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Thrombolysis for Evolving Myocardial Infarction

[+] Article, Author, and Disclosure Information

Grant support: The development of this paper by the Clinical Efficacy Assessment Project was funded by the John A. Hartford Foundation.

▸Requests for reprints should be addressed to Linda Johnson White; Clinical Efficacy Assessment Project, Department of Health and Public Policy, American College of Physicians, 4200 Pine Street; Philadelphia, PA 19104.

© 1985 American College of PhysiciansAmerican College of Physicians

Ann Intern Med. 1985;103(3):463-469. doi:10.7326/0003-4819-103-3-463
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This excerpt has been provided in the absence of an abstract.

The commonest cause of transmural myocardial infarction is thrombotic occlusion of a coronary artery (1, 2). With improved therapy for life-threatening arrhythmias in the setting of acute myocardial infarction, cardiac pump failure has emerged as the principal in-hospital cause of death in these patients. Efforts to decrease mortality related to pump failure have focused on reducing the extent of myocardial damage by reducing myocardial oxygen demand and improving myocardial oxygen supply. Thrombolytic therapy in the setting of acute myocardial infarction involves the use of pharmacologic agents to lyse coronary thrombi and to reperfuse jeopardized myocardium, thereby improving myocardial oxygen supply.


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