Ventricular function and coronary hemodynamics in hypertensive heart disease

Abstract

Left ventricular function, wall geometry and coronary hemodynamics were analyzed in 114 patients with essential hypertension during diagnostic left heart catheterization, left ventriculography and coronary arteriography. Results of the study were as follows: 1. 1. Left ventricular function (as assessed from the cardiac index, stroke volume index, ejection fraction, mean velocity of circumferential fiber shortening, mean normalized systolic ejection rate, isovolumic indexes) was normal in patients with hypertensive hypertrophy, even with a large increase in muscle mass and even in the presence of concomitant coronary artery disease. Left ventricular function was impaired when regional contraction abnormalities or ventricular dilatation, or both, occurred and was inversely related to both cardiac size and systolic wall stress. 2. 2. Coronary blood flow (+18 percent), coronary resistance (+38 percent) and myocardial oxygen consumption (MVO 2) (+21 percent) were increased in essential hypertension. Coronary reserve was reduced even in hypertensive hypertrophy without evidence of coronary artery disease. MVO 2 per mass unit was directly correlated with systolic wall stress per cross-sectional area of the left ventricular wall. 3. 3. The appropriateness of left ventricular hypertrophy may be defined by the relation between pressure, mass to volume ratio and systolic wall stress. In hypertensive heart disease at least two types of inappropriate left ventricular hypertrophy occur: (a) low stress hypertrophy, with an increased mass to volume ratio, with normal left ventricular function and with normal or reduced MVO 2; and (b) high stress hypertrophy, with normal or low mass to volume ratio, impaired left ventricular function and increased MVO 2. It is concluded that the appropriateness of left ventricular hypertrophy, as a result of mass to volume ratio and stress, is a major determinant of left ventricular performance and of myocardial oxygen consumption, and that the individual history of left ventricular pressure load specifically may influence left ventricular function.