Abstract
Until about 15 years ago the prevailing view of the pathogenesis of acute myocardial infarction was that it was based on total or subtotal atherosclerotic coronary obstructions causing a major decrease in antegrade flow. Fresh thrombi, which were often found during autopsy, were thought to be the result rather than the cause of the infarction [4], With the increasing availability of coronary arteriography for acute myocardial infarction came a major change in the understanding of the pathophysiology of the disease. DeWood et al. [9], using serial coronary arteriograms, showed that a fresh, occluding coronary thrombus is the cause and can be found in the majority of acute myocardial infarctions. While within the first 6 h the rate of total occlusions was 85%, this fell to 68% in the 6th–12th h — and to 64% in the 12th–24th h. These results also demonstrated that spontaneous thrombolysis occurs in about 20% of all patients within the 1st day.
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© 1991 Springer-Verlag Berlin Heidelberg
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Meyer, J. (1991). Fibrinolysis in Myocardial Infarction: Lessons for Cerebrovascular Disease. In: Hacke, W., del Zoppo, G.J., Hirschberg, M. (eds) Thrombolytic Therapy in Acute Ischemic Stroke. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-76439-4_3
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DOI: https://doi.org/10.1007/978-3-642-76439-4_3
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