Key result
Genetic variation in platelet surface receptors may be associated with platelet hyperreactivity, increased risk of myocardial infarction, and variable benefit from antithrombotic drug treatments.
This review summarizes current knowledge on platelet glycoprotein genetics, its association with myocardial infarction risk, and pharmacogenetic implications for antithrombotic therapies.
May inform future pharmacogenetic antithrombotic strategies in coronary disease; leaves open prospective validation before clinical use.
Platelet aggregation and coronary thrombosis have a central role in the development of acute coronary syndromes and myocardial infarction (MI). Therapies aimed at inhibiting platelet aggregation have shown great benefit in individuals with coronary disease or with multiple risk factors for coronary disease. Genetic variation in platelet surface receptors mediating thrombus formation has been suggested to be associated with platelet hyperreactivity, with increased risk of MI and possibly with the benefit received from various antithrombotic drug treatments. This review focuses on discrepancies and their likely explanations in studies on platelet glycoprotein genetics. Current knowledge on important issues concerning coronary event phenotypes and pharmacogenetics is analyzed. Possible future applicability of these data to patient treatment is also discussed.
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Mikkelsson et al. (2005) conducted a review in Acute coronary syndromes and myocardial infarction. Genetic variation in platelet surface receptors was evaluated. Genetic variation in platelet surface receptors may be associated with platelet hyperreactivity, increased risk of myocardial infarction, and variable benefit from antithrombotic drug treatments.
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