Effects of nifedipine on left ventricular distensibility, relaxation and filling dynamics during pacing-induced myocardial ischemia

Abstract

Diastolic left ventricular properties were assessed in 8 patients with coronary artery disease at rest and during postpacing states before and after nifedipine (10 mg sublingually). Typical anginal pain developed in all patients during pacing tachycardia before but not after nifedipine. Postpacing increases in end-diastolic pressure (10 ± 5 [mean ± standard deviation]to 23 ± 9 mm Hg) and volume (99 ± 29 to 113 ± 27 ml) were greatly attenuated with nifedipine (13 ± 7 and 97 ± 22 ml, respectively). These responses were associated with normalization of postpacing shifts of the ventricular diastolic pressure-volume curve upward or more to the right. The time constant of ventricular relaxation was prolonged by pacing tachycardia (44 ± 10 to 62 ± 5 ms) and was reduced to the control level in postpacing beats after nifedipine. The peak rate of early ventricular filling was affected neither by pacing stress nor by nifedipine. When regional myocardial function was expressed by a radial coordinate system, the nonischemic segment responded to the control pacing with an increase in end-diastolic length and comparable augmentation of the stroke excursion, while the ischemic segment showed a marked reduction in stroke excursion with end-diastolic length unchanged. Thus, the diastolic pressure-length relation moved up to the higher portion of the single curve in the nonischemic segment, while it shifted directly upward in the ischemic segment. These responses were markedly attenuated with nifedipine. The peak rate of segmental lengthening increased in postpacing beats before and after nifedipine in the normal segment, while it decreased by pacing stress with significant improvement with nifedipine in the ischemic segment. Thus, the net global changes in left ventricular diastolic function are determined by the complex interaction of changes in the regional myocardium, and favorable effects of nifedipine on global responses to transient ischemia are largely mediated by selective improvement of the ischemic segment.