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Modification of Myocardial Infarction Size After Coronary Occlusion

[+] Article, Author, and Disclosure Information

Grant support: 72-2949, National Heart and Lung Institute, National Institutes of Health; and by the John A. Hartford Foundation.

▸Requests for reprints should be addressed to Peter R. Maroko, M.D., Harvard Medical School, 25 Shattuck St., Boston, MA 02115.

Boston, Massachusetts

Ann Intern Med. 1973;79(5):720-733. doi:10.7326/0003-4819-79-5-720
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Several pharmacologic and hemodynamic interventions were found to alter acute ischemic injury of the myocardium and subsequent necrosis after coronary occlusion. Reduction in myocardial damage occurred when myocardial oxygen needs were reduced (beta-blocking agents, intra-aortic balloon counterpulsation, and digitalis in the failing heart), when coronary perfusion was improved (reperfusion, elevation of coronary perfusion pressure, nitroglycerin), when the provision of energy by means of anaerobic glycolysis was augmented (glucose-insulin-potassium, hypertonic glucose), when the diffusion of oxygen and of substrates to the ischemic cells was improved (hyaluronidase), and when the autolytic and heterolytic processes in the myocardium after coronary occlusion were stabilized (hydrocortisone). Interventions that increase myocardial oxygen consumption (tachycardia, isoproterenol, digitalis, glucagon, and bretylium in the non-failing heart) and that decrease coronary perfusion (arterial hypotension) increase myocardial ischemic damage. In pilot studies this concept of reduction in infarct size is being applied to patients, and initial results with hyaluronidase are promising.





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