Platelet Function Evaluation in Cardiovascular Diseases
Myocardial infarction (MI), commonly termed "heart attack", occurs when the blood supply to part of the heart muscle (the myocardium) is severely reduced or blocked. 70% of MI cases are the result of Vulnerable Plaque (VP). Vulnerable Plaque is characterized by fatty buildup leading to the development of a substantial necrotic core within the artery wall with a thin fibrous cap covering it and significant extent of macrophage infiltration (inflammation). Vulnerable plaques characteristically contain a lipid pool of more than 40% of volume, while the thin, fibrous cap is less than 100 microns. When vulnerable plaque lesions rupture, the content of the lesion spills into the bloodstream. The cytokines on the artery wall capture blood cells (mainly platelets) that rush to the site of injury and create a thrombus which can become large enough to block the artery. Thus, it is the aggregation of platelets inside the blood vessel which blocks the artery. Therefore, an effective evaluation of the patient's platelet function, following by timely preventive treatment with anti-aggregatory (antiplatelet) drugs may be crucial to saving the lives of patients in the event of MI.
The treatment with platelet aggregation inhibitors (antiplatelet drugs) which help to prevent the formation of potentially harmful blood clots has become a cornerstone of cardiovascular medicine. Aspirin and clopidogrel have emerged as critical therapies in the treatment of cardiovascular disease.
Mechanism of Action: The mechanism of action of clopidogrel is irreversible blockade of the adenosine diphosphate (ADP) receptor on platelet cell membranes. This receptor named P2Y12 plays an important role in platelet aggregation, and specifically in the cross-linking of platelets by fibrin. The blockade of this receptor inhibits platelet aggregation by blocking activation of the glycoprotein IIb/IIIa pathway. Plavix is an expensive drug costing approximately $3 a day or about $100 a month.
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