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European Heart Journal 1996 17(Supplement E):2-8; doi:10.1093/eurheartj/17.suppl_E.2
Copyright © 1996 by the European Society of Cardiology.
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© 1996 1996 The European Society of Cardiology

The rationale for thrombolytic therapy

R. M. Califf

Division of Cardiology, Department of Medicine, Duke University Medical Center Durham, North Carolina, U.S.A.

Correspondence. Robert M. Califf, MD, Professor of Medicine, Box 33123, Duke University Medical Center, Durham, North Carolina, U.S.A. 27710

Substantial progress has been made toward understanding the pathophysiological processes that lead to acute myocardial infarction. Research has shown that the mechanism of infarction is the rupture of an atherosclerotic plaque with a subsequent thrombogenic response from exposed subendothelial tissue, leading to additional or complete obstruction of the vessel. Myocardial cell death then proceeds in a wavefront fashion from the subendo cardium to the epicardium. Time to myocardial reper fusion and the extent of collateral flow are the primary determinants of final infarct area. This knowledge led to the development of therapeutic strategies to achieve early and sustained reperfusion of the infarct-related vessel, the presumption being that this would result in increased myocardial salvage and better residual left ventricular function in addition to reductions in infarct expansion and electrical instability.

The results of several large thrombolytic trials have supported this model, showing that patients who receive thrombolytic therapy derive a constant relative survival benefit when compared with control patients. The largest comparative thrombolytic trial to date has shown that therapies that result in early, more complete reperfusion are indeed associated with lower mortality; however, these therapies may be associated with higher rate of complications such as intracranial haemorrhage and reocclusion. Future evaluations must include assessment of the benefits relative to the risks of newer, more potent thrombolytic regimens.

Key Words: Acute myocardial infarction • thrombolysis • myocardial reperfusion • open vessel concept • tissue plasminogen activator • streptokinase • heparin


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