Circulation, Vol 75, 964-972, Copyright © 1987 by American Heart Association
T Wisenbaugh, JL Elion and SE Nissen
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)
ARTICLES
Influence of aortic valve disease on systolic stiffness of the human left ventricular myocardium