Low-Dose Aspirin for Atherothrombosis Prevention: Efficacy, Risks, and Controversies

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Abstract

Atherosclerosis is a chronic inflammatory illness in which immune systems work with metabolic risk factors to start, spread, and activate vascular lesions. It is the main cause of ischemic coronary artery disease and cerebrovascular disease. Myocardial infarction or ischemic stroke may result from arterial thrombosis, an acute complication that appears on the surface of a torn atheromatous plaque or as a result of endothelial erosion. The growth and advancement of atheromatous plaques may be aided by platelets, which are important biological elements of arterial occlusive thrombi. Additionally, essential to hemostasis, the physiological procedure that stops bleeding following tissue trauma and vascular injury, are platelets. Although the adhesion and activation of platelets can be seen as a repair-oriented response to sudden fissuring or rupture of an atheromatous plaque, unchecked progression of such a process through a series of self-sustaining amplification loops may result in intraluminal thrombus formation, vascular occlusion, and transient ischemia or infarction. Due to their adhesive qualities and ability to quickly activate in response to a variety of stimuli, platelets can contribute in both healthy hemostasis and atherothrombosis. By selectively blocking important platelet enzymes or receptors, antiplatelet medications currently on the market interfere with specific steps in the activation process, lowering the risk of arterial thrombosis through mechanisms that cannot be separated from an increased risk of bleeding complications.

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