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Circulation. 1997;95:892-898

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(Circulation. 1997;95:892-898.)
© 1997 American Heart Association, Inc.


Articles

Angina Pectoris in Patients With Aortic Stenosis and Normal Coronary Arteries

Mechanisms and Pathophysiological Concepts

Barbara K. Julius, MD; Martin Spillmann, MD; Giuseppe Vassalli, MD; Bruno Villari, MD; Franz R. Eberli, MD; Otto M. Hess, MD

the Division of Cardiology, University Hospital, Zurich, Switzerland.

Correspondence to Otto M. Hess, MD, Cardiology, University Hospital, 3010 Bern, Switzerland.

Background The incidence of angina pectoris (AP) in patients with severe aortic stenosis (AS) and normal coronary arteries has been reported to be 30% to 40%. The exact pathophysiological mechanism, however, is not known. The purpose of this work was to evaluate the various hemodynamic and angiographic determinants of myocardial perfusion in 61 patients with severe AS.

Methods and Results In a retrospective analysis, 61 patients with severe AS and without significant coronary artery disease were studied. Thirty-three patients with atypical chest pain and angiographically normal arteries served as control subjects. Patients were divided into two groups: 32 with AP and 29 without AP. Quantitative coronary angiography was performed in 59 patients and 22 control subjects. Coronary flow reserve was determined in 29 patients and 7 control subjects by use of coronary sinus thermodilution technique. Patients with AP had a lower left ventricular (LV) muscle mass, an increased LV peak systolic pressure, and increased wall stress than those without AP. Vessels of the left coronary artery were smaller and coronary flow reserve was lower in patients with AP than in those without. Inadequate LV hypertrophy with an increased wall stress was found in patients with AP but not in patients without AP.

Conclusions Myocardial ischemia in patients with severe AS can occur in the absence of coronary artery disease and appears to be due to inadequate LV hypertrophy with high systolic and diastolic wall stresses and a reduced coronary flow reserve. The cause of inadequate LV hypertrophy, however, remains unclear.


Key Words: hypertrophy • angina • hemodynamics • valves • myocardium




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