Direct cardiac and peripheral vascular effects of intracoronary and intravenous nifedipine

Abstract

The hemodynamic effects of a new parenteral formulation of nifedipine administered by the intravenous (1 mg) and intracoronary (IC) (0.1 and 0.2 mg) routes were studied in 10 patients with symptomatic coronary artery disease undergoing diagnostic right- and left-sided cardiac catheterization. Intravenous nifedipine (1 mg) reduced systemic vascular resistance by 34% (p < 0.01), increased cardiac output by 28% (p < 0.01) and decreased mean arterial pressure by 10% (p < 0.01). It had less effect on peak positive dP/dt (-8% p < 0.025) and on peak negative dP/dt (-15% p < 0.01). Coronary blood flow increased 20% (p < 0.025). In contrast, IC nifedipine (0.2 mg) increased coronary blood flow 46% (p < 0.025), depressed contractility as assessed by peak positive dP/dt (-26% p < 0.01) and prolonged diastolic relaxation time. The effect of 0.1 mg was similar but less pronounced. These data suggest that the primary therapeutic effect of nifedipine administered systemically to patients at rest results from an increase in coronary blood flow and, to a lesser extent, from afterload reduction; its myocardial depressant effects are small, transient and masked by reflex catecholamine release. IC nifedipine increases coronary blood flow, has a transient negative inotropic effect and prolongs relaxation. The relative importance of these myocardial effects in preventing myocardial ischemia is not known.