Impaired maximal rate of left ventricular relaxation in patients with coronary artery disease and left ventricular dysfunction.

Abstract

It has been suggested that the rate of left ventricular (LV) relaxation is related to the inotropic state, end-systolic fiber length and peak LV pressure, but little information is available regarding the rate of LV relaxation in patients with coronary artery disease (CAD) and LV dysfunction. To assess the rate of LV relaxation we obtained high-fidelity LV pressure measurements with manometer-tip catheters in 39 patients. The signal was analyzed by a digital computer to yield the maximal rate of pressure rise (pos dP/dt) and the maximal rate of pressure fall (neg dP/dt). Selective coronary arteriography and biplane LV angiography with determination of LV volumes, ejection fraction (EF) and percent abnormally contracting segments (ACS) when present, were performed in all patients. In 10 patients with normal LV function (EF greater than 0.50, no asynergy) mean neg dP/dt (2074 +/- 121 mm Hg/sec) was significantly (p less than 0.01) greater than in 29 patients with CAD and LV dysfunction (1695 +/- 66 mm Hg/sec). In nine patients with LV dysfunction and EF less than 0.35, mean neg dP/dt was reduced to 1405 +/- 107 mm Hg/sec, significantly (p less than 0.01) lower than in patients with normal LV function. Neg dP/dt correlated well with pos dP/dt (r = 0.75), with EF (r = 0.74), and with ACS (r = -0.74), and less well with LV end-systolic volume (r = 0.67). There was very poor correlation between neg dP/dt and peak LV pressure (r = 0.30). These data suggest that the rate of LV relaxation, as assessed by neg dP/dt, is impaired in patients with CAD and LV dysfunction, and the extent of impairment is related to the severity of the dysfunction as determined hemodynamically by pos dP/dt, and angiographically by EF and ACS. In these patients the maximal rate of LV relaxation is inversely related to LV end-systolic volume, and is not related to peak LV pressure.