EFFECTS OF INTRAVENOUS VERAPAMIL ON LEFT-VENTRICULAR RELAXATION AND FILLING IN STABLE ANGINA-PECTORIS

Left ventricular (LV) diastolic function is often impaired in coronary artery disease (CAD). To assess whether verapamil could improve LV diastolic properties, 12 patients with CAD undergoing right-and left-sided cardiac catheterization, as well as simultaneous radionuclide angiography, were studied before and during intravenous administration of verapamil (0.1 mg/kg as a bolus followed by 0.007 mg/kg/min). The heart rate was kept constant by atrial pacing in both studies. LV pressure-volume relations were obtained. Verapamil decreased LV systolic pressure (130 ± 22 to 117 ± 16 mm Hg, p < 0.01) and the end-systolic pressure/volume ratio (2.4 ± 1.3 to 1.6 ± 0.5 mm Hg/ml, p < 0.05), and increased LV end-diastolic (13 ± 4 to 16 ± 4 mm Hg, p < 0.02) and pulmonary capillary pressures (10 ± 5 to 12 ±5 mm Hg, p < 0.005). Despite such negative inotropic effects, cardiac index increased (3.4 ± 0.7 to 3.9 ± 0.6 liters/min/m2, p < 0.02). The time constant of isovolumic relaxation shortened (63 ± 14 to 47 ± 9 ms, p < 0.02); peak filling rate increased (370 ± 155 to 519 ± 184 ml/s, p < 0.001; 2.6 ± 1.1 to 3.3 ± 0.9 end-diastolic counts/s, p < 0.02; and 4.1 ± 1.6 to 5.5 ±1.5 stroke counts/s, p < 0.001). Percentage changes in peak filling rate were related to percentage changes in the time constant of isovolumic relaxation, the pressure asymptote, pulmonary capillary pressure, end-diastolic volume, and an index of LV diastolic asynchrony (r = 0.930, R2 = 0.864, F = 7.636, p = 0.014). Late diastolic filling was not affected by verapamil. Thus, intravenous verapamil administration in patients with CAD improved LV isovolumic relaxation and early filling. These effects are likely the consequence of both the drug's direct action on myocardium and changes in the loading conditions. © 1990.