Determinants of ejection performance in aortic stenosis.

Abstract

The cause of reduced ejection performance in patients with aortic stenosis is controversial. The relative contribution of afterload and contractility was evaluated in 76 patients with pure or predominant valvular aortic stenosis studied by left ventricular micromanometry and quantitative cineangiography. Thirteen patients without detectable heart disease served as controls. The ejection performance was assessed in terms of the mean normalized systolic ejection rate (MNSER, normal .gtoreq. 2.0 end-diastolic volumes (EV)/s), contractility by total pressure Vmax (normal .gtoreq. 1.47 muscle lengths/s) and/or peak measured velocity of shortening (normal .gtoreq. 1.14 muscle lengths/s) and afterload by peak systolic circumferential wall stress (normal < 460 dyn .cntdot. 103/cm2). The patients were divided into 4 groups according to the level of isovolumic contractility and peak systolic wall stress. In group 1, contractility and wall stress were normal. In group 2, contractility was normal and wall stress was increased. Wall stress was normal in group 3 and increased in group 4; in both groups, the isovolumic contractile indexes were depressed. At normal (groups 1 and 3) or increased (groups 2 and 4) wall stress, MNSER was significantly (P < 0.01) smaller in patients with reduced isovolumic contractility (1.72 EDV/s in group 3 and 1.48 EDV/s in group 4) than in the corresponding groups with normal contractility (2.34 EDV/s in group 1 and 2.13 EDV/s in group 2). Conversely, with a normal (control group and groups 1 and 2) or depressed (groups 3 and 4) contractile state, there was a significant inverse linear relationship between MNSER and systolic wall stress. The slopes of the 2 curves were almost identical, but the intercept on the y-axis (MNSER) was significantly (P < 0.001) smaller in patients with depressed contractility (3.09 EDV/s) than in those with normal contractility (2.59 EDV/s). Both altered contractility and increased afterload are operative in depressing left ventricular ejection performance. The observation that contractile state can be normal or impaired at normal and increased systolic wall stress is evidence for nonuniform myocardial quality in adequate and inadequate hypertrophy. The significantly higher left ventricular angiographic muscle mass in groups 3 and 4 than in groups 1 and 2 is consistent with the concept that whether or not hypertrophy is adequate or inadequate in terms of maintaining normal systolic stress, advanced myocardial hypertrophy leads to depression of contractility.