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Part of the book series: Developments in Cardiovascular Medicine ((DICM,volume 203))

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Abstract

Rupture of an atherosclerotic plaque with subsequent platelet aggregation and coronary artery thrombosis is the central pathophysiologic event in the spectrum of acute coronary syndromes which range from unstable angina to myocardial infarction [1-3]. Plaque rupture provides a stimulus for the conversion of physiologic hemostatic mechanisms into pathologic processes which can result in occlusion of the coronary arterial lumen and myocardial necrosis. Whether plaque rupture results in complete coronary or partial arterial occlusion has been hypothesized to depend on a number of factors including the depth of arterial injury, the degree of luminal occlusion by plaque material, and the status of the coagulation system [4]. Plaque rupture occurs primarily at lipid-rich pools at the shoulder of the plaque which constitute areas of structural weakness [2]. Attempts to alter the lipid content of the plaque by decreasing plasma lipoprotein levels comprise the cornerstone of current attempts to prevent the conversion of stable coronary arterial atherosclerosis into unstable syndromes and may reflect the reasons for the reduction of acute ischemic events observed in large trials of lipid lowering therapy [5,6]. Management of luminal occlusion consists largely of mechanical interventions. Medical stabilization of patients with unstable syndromes is generally directed at the coagulation system.

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Bitar, J., Dabaghi, S., Sekili, S., Kleiman, N.S. (1998). Novel Antithrombotic Strategies. In: Wilensky, R.L. (eds) Unstable Coronary Artery Syndromes Pathophysiology, Diagnosis and Treatment. Developments in Cardiovascular Medicine, vol 203. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5715-9_7

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  • DOI: https://doi.org/10.1007/978-1-4615-5715-9_7

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4613-7617-0

  • Online ISBN: 978-1-4615-5715-9

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