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Risk Stratification and Role of Implantable Defibrillators for Prevention of Sudden Death in Patients with Hypertrophic Cardiomyopathy Barry J

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Risk Stratification and Role of Implantable Defibrillators for Prevention of Sudden Death in Patients with Hypertrophic Cardiomyopathy Barry J Circulation Journal REVIEW Official Journal of the Japanese Circulation Society http://www.j-circ.or.jp Risk Stratification and Role of Implantable Defibrillators for Prevention of Sudden Death in Patients With Hypertrophic Cardiomyopathy Barry J. Maron, MD Hypertrophic cardiomyopathy (HCM) is the most common cause of sudden cardiac death (SCD) in young peo- ple, including trained athletes. It is now 30 years since the introduction of implantable cardioverter-defibrillators (ICDs) to clinical cardiovascular practice and coronary artery disease, and now device therapy represents the most significant therapeutic innovation and the only definitive strategy for prolonging the life of HCM patients. ICDs have proved effective in preventing SCD in young HCM patients with appropriate intervention rates of 11% for secondary and 4% for primary prevention, despite massive left ventricular (LV) hypertrophy, LV outflow obstruc- tion, diastolic dysfunction or microvascular ischemia. Targeting candidates for prophylactic ICD therapy can be complex, compounded by the unpredictability of the arrhythmogenic substrate, the absence of a dominant risk factor, and difficulty in assembling randomized trials. However, a single major risk factor is often sufficient to justify an ICD, although additional markers and other disease features can resolve ambiguous decision-making. Nevertheless, the absence of all risk factors does not convey absolute immunity to SCD. The current risk factor algorithm, when combined with a measure of individual physician judgment (and patient autonomy considerations), is an effective guide to identifying high-risk HCM patients. ICDs have altered the natural history of HCM for many patients and provided an opportunity to achieve many decades of productive life, and the potential for normal or near-normal longevity. Indeed, prevention of SCD has now become a new paradigm in the management of HCM. (Circ J 2010; 74: 2271 – 2282) Key Words: Defibrillation; Hypertrophic cardiomyopathy; Implantable cardioverter-defibrillator (ICD); Sudden cardiac death isk of sudden cardiac death (SCD) in patients with be superior to conventional antiarrhythmic drugs, for second- hypertrophic cardiomyopathy (HCM) has been rec- ary and primary SCD prevention in high-risk patients with R ognized since the initial contemporary description CAD or nonischemic cardiomyopathy.19 of the disease 50 years ago.1–7 SCD is the most visible and devastating complication of HCM,4–7 but it is only in the ICD in HCM past 10 years that the aspiration to prevent SCD has been In their seminal 1980 paper, Mirowski et al reported 3 pa- realized with the systematic use of implantable cardioverter- tients at exceptionally high risk for SCD after surviving 2 or defibrillators (ICDs) in high-risk HCM patients.8–17 Indeed, more cardiac arrests.18 In the laboratory, the implanted de- SCD prevention represents a turning point in the management fibrillator operated spontaneously and automatically to abort of HCM, by altering the natural history of the disease.8–10 ventricular fibrillation (VF). Notably, 2 of the 3 original pa- With the rate of ICD implants in HCM increasing sharply, tients had HCM, but for the ensuing 2 decades patients with it is timely to review the overall experience with this therapy HCM were largely ignored with regard to ICD therapy. in this complex disease. Pharmacologic therapy has failed to provide HCM patients with reliable protection against SCD. Historically, such medi- cations have included β-blockers and verapamil, for which Historical Perspectives of ICD Therapy there are no prospective data, type IA antiarrhythmic agents General such as quinidine and procainamide (abandoned because of The ICD was developed by Drs Michel Mirowski and Morton the potential for proarrhythmia), and amiodarone,9,10,20 which Mower in the early 1980s for patients with coronary artery is impractical for long-term administration to young patients disease (CAD).18 Over the past 20 years a number of prospec- given its potential for important side-effects. For example, tive, controlled and randomized trials have shown ICDs to in a large retrospective study, almost 30% of patients taking Received September 15, 2010; accepted September 16, 2010; released online October 16, 2010 Hypertrophic Cardiomyopathy Center, Minneapolis Heart Institute Foundation, Minneapolis, MN, USA Mailing address: Barry J. Maron, MD, Hypertrophic Cardiomyopathy Center, Minneapolis Heart Institute Foundation, 920 E. 28th Street, Suite 620, Minneapolis, MN 55407, USA. E-mail: [email protected] ISSN-1346-9843 doi: 10.1253/circj.CJ-10-0921 All rights are reserved to the Japanese Circulation Society. For permissions, please e-mail: [email protected] Circulation Journal Vol.74, November 2010 2272 MARON BJ Figure 1. Sudden cardiac death (SCD) and age. (Top) SCD is most common before ap- proximately 25 years of age, whereas heart failure and stroke generally occur later in life.7 (Reproduced with permission.) (Bottom) Single most frequent cause of SCD in young competitive athletes in the U.S.. ARVC, arrhyth- mogenic right ventricular cardiomyopathy; AS, aortic valve stenosis; CAD, coronary artery disease; CHD, congenital heart disease; CM, cardiomyopathy; LAD, left anterior de- scending; MVP, mitral valve prolapse; WPW, Wolff-Parkinson-White. *Regarded as possible (but not definitive) evidence for hypertrophic cardiomyopathy at autopsy with mildly in- creased LV wall thickness (15–19 mm) and heart weight (447±76 g). †Includes most com- monly, Kawasaki disease, sickle cell trait and sarcoid. (Reproduced from Maron BJ, et al. Circulation 2009; 119: 1085 – 1092, with per- mission.) amiodarone (as an adjunct to ICD therapy) experienced appro- 10 years from less selected regional or community-based priate ICD interventions.9,10 Furthermore, in an Italian HCM cohorts placed annual HCM mortality rates at a much more cohort largely devoid of ICD implants, cardioactive and anti- realistic ≤1%.3,4,7,21 arrhythmic drugs were ineffective in protecting patients from Nevertheless, the traditional profile of SCD in HCM re- lethal ventricular tachyarrhythmias (VT), and SCD occurred mains unchanged; that is, it usually occurs without warning in 20% of those taking amiodarone.20 in asymptomatic or mildly symptomatic young patients (pre- The ICD era in HCM treatment essentially began in earnest dominantly <25 years of age)3,4,7,13 In this respect, HCM is with the highly visible publication in 2000 of the first size- the most common cause of sudden death in competitive able series of patients.8 This report triggered enthusiasm for athletes in the U.S. (Figure 1).6 device therapy in HCM patients and subsequently greater Although SCD risk is lower in midlife and beyond, achiev- numbers of ICDs were implanted prophylactically. Interest in ing this measure of longevity does not confer immunity to defibrillator therapy for HCM patients has stimulated more SCD7,13 (Figure 1). No relationship between SCD risk and widespread application to other genetic heart diseases (ie, gender has been identified,22 and although no differences in ion channelopathies (long QT and Brugada syndromes) and risk according to race are known, SCD is common in African- arrhythmogenic right ventricular cardiomyopathy).13 American competitive athletes with HCM.6 Profile of SCD in HCM Estimates of the SCD rate in HCM unavoidably emanate from Selection of HCM Patients for ICDs hospital-based cohorts, and in the older literature were as high Conventional Risk Markers as 6%/year, which we now recognize as overestimates based There has been a substantial investigative effort in ICD deci- on tertiary center data contaminated by the preferential re- sion-making toward reliably identifying the relatively small ferral of high-risk patients.3,4 However, reports over the past subset of patients within the broad HCM disease spectrum Circulation Journal Vol.74, November 2010 Implanted Defibrillators in HCM 2273 Figure 2. Risk stratification for sud- den cardiac death (SCD). (Top) Pyra- mid profile currently used to iden- tify patients at highest risk for SCD who are potential candidates for an implantable cardioverter-defibrillator (ICD). BP, blood pressure; LV, left ventricular; LVH, left ventricular hy- pertrophy; NSVT, nonsustained ven- tricular tachycardia; VT, ventricular tachycardia. *Following alcohol sep- tal ablation, sustained VT has been reported in a significant minority of patients (≈10%) over the short term.36 (Reproduced with permission.) (Bot- tom) Direct relation between magni- tude of LV hypertrophy (maximum [max] wall thickness by echocardiog- raphy) and SCD risk. Mild hypertro- phy generally conveys lower risk and extreme hypertrophy (wall thick- ness ≥30 mm) is associated with the highest risk.23 (Reproduced with per- mission.) who are at unacceptably high risk for SCD.3,4,7–10,13,23–27 There ≥1 episode of unexplained, recent syncope; (3) massive LV is universal agreement concerning the prudence of second- hypertrophy (thickness ≥30 mm); (4) nonsustained VT on ary prevention with ICDs for patients who have survived a serial ambulatory 24-h (Holter) ECGs; and (5) hypotensive cardiac arrest with documented VF or an episode of sustained or attenuated blood pressure response to exercise (Figure 2). VT, because of the relatively high recurrence rates in this However, the exercise blood pressure response is tested less subgroup.4 commonly than other risk factors13 and it rarely represents the However, selection of patients most likely to benefit from
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