Why the study?
Uncontrolled platelet activation and accumulation after atherosclerotic plaque rupture in coronary arteries can lead to occlusive thrombosis and myocardial infarction.
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Design
Review
Platelet roles in thrombosis and inflammation warrant integrated caution; leaves open targeted modulation research.
Abstract—Platelets play a key role in the development of thrombosis and inflammation. These cells are the key participants in pathological thrombosis due to their ability to attach to damaged areas of blood vessels and further accumulation at the sites of damage. Although platelet activation and adhesion should be considered as a physiological response to a sudden rupture of an atherosclerotic plaque, which frequently contributes to its repair, the uncontrolled progression of such a process in the coronary arteries may result in the formation of a thrombus occluding the lumen of the vessel, that cause the development of myocardial infarction. This review is mainly devoted to the consideration of the correction of platelet function using antiplatelet drugs, which have led to significant positive changes in the fight against acute coronary syndrome and myocardial infarction.
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Bouryachkovskaya et al. (2023) studied this question.
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