Regional wall motion from radiopaque markers after intravenous and intracoronary injections of nifedipine

In 11 patients, 1 mg of i.v. nifedipine was administered over 3 minutes and regional wall motion was studied during atrial pacing. The dominant effect of nifedipine at basal heart rate (HR) was a lowering of peak left ventricular pressure (152 to 128 mm Hg) with an increase in HR from 70 to 86 beats/min. During pacing, nifedipine produced (p < 0.02) a similar reduction in pressure at all rates, which is a mechanism reducing or sparing myocardial oxygen consumption. At the highest paced rate, the maximal velocity (Vmax) of the contractile element was significantly (p < 0.02) increased from 61 to 68 sec^-1 and the regional shortening fractions were increased over the entire pacing range: basal HR, 13.7% to 14.6% (p < 0.025); HR 120 beats/min, 11.6% to 13.5% (p < 0.005); maximal HR, 10.9% to 11.8% (p < 0.05). No evidence of a negative inotropic effect after i.v. administration of nifedipine was observed, myocardial oxygen consumption was probably reduced and there was an increase in regional function. Nifedipine (0.1 mg within 10 seconds) was selectively injected into bypass grafts at a constant paced rate in 10 patients. Seventeen marker pair regions were directly supplied by bypasses selectively injected with nifedipine (group A), and nine were independently perfused (group B). The pressure-derived variables showed a direct negative inotropic effect and a slowed relaxation phase. Thirty seconds after injection, minimal marker separation in group A occurred 78 msec after end-systole (ES), whereas before injection, minimal marker separation occurred 39 msec before ES (p < 0.0001). At the same time, the relation between minimal marker separation and ES in group B was unaffected. In consequence, the regional shortening fraction in group A contributing to left ventricular ejection decreased significantly 30 seconds after injection (-32%,p < 0.01), while that calculated simply from minimal and maximal marker separation remained unchanged (-9%, NS). Active regional contraction starting after the beginning of ejection and ending after ES must be considered as asynchrony and can be considered responsible for the slowed isovolumic contraction and relaxation of the whole ventricle. The dominant effect of i.v. nifedipine at clinical dosage levels is a lowering of systemic blood pressure, possibly reducing oxygen demand. When regionally administered, nifedipine exerts a direct negative inotropic effect, but after i.v. injection, this effect is overridden by reflex increases in contractility and in heart rate as a result of lowered systemic arterial pressure.