Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation
Search: search_blue_button Advanced Search
Circulation. 1986;73:727-733

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Feldman, R. L.
Right arrow Articles by Pepine, C. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Feldman, R. L.
Right arrow Articles by Pepine, C. J.
Right arrowPubmed/NCBI databases
*Compound via MeSH
*Substance via MeSH
Hazardous Substances DB
*PROPRANOLOL HYDROCHLORIDE

Circulation, Vol 73, 727-733, Copyright © 1986 by American Heart Association


ARTICLES

Effect of propranolol on myocardial ischemia occurring during acute coronary occlusion

RL Feldman, RG MacDonald, JA Hill, MC Limacher, CR Conti and CJ Pepine

In 16 patients undergoing angioplasty of the left anterior descending coronary artery, the clinical, electrocardiographic, and hemodynamic effects of short-term intravenous nonselective beta-adrenergic blockade with propranolol (0.1 mg/kg) were assessed during temporary occlusion of the artery. Myocardial ischemia during coronary occlusion was prevented, delayed in onset, or diminished in magnitude by propranolol in 10 of the 16 patients. Propranolol decreased values for indexes of myocardial oxygen demand, such as heart rate and blood pressure and their product, in all patients. Surprisingly, in patients who derived clinical benefit, propranolol did not change indexes of myocardial oxygen supply to the left ventricular region perfused by the occluded artery. For example, great cardiac vein flow (40 +/- 15 to 41 +/- 17 ml/min, p = NS) and coronary collateral resistance (2.1 +/- 1.0 to 2.1 +/- 1.1 mm Hg/ml/min, p = NS) were unchanged. In contrast, a worsening of supply occurred in patients who were not benefited: great cardiac vein flow (50 +/- 10 to 39 +/- 6 ml/min, p less than .05) decreased and coronary collateral resistance (1.6 +/- 0.5 to 2.0 +/- 0.6 mm Hg/ml/min, p less than .05) increased. Information obtained from this study demonstrates the value of this new experimental preparation in helping assess potential clinical effectiveness of drug interventions during the initial phase of acute coronary occlusion and providing insight into the mechanisms of drug effect.


This article has been cited by other articles:


Home page
CirculationHome page
F. W. Wang, A. Osman, J. Otero, G. A. Stouffer, S. Waxman, A. Afzal, A. Anzuini, and B. F. Uretsky
Distal Myocardial Protection During Percutaneous Coronary Intervention With an Intracoronary {beta}-Blocker
Circulation, June 17, 2003; 107(23): 2914 - 2919.
[Abstract] [Full Text] [PDF]


Home page
Cardiovasc ResHome page
M. Billinger, M. Fleisch, F. R. Eberli, B. Meier, and C. Seiler
Collateral and collateral-adjacent hyperemic vascular resistance changes and the ipsilateral coronary flow reserve: Documentation of a mechanism causing coronary steal in patients with coronary artery disease
Cardiovasc Res, February 16, 2001; 49(3): 600 - 608.
[Abstract] [Full Text] [PDF]


Home page
CirculationHome page
J. J. Piek, R. A. M. van Liebergen, K. T. Koch, R. J. de Winter, R. J. G. Peters, and G. K. David
Pharmacological Modulation of the Human Collateral Vascular Resistance in Acute and Chronic Coronary Occlusion Assessed by Intracoronary Blood Flow Velocity Analysis in an Angioplasty Model
Circulation, July 1, 1997; 96(1): 106 - 115.
[Abstract] [Full Text]


Home page
J CARDIOVASC PHARMACOL THERHome page
Y. Birnbaum, K. Przyklenk, and R. A. Kloner
Time Frame of Ischemic Preconditioning: Is It Clinically Relevant?
Journal of Cardiovascular Pharmacology and Therapeutics, October 1, 1996; 1(4): 339 - 346.
[PDF]