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Part of the book series: Contemporary Cardiology ((CONCARD))

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Abstract

Angiographic and pathologic studies have contributed greatly to our understanding of the pathogenesis of acute coronary syndromes. “Vulnerable” atherosclerotic plaques, characterized by thin fibrous caps, lipid-rich cores, and infiltration of leukocytes, undergo ulceration, fissure, or rupture (1–3). Exposure of subendothelial collagen leads to adhesion and activation of platelets. The coagulation cascade is initiated by subendothelial tissue factor as well as vasoactive substances secreted by activated platelets. These processes result in platelet aggregation, thrombin generation, and fibrin deposition, ultimately leading to coronary thrombosis. In the case of ST-segment elevation acute myocardial infarction (AMI), the thrombosis is usually occlusive, resulting in transmural myocardial necrosis (4). Reperfusion therapy, whether catheter-based or pharmacologic, is critically needed to restore antegrade flow to the infarct-related artery and thus arrest the propagating wave of necrosis (5). To preserve myocardium and reduce morbidity and mortality, reperfusion must be rapid, complete, and sustained.

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Cantor, W.J. (2002). Rationale and Lexicon of Primary Angioplasty. In: Tcheng, J.E. (eds) Primary Angioplasty in Acute Myocardial Infarction. Contemporary Cardiology. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-155-8_1

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  • DOI: https://doi.org/10.1007/978-1-59259-155-8_1

  • Publisher Name: Humana Press, Totowa, NJ

  • Print ISBN: 978-1-4757-6248-8

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