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.