Influence of aortic valve disease on systolic stiffness of the human left ventricular myocardium.

The new concept of systolic myocardial stiffness was applied to the study of ejection mechanics in aortic valve disease. Frame-by-frame analysis of stress (sigma) and volume (V) was performed for two differently loaded beats in 26 patients who underwent simultaneous cineangiography and micromanometry: nine normal subjects, eight with isolated aortic regurgitation (AR), and nine with aortic stenosis (AS). Maximum myocardial stiffness (maxEav) was defined as the slope of the end-systolic (es) stress-strain relationship. End-systole was defined as the frame where stiffness was maximal, and strain was defined as epsilon = loge (Dm/Dom), where Dm is left ventricular midwall diameter and Dom is the theoretical Dm at zero stress. Expressed in terms of cavity volume, epsilon = gamma X loge (V/Vo), where gamma is the geometric factor relating Dm to V during systole. Vo was obtained by extrapolating to sigma es = 0 the function, sigma es = maxEav X gamma X loge (Ves/Vo), which was fit to the end-systolic data. Vo always had a value greater than zero. MaxEav was preserved in the AR group (1575 +/- 565) and increased in the AS group (1877 +/- 544; p = .02) compared with normal (1320 +/- 268), suggesting maintenance of contractile force per unit of myocardium in these two lesions. However, theoretical "unloaded" shortening fraction (SFo) was depressed in the AS group (0.30 +/- 0.06; p = .01) compared with normal (0.37 +/- 0.04), preserved in the AR group (0.34 +/- 0.07; p = .24), and inversely related to maxEav (r = -.66, p = .01), suggesting a disparity between shortening potential and force potential.(ABSTRACT TRUNCATED AT 250 WORDS)