Inotropic, vascular and neuroendocrine effects of nifedipine in heart failure: comparison with nitroprusside

To evaluate the short-term hemodynamic and neuroendocrine effects of nifedipine in heart failure, it was compared with nitroprusside, a balanced vasodilator without known inotropic effect, in equihypotensive doses during right and left heart catheterization in nine patients with heart failure. Mean arterial pressure decreased from 89 +/- 12 to 76 +/- 14 mm Hg with nitroprusside, and from 90 +/- 12 to 75 +/- 13 mm Hg with sublingual nifedipine. Right atrial, pulmonary artery, pulmonary capillary wedge and left ventricular end-diastolic pressures decreased significantly with nitroprusside, but not with nifedipine. Cardiac index and stroke volume index increased to a similar extent with both drugs; in contrast, stroke work index increased significantly with nitroprusside, but not with nifedipine. Peak rate of left ventricular pressure development (dP/dt) (measured with a micromanometer-tipped catheter in seven patients) was unchanged with nitroprusside, but decreased significantly with nifedipine (747 +/- 292 to 639 +/- 238 mm Hg/s; p less than 0.002). There was no change in heart rate with either medication. Plasma norepinephrine and epinephrine concentrations were not altered significantly by either drug. Plasma renin activity was not changed by nitroprusside infusion, but was increased after the administration of nifedipine. Thus, in contrast to the balanced vasodilator action of nitroprusside, the effect of nifedipine is predominantly on the arterial circulation. In these patients with heart failure, reflex sympathetic stimulation did not occur in response to a decrease in systemic arterial pressure by either vasodilator. A negative inotropic effect occurred after the administration of nifedipine, but not nitroprusside.