[Effects of verapamil on systolic time intervals and relaxation time in hypertrophic cardiomyopathy (author's transl)].

In order to determine the effect of verapamil, a calcium-channel blocking agent, on systolic performance and relaxation in hypertrophic cardiomyopathy (HCM), 12 patients with HCM and 10 normal subjects were studied. Echocardiograms, phonocardiograms, carotid pulses, and apex cardiograms were recorded simultaneously at the control state and 5, 10, and 15 min after intravenous injection of 10 mg of verapamil. After verapamil administration, heart rate was unchanged, while systolic blood pressure was slightly reduced in both groups. In normal subjects no significant changes were observed in systolic time intervals, such as ET, delta ET, PEP, delta PEP and PEP/ET, and mean VCF, except slightly prolonged delta ET after 5 min of the injection. The duration of isovolumic relaxation, (IIa-D) interval, taken as the period from the aortic valve closure (IIa) to the onset of mitral valve cusp separation and the time from IIa to the O point of the apex cardiogram, (IIa-O) interval, were 58 +/- 5 and 123 +/- 16 msec, respectively. The maximum velocity of the left ventricular posterior wall in early diastole (PWDV) was 128 +/- 10 mm/sec. These intervals and the velocity were not significantly changed after verapamil administration. In patients with HCM, ET and delta ET were unchanged, but PEP and delta PEP prolonged at 10 and 15 min after verapamil administration. PEP/ET was increased and mean VCF was reduced at 15 min after injection. In comparison with normal subjects, IIa-D interval and Ha-O interval were prolonged definitely at control, 92 +/- 21 and 190 +/- 28 msec, respectively. PWDV was slower than normal, 86 +/- 18 mm/sec at control. After verapamil, these intervals were shortened and PWDV fastened significantly. These results indicated that verapamil is regarded to have slight intrinsic negative inotropic action, suggesting the beneficial effect to reduce intraventricular pressure gradient, and also improve impaired myocardial relaxation in HCM.