Left ventricular contraction and relaxation in patients with coronary heart disease.

The relationship of left ventricular relaxation and compliance to the mechanism of elevation of left ventricular enddiastolic pressure during ischemia was investigated. Isovolumic left ventricular contraction, relaxation, and diastolic pressure-volume relationship were studied in controls and in coronary heart disease patients. Patients were studied at similar heart rates during ergometric exercise and pacing. Diastolic aortic, left ventricular systolic, and incisural pressure were not significantly different in both groups at rest, pacing, and exercise. Left ventricular dP/dtmax increased during pacing and exercise in controls (P smaller than 0.05; P smaller than 0.01) and in coronary heart disease patients (P smaller than 0.01 for both); whereas left ventricular dP/dtmin increased only in controls during exercise (P smaller than 0.01). Peak measured velocity of shortening (Vpm) and of lengthening (Vpmr) of the contractile elements was calculated as (dP/dt)/p. Vpm and Vpmr increased in controls during both pacing (P smaller than 0.05; P smaller than 0.02) and exercise (P smaller than 0.01 for both). In coronary heart disease patients Vpm increased during pacing (P smaller than 0.01) while Vpmr did not differ significantly. During exercise both Vpm and Vpmr were unchanged. In patients with coronary heart disease paced to angina, diastolic logarithmic pressure-volume relationship showed change in slope (P smaller than 0.05) of the regression line and upward shift in intercept b (+0.25; P smaller than 0.001). Ischemia produced an impaired contractile state, delayed relaxation and generation of active diastolic tone in the intact ventricle.