Hypertrophic Cardiomyopathy

Recent studies indicate that reversible 20`TI perfusion defects, compatible with silent myocardial ischemia, commonly develop during exercise in asymptomatic or mildly symptomatic patients with hypertrophic cardiomyopathy (HCM). To determine whether this represents a dynamic process that may be modified favorably by medical therapy, we studied 29 asymptomatic or minimally symptomatic patients with HCM, aged 12-55 years (mean, 28), with exercise 201T1 emission computed tomography under control conditions and again after 1 week of oral verapamil (mean dosage, 453 mg/day). Treadmill time increased slightly during verapamil (21.0+3.6 to 21.9±2.7 minutes, p<0.005), but peak heart rate-blood pressure product was unchanged (26.3+6.0x 103 compared with 25.0±6.4x103). Two midventricular short-axis images per study were divided into five regions each, and each of these 10 regions was then analyzed on a 0-2 scale by three observers blinded with regard to the patients' therapy. Average regional scores of 1.5 or less were considered to represent perfusion defects, and a change in regional score of0.5 or more was considered to constitute a significant change. During control studies, 15 patients (52%) developed perfusion defects with exercise (average, 3.7 regions per patient). In 14 of these patients, all perfusion defects completely reversed after 3 hours of rest; one patient had fixed defects. After administration of verapamil, exercise perfusion scores improved in 10 of the 14 patients (71%) with reversible defects; there was overall improvement in 34 of 50 (68%) regions with initially reversible perfusion defects. completely normalized all regional perfusion defects that were apparent during exercise under control conditions in eight patients (average, 3.9 regions per patient). No region developed a new or worse perfusion defect during verapamil in any patient. Thus, exercise-induced regional myocardial perfusion defects improved during verapamil in the majority of asymptomatic patients with HCM and in many cases improved completely. These data suggest that verapamil may prevent or diminish inducible silent ischemia in many asymptomatic patients with HCM. (Circulation 1989;79:1052-1060)

[1]  S. Larson,et al.  Myocardial perfusion abnormalities in patients with hypertrophic cardiomyopathy: assessment with thallium-201 emission computed tomography. , 1987, Circulation.

[2]  B. Maron,et al.  Relation between extent of left ventricular hypertrophy and occurrence of ventricular tachycardia in hypertrophic cardiomyopathy. , 1987, The American journal of cardiology.

[3]  W. Roberts,et al.  Intramural ("small vessel") coronary artery disease in hypertrophic cardiomyopathy. , 1986, Journal of the American College of Cardiology.

[4]  O. Hess,et al.  Does verapamil improve left ventricular relaxation in patients with myocardial hypertrophy? , 1986, Circulation.

[5]  Michael V. Green,et al.  Verapamil-induced improvement in left ventricular diastolic filling and increased exercise tolerance in patients with hypertrophic cardiomyopathy: short- and long-term effects. , 1985, Circulation.

[6]  T. Kozuka,et al.  Thallium perfusion and cardiac enzyme abnormalities in patients with familial hypertrophic cardiomyopathy. , 1985, American heart journal.

[7]  R. Bonow,et al.  Myocardial ischemia in patients with hypertrophic cardiomyopathy: contribution of inadequate vasodilator reserve and elevated left ventricular filling pressures. , 1985, Circulation.

[8]  R. Bonow,et al.  Use of calcium-channel blocking drugs in hypertrophic cardiomyopathy. , 1985, The American journal of cardiology.

[9]  D S Berman,et al.  Quantification of rotational thallium-201 myocardial tomography. , 1985, Journal of nuclear medicine : official publication, Society of Nuclear Medicine.

[10]  B. Maron,et al.  Echocardiographic analysis of ventricular septal dynamics in hypertrophic cardiomyopathy and other diseases. , 1984, The American journal of cardiology.

[11]  H. Rakowski,et al.  Muscular subaortic stenosis: the quantitative relationship between systolic anterior motion and the pressure gradient. , 1984, Circulation.

[12]  Michael V. Green,et al.  Effects of verapamil on left ventricular systolic and diastolic function in patients with hypertrophic cardiomyopathy: pressure-volume analysis with a nonimaging scintillation probe. , 1983, Circulation.

[13]  M. Schlüter,et al.  Influence of verapamil therapy on left ventricular performance at rest and during exercise in hypertrophic cardiomyopathy. , 1983, The American journal of cardiology.

[14]  E. Sonnenblick,et al.  Microvascular Spasm in the Cardiomyopathic Syrian Hamster: A Preventable Cause of Focal Myocardial Necrosis , 1982, Circulation.

[15]  C. Henschke,et al.  Pathophysiology of Chest Pain in Patients with Cardiomyopathies and Normal Coronary Arteries , 1982, Circulation.

[16]  Michael V. Green,et al.  Effects of Verapamil on Left Ventricular Systolic Function and Diastolic Filling in Patients with Hypertrophic Cardiomyopathy , 1981, Circulation.

[17]  J. Gottdiener,et al.  Patterns and significance of distribution of left ventricular hypertrophy in hypertrophic cardiomyopathy. A wide angle, two dimensional echocardiographic study of 125 patients. , 1981, The American journal of cardiology.

[18]  E. Sowton,et al.  Assessment of chest pain in hypertrophic cardiomyopathy using exercise thallium-201 myocardial scintigraphy. , 1980, British heart journal.

[19]  R. Okada,et al.  Improved diagnostic accuracy of thallium-201 stress test using multiple observers and criteria derived from interobserver analysis of variance. , 1980, The American journal of cardiology.

[20]  K. R. Anderson,et al.  Histopathological specificity of hypertrophic obstructive cardiomyopathy. Myocardial fibre disarray and myocardial fibrosis. , 1980, British heart journal.

[21]  B. Maron,et al.  Verapamil therapy: a new approach to pharmacologic treatment of hypertrophic cardiomyopathy. , 1980, Chest.

[22]  W. Bussmann,et al.  Treatment of hypertrophic obstructive cardiomyopathy with verapamil , 1980, British heart journal.

[23]  B. Maron,et al.  Verapamil therapy: a new approach to the pharmacologic treatment of hypertrophic cardiomyopathy. I. Hemodynamic effects. , 1979, Circulation.

[24]  B. Maron,et al.  Verapamil therapy: a new approach to the pharmacologic treatment of hypertrophic cardiomyopathy. II. Effects on exercise capacity and symptomatic status. , 1979, Circulation.

[25]  S. Gulotta,et al.  Idiopathic hypertrophic subaortic stenosis: evaluation of anginal symptoms with thallium-201 myocardial imaging. , 1979, The American journal of cardiology.

[26]  W. Roberts,et al.  Hypertrophic cardiomyopathy and transmural myocardial infarction without significant atherosclerosis of the extramural coronary arteries. , 1979, The American journal of cardiology.

[27]  B. Maron,et al.  Hypertrophic cardiomyopathy: a discussion of nomenclature. , 1979, The American journal of cardiology.

[28]  J. Roelandt,et al.  Progression to left ventricular dilatation in patients with hypertrophic obstructive cardiomyopathy. , 1979, American heart journal.

[29]  G. Pohost,et al.  The Influence of Left Ventricular Volume and Wall Motion on Myocardial Images , 1979, Circulation.

[30]  J. Griffith,et al.  Regional Contractility: Selective Depression of Ischemic Myocardium by Verapamil , 1976, Circulation.

[31]  R. Popp,et al.  Ventricular systolic septal thickening and excursion in idiopathic hypertrophic subaortic stenosis. , 1974, The New England journal of medicine.

[32]  W. Henry,et al.  Echocardiographic measurement of the left ventricular outflow gradient in idiopathic hypertrophic subaortic stenosis. , 1973, The New England journal of medicine.