Literature Review: Anticoagulant Therapy in the Management of Acute Myocardial Infarction

Abstract

Acute Myocardial Infarction (AMI) is a clinical condition resulting from an inadequate supply of oxygen to the myocardium, leading to sudden damage of cardiac muscle tissue. This condition typically arises from thrombotic occlusion of the coronary arteries following atherosclerotic plaque disruption. The thrombus formed in this process generally consists of platelet aggregates and fibrin. When an atherosclerotic plaque located within the coronary arterial wall undergoes disruption, either through rupture or erosion, its thrombogenic core becomes exposed to the bloodstream. This exposure triggers platelet activation and initiates the coagulation cascade, culminating in thrombus formation at the site of the plaque. The resulting thrombus may obstruct the artery and impede blood flow to the myocardium. Such obstruction induces ischemia, a state in which the cardiac muscle fails to receive adequate oxygen and nutrients necessary for optimal function. One of the therapeutic strategies employed in the management of AMI is anticoagulant therapy. Anticoagulants inhibit the coagulation cascade and prevent fibrin formation, which constitutes the main structural component of thrombi. An ideal anticoagulant is one that effectively prevents pathological thrombosis and mitigates reperfusion injury while preserving physiological hemostasis and minimizing bleeding risk. However, the use of anticoagulant and fibrinolytic agents may increase the likelihood of bleeding events, which represent their principal adverse effects. In severe cases, excessive bleeding may occur, significantly elevating the risk of mortality. Therefore, appropriate selection of anticoagulant agents, careful patient stratification, precise dosing, and meticulous clinical monitoring of coagulation parameters are required to reduce these risks.