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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)

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