Key result
Platelet activation plays a central role in vessel occlusion and unstable coronary syndromes, regulated by a complex myriad of cellular and plasma-derived mediators.
This review highlights the complex molecular regulation of platelet-dependent thrombosis and its central role in unstable coronary syndromes.
Supports platelet activation as key in ACS; leaves open which mediators to target therapeutically.
Hemostasis is a normal process preventing the sequelae of uncontrolled hemorrhage. In certain settings, these same processes cause adverse clinical events due to thrombotic occlusion of a vessel. The majority of unstable coronary syndromes result from disruption of an atherosclerotic plaque, leading to the exposure of subintimal contents, which triggers coagulation and the formation of a platelet-rich thrombus. The central role of platelet activation in the events that lead to vessel occlusion is well known. However, this process is complex and influenced by a myriad of cellular and plasma-derived mediators that regulate the balance between occlusive and nonocclusive thrombosis.
No takes yet. Share an insight, caveat, or question.
Jane E. Freedman (2005) conducted a review in Thrombosis and unstable coronary syndromes. Platelet activation plays a central role in vessel occlusion and unstable coronary syndromes, regulated by a complex myriad of cellular and plasma-derived mediators.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: