Left ventricular dynamics, energetics and coronary hemodynamics in hypertrophic heart disease.
The relations between left ventricular mass, mass to volume ratio, systolic wall stress and myocardial oxygen consumption were analyzed in 187 patients with chronic heart disease. The degree of left ventricular hypertrophy is determined by mass, the mass to volume ratio, and pressure and, hence, systolic wall stress. In chronic heart disease at least two types of inappropriate left ventricular hypertrophy may occur: (1) low stress hypertrophy with an increased mass to volume ratio, normal left ventricular function and normal or reduced oxygen consumption (MVO2), whereas (2) high stress hypertrophy has a normal or low mass to volume ratio, impaired left ventricular function and an increased MVO2). Left ventricular oxygen consumption per viable mass unit (MVO/2) is significantly correlated with the systolic force per unit cross-sectional area of the left ventricular wall, that is, to left ventricular systolic wall stress. The range of systolic wall stress was 100-450 X 10(3) dynes/cm2. A similar reserve capacity is present for both the metabolic and the coronary reserves. The coronary reserve is governed by both the vascular and the myocardial component of coronary resistance. In coronary artery disease the coronary reserve (normal = 4.9) may be diminished by more than 50%, due to an increased vascular component of coronary resistance, whereas an abnormal increase of the myocardial (= extravascular) component of coronary resistance is present in dilated heart disease, where marked reduction in coronary reserve may occur, despite a normal coronary arteriogram. In addition to these diseases, a large variety of disturbances of coronary microcirculation of vascular, rheological and metabolic origin exists leading to reduction in the oxygen supply of the heart despite normal large coronary arteries.
D001022:Aortic Valve Insufficiency / Q000503:physiopathology; D001024:Aortic Valve Stenosis / Q000503:physiopathology; D006332:Cardiomegaly / Q000209:etiology* / Q000503:physiopathology; D003326:Coronary Circulation; D003327:Coronary Disease / Q000503:physiopathology; D006321:Heart / Q000503:physiopathology*; D006352:Heart Ventricles / Q000503:physiopathology; D006801:Humans; D006973:Hypertension / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism*; D010101:Oxygen Consumption; D012039:Regional Blood Flow; D013599:Systole