Section 5
Chapter 4,781

Arterial vasodilator, systemic and coronary hemodynamic effects of nisoldipine in congestive heart failure secondary to ischemic or dilated cardiomyopathy

Kiowski, W.; Erne, P.; Pfisterer, M.; Mueller, J.; Buehler, F.R.; Burkart, F.

American Journal of Cardiology 59(12): 1118-1125


ISSN/ISBN: 0002-9149
PMID: 3578053
DOI: 10.1016/0002-9149(87)90859-9
Accession: 004780281

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The systemic and coronary hemodynamic and neurohumoral effects of nisoldipine, a calcium antagonist drug with high vascular specificity, were investigated in 17 patients with chronic congestive heart failure (CHF). Brachial artery infusions (n = 9) decreased forearm vascular resistance in a dose-dependent manner, attesting to its powerful arterial vasodilator properties. A dose of 3 .mu.g/kg intravenously decreased mean blood pressure 16% and systemic vascular resistance 33%, while increasing stroke index 19% and ejection fraction 21% at rest and similarly during exercise. Pulmonary capillary wedege pressure decreased significantly during exercise. Intravenous infusion of nisoldipine increased rest coronary sinus flow 10% (p < 0.05, n = 7), decreased rest and exercise coronary vascular resistance 28% and 19% (p < 0.01) and rest myocardial oxygen consumption 14% (p < 0.05). In 13 patients similar systemic hemodynamic results were found after treatment with oral nisoldipine, 2 .times. 20 mg for 4 weeks. Stroke index and stroke work index increased long-term more than acutely (31% and 12.4% vs. 19% and 4.5% at rest, both p < 0.05), which may indicate a compensated mild cardiodepressant effect of intravenous nisoldipine. Changes in forearm vascular resistance after intraarterial administration did not correlate with changes of systemic vascular resistance after intravenous administration, suggesting that factors other than vascular calcium entry blockade importantly influence hemodynamic responses. Elevated control plasma norepinephrine and renin levels, on average, did not change during chronic therapy but individual changes were compatible with a reduction of sympathetic activity in patients with hemodynamic improvement. Three patients died during the study; their deaths were probably unrelated to a potential negative inotropic effect of nisoldipine. Nisoldipine may be of value for treatment of CHF, particularly in patients with coronary artery disease.

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