Afterload dependent prolongation of left ventricular relaxation: importance of asynchrony.

Abstract

Acute increases in afterload and in left ventricular asynchrony both independently prolong left ventricular isovolumetric relaxation. The aim of the study was to investigate whether an increased left ventricular afterload augments left ventricular asynchrony, which in turn could mediate the afterload dependent prolongation of left ventricular isovolumetric relaxation. Seven chloralose anaesthetised open chest dogs were instrumented with a left ventricular pressure gauge and two pairs of ultrasonic wall thickness crystals in the antero-apical and postero-basal left ventricular wall. At a constant heart rate of 149(SEM 7) beats.min-1, left ventricular pressure was acutely increased by brief manual clamping of the descending (AOCD) and ascending AOCA) thoracic aorta. Left ventricular asynchrony was quantified by the phase difference of the first Fourier harmonic between postero-basal and antero-apical wall motion. Global left ventricular relaxation was measured as the time constant of isovolumetric pressure fall, tau. Regional myocardial relaxation was assessed as the mean rate to half end diastolic thinning. AOCD increased left ventricular peak systolic pressure from 141.9(6.9) mm Hg to a maximum of 182.0(5.1) mm Hg and tau from 34.3(2.4) ms to 48.0(5.0) ms (p less than 0.05). Simultaneously, phase difference increased markedly during AOCD, from 12.7(3.5) degrees to 24.4(2.2) degrees (p less than 0.05). At matched left ventricular peak systolic pressures, AOCA increased tau from 33.4(2.5) ms to only 42.5(4.3) ms (p less than 0.05 v control and AOCD). Concomitantly, the increase in phase difference was smaller and statistically non-significant, at 13.7(2.9) degrees v 17.1(2.5) degrees. During 13 out of the 14 aortic clampings (7 AOCD, 6 AOCA), tau correlated linearly with phase difference [mean r = 0.74(0.03)]. In contrast to their effects on global left ventricular relaxation and asynchrony, neither AOCD nor AOCA influenced the rate to half end diastolic thinning. (1) left ventricular asynchrony may increase during an acute augmentation of left ventricular afterload; (2) this increased left ventricular asynchrony possibly contributes to the afterload dependent prolongation of left ventricular isovolumetric relaxation rate.