This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Ferlinz, J. Articles by Aronow, W. S. Search for Related Content PubMed PubMed Citation Articles by Ferlinz, J. Articles by Aronow, W. S.

Circulation, Vol 59, 313-319, Copyright © 1979 by American Heart Association

ARTICLES

Effects of verapamil on myocardial performance in coronary disease

J Ferlinz, JL Easthope and WS Aronow

Verapamil, a calcium antagonist, has been used extensively for treatment of cardiac arrhythmias. Concern persists, however, that it may seriously depress myocardial function in cardiac patients. To investigate this possibility, 20 patients with coronary artery disease (CAD) but no heart failure were given intravenous verapamil (0.1 mg/kg bolus, followed by 0.005 mg/kg/min infusion), and studied hemodynamically and angiographically. Verapamil markedly lowered mean aortic pressure (94 +/- 17 to 82 +/- 13 mm Hg, p less than 0.0005) and systemic vascular resistance (1413 +/- 429 to 1069 +/- 235 dyn-sec-cm5, p less than 0.0005). Simultaneously, all indices of left ventricular (LV) performance greatly improved: cardiac index rose from 2.8 +/- 0.6 to 3.1 +/- 0.7 1/min/m2 (p less than 0.0005), mean velocity of circumferential fiber shortening increased from 0.85 +/- 0.39 to 0.97 +/- 0.46 circ/sec (p less than 0.01), and ejection fraction improved from 55 +/- 16 to 61 +/- 18% (p less than 0.01). No significant changes were noted in the heart rate before and after verapamil administration, and verapamil did not worsen the extent of LV asynergy in the majority of patients. In patients with CAD, the intrinsic negative inotropic effect of verapamil is of negligible importance because its potent vasodilatory properties more than compensate for any intrinsic decrease in LV contractility, and thereby improve the overall cardiac function.

This article has been cited by other articles:

				A. L. Waldo, V. J. Plumb, J. G. Arciniegas, R. W. Henthorn, and S. H. Zimmern Verapamil Therapy in the Treatment of Supraventricular Arrhythmias Following Open Heart Surgery Angiology, December 1, 1983; 34(12): 755 - 763. [PDF]

				B. N. Singh, K. Nademanee, and G. Feld Antiarrhythmic Effects of Verapamil Angiology, September 1, 1983; 34(9): 572 - 590. [PDF]

				B. N. Singh Pharmacological Basis for the Therapeutic Applications of Slow-Channel Blocking Drugs Angiology, August 1, 1982; 33(8): 492 - 515. [PDF]

				J. Kieval and R. J. Myerburg The Hemodynamic Effects of Calcium Channel Blocking Agents: A Brief Review Angiology, August 1, 1982; 33(8): 516 - 521. [PDF]

				M. D. Winniford, J. T. Willerson, and L. D. Hillis Calcium Antagonists in the Treatment of Individuals with Ischemic Heart Disease Angiology, August 1, 1982; 33(8): 522 - 539. [Abstract] [PDF]