular, or arterial abnormalities Aortic involvement is estimated to occur in 15% of patients with giant cell arteritis Inflammation often involves the proximal aorta and aortic valve cusps, resulting in dilatation of the vessel and aortic regurgitation.1 Other rheumatologic diseases that prominently involve the aorta include ankylosing spondylitis and psoriatic arthritis Valvular abnormalities are found by transesophageal echocardiography in 50% of patients with systemic lupus erythematosus.2 The most common involvement, termed Libman-Sacks endocarditis, represents noninfectious valve thickening, usually on the atrial side of the mitral valve and the arterial side of the aortic valve Over time, fibrosis may result in valvular insufficiency Much less commonly, the vegetations may occlude the valve orifice, causing stenosis Clinical manifestations of Libman-Sacks lesions, such as infective endocarditis or peripheral embolism, are rare.2 Although pulmonary hypertension can develop in many rheumatologic disorders, it is a particularly prominent feature of scleroderma and is one of the leading causes of morbidity and mortality in that condition.3 Behỗet disease typically results in inflammation of the thoracic aorta and branch vessels, leading to stenoses and aneurysmal dilatation of the subclavian and carotid arteries.4 Thoracic and abdominal aortic aneurysms may also result REFERENCES Weyand CM, Goronzy JJ: Medium and large vessel vasculitis N Engl J Med 349:160, 2003 Perez-Villa F, Font J, Azqueta M, et al: Severe valvular regurgitation and antiphospholipid antibodies in systemic lupus erythematosus: a prospective, long-term follow-up study Arthritis Rheum 53:460, 2005 McMahan ZH, Hummers LK: Systemic sclerosis—challenges for clinical practice Nat Rev Rheumatol 9:90, 2013 Ambrose NL, Haskard DO: Differential diagnosis and management of Behỗet syndrome Nat Rev Rheumatol 9:79, 2013 This page intentionally left blank This page intentionally left blank This page intentionally left blank This page intentionally left blank Smarter search Faster answers Smarter, Faster Search for Better Patient Care Unlike a conventional search engine, ClinicalKey is specifically designed to serve doctors by providing 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Visit ClinicalKey.com for more information and subscription options ... clinically relevant information you need to effectively use this therapy to treat and manage end-stage cardiovascular disease BRAUNWALD’S HEART DISEASE REVIEW AND ASSESSMENT This page intentionally... nuclear scintigraphy or echocardiography? A A 53-year-old woman with hypertension and left ventricular hypertrophy by echocardiography who has developed exertional chest pressure B A 74-year-old man... cm   title: Heart disease review and assessment   “Study guide designed to accompany the tenth edition of Braunwald’s heart disease: a textbook of cardiovascular medicine, edited by Dr Douglas
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Xem thêm: Braunwalds heart disease review and assessment khotailieu y hoc , Braunwalds heart disease review and assessment khotailieu y hoc , 130–D, 131–A, 132–C, 133–B (Braunwald, pp. 133-135, 146-147, 1638-1639, 1687), 291–A, 292–C, 293–B, 294–B (Braunwald, pp. 463-464, 469; Figure 22-8), D (Braunwald, pp. 982, 989; Table 45-2), B (Braunwald, pp. 1106, 1246; see also Answer to Question 331), C (Braunwald, p. 1296; see also Answer to Question 352), 432–A, 433–A, 434–C, 435–B (Braunwald, pp. 988, 989-990; Table 45-4), B (Braunwald, pp. 1407-1412; see also Answer to Question 444), A (Braunwald, p. 1689; Table 74-3), A (Braunwald, pp. 1570-1571; see also Answer to Question 451), D (Braunwald, pp. 1474-1477; see also Answer to Question 522), D (Braunwald, pp. 1446-1458; see also Answer to Question 507), 625–A, 626–A, 627–B, 628–B, 629–D (Braunwald, pp. 1613-1615, 1620-1621), 703–D, 704–B, 705–A, 706–C (Braunwald, pp. 1844-1845, 1846-1847, 1853, 1854, 1856, 1858-1859; see also Answers to Questions 670 to 674)

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