The effects of intravenous nifedipine on cardiac hemodynamics and contractility in patients with coronary artery disease in the presence or absence of beta adrenergic blockade.

We studied the acute effects of intravenous nifedipine on hemodynamics and left ventricular function of CAD patients without previous treatment (group 1) and of 10 CAD patients receiving acebutolol (9 mg/kg daily) and who had been shown to be adequately beta blocked (reduction in heart rate by 25%) (group 2). Intravenous nifedipine (15 micrograms/kg) significantly reduced systemic peripheral resistances in both groups: this was associated with decreased systolic blood pressure and increased left ventricular cardiac output with a slight nonsignificant increase of ejection fraction. There was a significant increase in heart rate in both groups, the chronotropic response to nifedipine being attenuated in patients receiving acebutolol. Left ventricular end-diastolic pressure did not change in the first group, but it was significantly decreased in the second group, with a concomitant increase of end-diastolic left ventricular volume, suggesting an amelioration of diastolic compliance. The effect of nifedipine on intrinsic myocardial contractility was quite different, depending on the presence of beta adrenergic blockade. When given to patients of group 1, nifedipine significantly increased dP/dtmax, Vcemax, and Vmaxd. The same indices, however, were significantly depressed when nifedipine was given to the patients of group 2 receiving acebutolol. This study shows that intravenous nifedipine can be usefully administered to patients with coronary artery disease who have been on adequate beta-blocking doses of acebutolol with relative safety. Under these conditions nifedipine increases cardiac output in association with arterial dilation, despite evidence for a negative inotropic effect. These data also suggest that such an intrinsic negative inotropic effect would normally be masked by compensatory sympathetic activity.