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This article explores the pathogenesis and factors influencing plaque rupture in Acute Coronary Syndromes (ACS). It discusses the structure of thrombus following plaque disruption and the role of platelet adhesion, activation, and aggregation. The therapeutic interventions against platelet activation and aggregation, including the mechanism of action of GP IIb-IIIa inhibitors, are also discussed. Additionally, it highlights the ischemic complications of percutaneous coronary intervention (PCI) and microembolization.
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Acute Coronary Syndromes (ACS) Van de Werf F. Throm Haemost. 1997; 78(1):210-213.
Pathogenesis of ACS White HD. Am J Cardiol. 1997; 80(4A):2B-10B.
Factors affecting plaque rupture/fissure • Sudden changes in intraluminal pressure or tone • Bending and twisting of an artery during each heart contraction • Lipid content of plaque • Thickness of fibrous cap • Plaque shape • Mechanical injury White HD. Am J Cardiol. 1997; 80(4A):2B-10B.
Pathogenesis of ACS White HD. Am J Cardiol. 1997; 80(4A):2B-10B.
Structure of thrombus following plaque disruption Adapted from Davies MJ. Circulation. 1990; 82 (suppl II): 11-38—11-46.
Platelet adhesion, activation, and aggregation White HD. Am J Cardiol. 1997; 80(4A):2B-10B.
GP IIb-IIIa: the final commonpathway to platelet aggregation White HD. Am J Cardiol. 1997; 80(4A):2B-10B.
Therapeutic interventions against platelet activation and aggregation White HD. Am J Cardiol. 1997; 80(4A):2B-10B.
Mechanism of action: GP IIb-IIIa inhibitors White HD. Am J Cardiol. 1997; 80(4A):2B-10B.
Thrombus formation Percutaneous coronaryintervention Plaque rupture/fissure Intracoronary stenting Microembolization Ischemic Complications of PCI White HD. AM J Cardiol. 1997; 80(4A): 2B-10B.