Copyright © 1990 by the European Society of Cardiology.
© 1990 The European Society of Cardiology
Coronary microangiopathy and cardiac hypertrophy
Medizinische Klinik and Poliklinik B, University of Düsseldorf F.R.G.
Correspondence: Martin Vogt MD, Medizinische Klinik und Poliklinik B, Universität Düsseldorf, Abteilung für Kardiologie, Pneumologie und Angiologie, Moorenstrasse 5, D-4000 Düsseldorf 1, West Germany
Even in the absence of coronary heart disease, coronary vasodilator reserve is frequently impaired in hypertensive patients. To study, whether the reduced coronary reserve is due to the degree of left ventricular hypertrophy or is a consequence of primary vascular alterations, coronary reserve was determined in 54 hypertensiue patients with angina pectoris and angiographically normal coronary arteries. Twelve normotensive persons were studied for control purposes. Coronary blood flow was measured quantitatively by the gas chromatographic argon method. Coronary reserve was determined by measuring coronary resistance before and after dipyridamole (0·5 mg (kg body weight)–1 i.v.). Left ventricular muscle mass was determined by ventriculography. In hypertensive patients, minimal coronary resistance was markedly increased by 124% and coronary reserve signfiantly reduced by about 38% compared with healthy normotensives. Hypertensives and normotensives did not differ with respect to myocardial oxgyen consumption per unit weight myocardrum (11·9 ± 2·3 vs 11·4 ± 2·4 ml O2 100g–1 min, n.s.) and resting coronary pow (92·1 ± 20·8 vs 91·4 ± l8·9 ml min–1 min, n.s.). No significant correlation was found between minimal coronary resistance and coronary reserve and left ventricular murcle mass and between coronary reserve and diastolic wall stress. Accordingly, the reduced coronary regulation capacity in hypertensives does not parallel the degree of left ventricular hypertrophy and is not due to an increased myocardial oxygen consumption under resting conditions. Consequently, the impaired coronary reserve in hypertensive patients seems to be the consequence of primary microvascular lesions, which are independent of the process of left ventricular hypertrophy.
Key Words: arterial hypertension coronary reserve left ventricular hypertrophy microvascular angina pectoris media hypertrophy