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Intracoronary Thrombolysis in Evolving Myocardial Infarction

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Supported in part by grant HL17651, Specialized Center of Research.

Division of Cardiology, Cedars-Sinai Medical Center and University of California School of Medicine, Los Angeles; Los Angeles, California

Ann Intern Med. 1981;95(4):500-502. doi:10.7326/0003-4819-95-4-500
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This excerpt has been provided in the absence of an abstract.

Extensive myocardial necrosis remains the principal cause of death and morbidity among patients hospitalized with acute myocardial infarction. The clinical impact of interventions designed to reduce necrosis by reducing myocardial oxygen demand, augmenting collateral blood supply, or correcting ischemic cellular defects has been disappointing. As a result, the conviction that restoring blood flow to the ischemic myocardium is needed for clinically significant reduction of necrosis is becoming stronger.

The rate of myocardial necrosis is known to differ widely in experimental animals, from virtually no necrosis after several hours of coronary artery occlusion to transmural necrosis after only 40 minutes of


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