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Calcium antagonists and stunned myocardium: importance for clinicians?

Authors: K Przyklenk|||R A Kloner

Journal: Cardiovascular drugs and therapy

Publication Type: Journal Article

Date: 1991

DOI: 10.1007/BF00053557

ID: 1756142

Affiliations:

Affiliations

    Heart Institute, Hospital of the Good Samaritan, Los Angeles, CA 90017.|||

Abstract

Experimental evidence indicates that calcium antagonists enhance the recovery of contractile function in canine myocardium stunned by a brief, 15-minute episode of transient coronary artery occlusion. In fact, both nifedipine and verapamil have been shown to improve systolic contraction, even when treatment was delayed, that is, when the agents were administered 30 minutes after reperfusion. The beneficial effects of delayed treatment were not a consequence of myocardial high-energy phosphate preservation. Furthermore, as low-dose intracoronary nifedipine enhanced the recovery of function in the absence of systemic hemodynamic or coronary vasodilatory effects, the improved function associated with delayed administration of calcium antagonists could not be attributed solely to afterload reduction or increased coronary blood flow. These data suggest that calcium-channel blockers exert a direct effect on the previously ischemic tissue, perhaps by subtle modulation of calcium transport or flux within the stunned myocytes. Although the precise mechanism of action of these agents remain unresolved, these intriguing experimental results raise the possibility that calcium antagonists may provide a clinically useful means of attenuating postischemic dysfunction of viable myocardium salvaged by thrombolysis, angioplasty, or cardiopulmonary bypass. The potential role of calcium-channel blockers in these clinical instances of stunned myocardium awaits further evaluation.


Chemical List

    Calcium Channel Blockers

Reference List

    Circulation. 1991 Feb;83(2):681-8|||Circ Res. 1983 Feb;52(2 Pt 2):I129-38|||Circulation. 1989 Nov;80(5):1115-27|||Circulation. 1984 Oct;70(4):734-41|||J Am Coll Cardiol. 1988 Mar;11(3):614-23|||Am J Cardiol. 1987 Jan 30;59(3):84B-94B|||Circ Res. 1989 Sep;65(3):838-46|||Am J Cardiol. 1987 Jan 30;59(3):75B-83B|||Circulation. 1989 Oct;80(4):1049-62|||J Am Coll Cardiol. 1987 Sep;10(3):710-2|||Circ Res. 1987 May;60(5):700-7|||Am J Med. 1989 Jan 16;86(1A):14-22|||Basic Res Cardiol. 1990 Jan-Feb;85(1):45-54|||J Mol Cell Cardiol. 1983 Oct;15(10):659-71|||Am J Physiol. 1989 Feb;256(2 Pt 2):H368-74|||Am J Cardiol. 1989 Nov 7;64(17):84I-91I; discussion 91I-93I|||J Am Coll Cardiol. 1985 Nov;6(5):1026-34|||J Clin Invest. 1987 Mar;79(3):950-61|||Proc Natl Acad Sci U S A. 1980 Sep;77(9):5471-5|||J Clin Invest. 1988 Sep;82(3):920-7|||J Am Coll Cardiol. 1990 Mar 1;15(3):737-47|||Am J Pathol. 1981 Feb;102(2):262-70|||Pharmacol Res Commun. 1988 Jan;20(1):13-21|||J Cardiovasc Pharmacol. 1985 Jan-Feb;7(1):158-66|||J Am Coll Cardiol. 1989 Apr;13(5):1176-83|||Am J Cardiol. 1989 Nov 7;64(17):94I-100I|||Circulation. 1986 Oct;74(4):843-51|||Circulation. 1982 Dec;66(6):1146-9|||J Mol Cell Cardiol. 1982 Sep;14 Suppl 3:99-103|||Am J Pathol. 1972 Jun;67(3):441-52|||J Clin Invest. 1988 Aug;82(2):476-85