Ischemia-induced impairment of left ventricular relaxation: Relation to reduced diastolic filling rates of the left ventricle

Abstract

An investigation was performed in order to better define the cause of reduced diastolic filling rates of the left ventricle (LV) observed in the setting of acute myocardial ischemia. Seven closed chest, anesthetized pigs were instrumented by placing a micromanometer-tip catheter in the LV and a balloon tip catheter in the midportion of the left anterior descending coronary (LAD) artery. The animal's red blood cells were labeled with technetium-99m and LV time-activity curves obtained by means of a computer-controlled, nonimaging cardiac probe (collimated, 3.5 cm DIA, sodium iodide crystal). Nuclear data obtained simultaneously with LV pressure data were used to evaluate diastolic pressure-count rate (i.e., volume) relations of the LV under control conditions and at 5 and 10 minutes after balloon occlusion of the animal's LAD. Diastolic filling rates, the time constant (“T”) of ventricular relaxation, the chamber passive stiffness constant (“K”), and maximum negative left ventricular DP DT were computed for each experimental condition. Maximum negative DP DT decreased compared with control (1690 + 699 mm Hg/sec; mean ± 1 SD) at both 5 minutes (1040 ± 493, p < 0.01) and 10 minutes (1360 ± 588, p < 0.05) after occlusion. Likewise “T” was prolonged versus control (45.3 ± 6.4) at both 5 minutes (56.8 ± 12.8, p < 0.01) and 10 minutes (54.0 ± 8.7, p < 0.05) after occlusion. In contrast both “K” and calculated left ventricular pressure at zero counts (i.e., volume) remained constant throughout the study. Left ventricular end-diastolic pressure also did not change significantly during the study. The mean, maximal, and mid to late LV diastolic filling rates all were prolonged significantly ( p < 0.05) versus control at 5 minutes and 10 minutes after occlusion. The rate of early diastolic filling of the LV did not change significantly during the study, although it tended to decline along with the other rates. Thus, ischemia-induced changes in diastolic filling rates may be seen in the absence of changes in left ventricular chamber stiffness, and ischemia-induced impairment of left ventricular relaxation alone is sufficient to reduce the rate of diastolic filling of the LV.