Prognostic importance of the immediate hemodynamic response to nifedipine in patients with severe left ventricular dysfunction

Department of Medicine, Mount Sinai School of Medicine, City University of New York, New York.

To determine the clinical significance of the occurrence of hemodynamic deterioration after the administration of calcium channel blocking drugs, nifedipine (20 mg orally) was administered to 29 patients with severe left ventricular dysfunction. Thirteen patients showed hemodynamic improvement with the drug (Group 1), as shown by a notable increase in cardiac index associated with a modest decrease in mean arterial pressure. The other 16 patients exhibited hemodynamic deterioration after nifedipine (Group 2), as reflected by a decline in right and left ventricular stroke work indexes accompanied by a marked hypotensive response. These differences were not related to differences in the peripheral vascular response to nifedipine, because both groups showed similar decreases in systemic and pulmonary vascular resistances. Groups 1 (hemodynamic improvement) and 2 (hemodynamic deterioration) were similar with respect to all demographic variables and pretreatment left ventricular performance (cardiac index, left ventricular filling pressure and systemic vascular resistance). Yet, the 1 year actuarial survival in patients in Group 1 was substantially better than that in patients in Group 2 (67 versus 23%, p = 0.009). Group 2, however, had higher values for plasma renin activity (17.7 +/- 6.0 versus 4.3 +/- 1.4 mg/ml per h, p less than 0.05), lower values for serum sodium concentration (134.6 +/- 1.2 versus 139.2 +/- 0.6 mEq/liter, p less than 0.05) and higher values for mean right atrial pressure (15.8 +/- 2.0 versus 7.9 +/- 1.4 mm Hg, p less than 0.01) than did patients in Group 1.(ABSTRACT TRUNCATED AT 250 WORDS)

This article has been cited by other articles:

				C. B. Maxwell and A. T. Jenkins Drug-induced heart failure Am. J. Health Syst. Pharm., October 1, 2011; 68(19): 1791 - 1804. [Abstract] [Full Text] [PDF]

				F. G. Spinale, R. Mukherjee, R. S. Krombach, M. J. Clair, J. W. Hendrick, W. V. Houck, L. Hebbar, S. B. Kribbs, J. L. Zellner, and M. G. Dodd Chronic Amlodipine Treatment During the Development of Heart Failure Circulation, October 20, 1998; 98(16): 1666 - 1674. [Abstract] [Full Text] [PDF]

				S. B. Kribbs, W. M. Merritt, M. J. Clair, R. S. Krombach, W. V. Houck, M. G. Dodd, R. Mukherjee, and F. G. Spinale Amlodipine Monotherapy, Angiotensin-Converting Enzyme Inhibition, and Combination Therapy With Pacing-Induced Heart Failure Hypertension, March 1, 1998; 31(3): 755 - 765. [Abstract] [Full Text] [PDF]

				W. Z. Wang, A. Matsumori, T. Yamada, T. Shioi, I. Okada, S. Matsui, Y. Sato, H. Suzuki, K. Shiota, and S. Sasayama Beneficial Effects of Amlodipine in a Murine Model of Congestive Heart Failure Induced by Viral Myocarditis: A Possible Mechanism Through Inhibition of Nitric Oxide Production Circulation, January 7, 1997; 95(1): 245 - 251. [Abstract] [Full Text]

				S. S. Gottlieb, M. L. Kukin, M. Yushak, N. Medina, and M. Packer Adverse Hemodynamic and Clinical Effects of Encainide in Severe Chronic Heart Failure Ann Intern Med, April 1, 1989; 110(7): 505 - 509. [Abstract] [PDF]