Impaired Maximal Rate of Left Ventricular Relaxation in Patients with Coronary Artery Disease Left Ventricular Dysfunction

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It has been suggested that the rate of left ventricular (LV) relaxation is related to the inotropic state, end-systolic fiber length peak LV pressure, but little information is available regarding the rate of LV relaxation in patients with coronary artery disease (CAD) 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) the maximal rate of pressure fall (neg dP/dt). Selective coronary arteriography biplane LV angiography with determination of LV volumes, ejection fraction (EF) percent abnormally contracting segments (ACS), when present, were performed in all patients. In 10 patients with normal LV function (EF >0.50, no asynergy) mean neg dP/dt (2074+121 mm Hg/sec) was significantly (p ≤ 0.01) greater than in 29 patients with CAD LV dysfunction (1695 ± 66 mm Hg/sec). In nine patients with LV dysfunction EF < 0.35, mean neg dP/dt was reduced to 1405 ± 107 mm Hg/sec, significantly (p ≤ 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), with ACS (r = −0.74), less well with LV end-systolic volume (r = −0.67). There was very poor correlation between neg dP/dt 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 LV dysfunction, the extent of impairment is related to the severity of the dysfunction as determined hemodynamically by pos dP/dt, angiographically by EF ACS. In these patients the maximal rate of LV relaxation is inversely related to LV end-systolic volume, is not related to peak LV pressure.

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