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Review Article Open Access
Haemostatic function of platelets is vital & their pathological role is potentially lethal. In pathological states there is over activation and aggregation of blood platelets resulting in atherothrombosis causes various states from angina to acute coronary syndromes, stroke and peripheral artery diseases. Platelets are anuclear subcellular fragments derived from megakaryocytes that circulate in blood as small anucleate ovoid discs. Under normal conditions they do not interact with the intact endothelial cell lining throughout the vasculature. Disruption of this well-regulated balance leads to pathologic conditions, such as thrombosis and bleeding. Although controlled plug formation is desired for the prevention of excessive blood loss and for promoting wound healing, several pathological conditions may result in the formation of occlusive thrombi leading to severe clinical complications, including myocardial infarction and ischemic stroke. The formation of a stable platelet plug occurs in three different stages: platelet adhesion, amplification of platelet activation and platelet aggregation. Many strategies have been pursued to lower the risk of pathological thrombus formation by interfering either with platelet adhesion, activation or aggregation. We here review clinically established antiplatelet targets and promising new antiplatelet strategies that are under investigation.
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Author(s): Rahul Saini, Sunaina