From 1975 through 1993, 178 patients underwent surgical management of hypertrophic obstructive cardiomyopathy. Operations included isolated septal myectomy (n = 95), septal myectomy and coronary artery bypass grafting (n = 41), septal myectomy plus a valve procedure (n = 25), septal myectomy, valve procedure, and coronary artery bypass grafting (n = 14), and mitral valve replacement without septal myectomy (n = 3). Recent myectomy results were monitored with transesophageal echocardiography. After initial myectomy, 32 patients (20%) underwent a second pump run for more extensive myectomy only (n = 22), mitral valve replacement only (n = 5), or both (n = 2). In-hospital mortality was 6% (n = 11) and 4% (n = 6) for patients undergoing septal myectomy or septal myectomy plus coronary artery bypass grafting, respectively. Heart block occurred in 17 patients (10%). Left ventricular outflow tract systolic gradients decreased from a mean of 93 mm Hg to 21 mm Hg after myectomy. Late survival was 86% and 70% at 5 and 10 postoperative years, respectively, and 93% and 79% for patients undergoing septal myectomy alone or septal myectomy plus coronary artery bypass grafting, respectively. Only 3 of 131 in-hospital survivors of septal myectomy or septal myectomy plus coronary artery bypass grafting died late cardiac deaths, for a yearly mortality of 0.6%. However, the 5-year late survival of patients undergoing valve operation plus septal myectomy was 51%, and multivariate testing confirmed the adverse influence on late survival (p = 0.008), as well as adverse influences of increasing age (p = 0.016) and return to cardiopulmonary bypass for mitral valve replacement (p = 0.038). At follow-up 136 patients (94%) had New York Heart Association class I or II symptoms. For patients with hypertrophic obstructive cardiomyopathy, septal myectomy alone or in combination with coronary artery bypass grafting produces effective symptom relief, excellent long-term survival, and a low risk of late cardiac death.

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The direct effects of angiotensin II (Ang II) on human cardiac muscle were investigated using isolated trabecular muscles from failing and functionally normal hearts. (Circulation 1990;82:1973-1984 T wo developments in the field of cardiovascular physiology have renewed interest in the effects of angiotensin II (Ang II) on the myocardium. First, the observation that angiotensin converting enzyme inhibitors such as captopril are more efficacious in treating heart failure patients than direct-acting vasodilators1,2 suggests that the renin-angiotensin system or its perturbation may be involved in heart failure, although the mechanisms involved remain to be defined. Second, evidence for the existence of localized tissue renin-angiotensin systems3 and the demonstration that such a system