The effect of premature ventricular contraction on left ventricular relaxation, chamber stiffness, and filling in humans

Abstract

To investigate the influence of single spontaneous premature ventricular ectopic beats on left ventricular contraction, relaxation, chamber stiffness, and filling, we examined 21 patients with simultaneous micromanometer left ventricular pressure tracings and echocardiograms. Instantaneous left ventricular diameter and mitral valve inflow velocity were obtained by using of M-mode and pulsed Doppler echocardiography, respectively. The isovolumic relaxation time constants (T L and T D) were calculated by mean of a zero (T L) and variable (T D) asymptote pressure. The chamber stiffness constants were derived from the diastolic pressure-diameter (k d) and pressure-volume (k v) relationships. The extrasystolic beat was associated with marked impairments of relaxation, systolic function, and diastolic filling as seen by an increased T L (53 to 71 msec; p < 0.001), T D (59 to 89 msec; p < 0.005), time from maximum negative dp/dt to the lowest diastolic pressure (147 to 170 msec; p < 0.05), and decreased number of elasped T Ds (3.1 to 2.4; p < 0.05), end-systolic pressure-diameter ratio (2.4 to 1.7; p < 0.001), maximum positive dp/dt (1904 to 1326 mm Hg/sec; p < 0.001), shortening fraction (31% to 21%; p < 0.001), and peak early filling velocity (59 to 49 cm/sec; p < 0.001). Chamber stiffness constants were unchanged. Relaxation and chamber stiffness were unchanged during the postextrasystolic beat as reflected by T L, T D, maximum negative dp/dt, and k d and k v. Systolic function was potentiated during the postextrasystolic beat as reflected by an increased end-systolic pressure-diameter ratio (2.4 to 3.3 mm Hg/mm; p < 0.001), maximum positive dp/dt (1904 to 2362 mm Hg/sec; p < 0.001), and shortening fraction (31% to 42%; p < 0.001). Peak early filling velocity, one-third filling fraction, and total time-velocity integral of diastolic filling were unchanged. Relaxation and diastolic filling are significantly impaired during a premature ventricular beat. This may be due to an increase in the nonuniformity of relaxation coupled with unfavorable inotropic state and loading conditions. Despite enhanced systolic function and favorable loading conditions during the postextrasystolic contraction, diastolic function and filling were not improved. This may represent slowing of the actin-myosin cross-bridge inactivation process or an increase in the nonuniformity of relaxation.