ABSTRACT
Recent data suggest that inherited prothrombotic risk factors are associated with acute coronary syndromes. Glycoprotein III a [GP III a] is part of the platelet fibrinogen receptors, the common final pathway of platelet aggregation. PI A1/A2 genetic polymorphism in GP III a, due to a leucine to proline amino-acid substitution at residue 33, has become a fashionable candidate polymorphism in coronary artery disease [CAD]. The aim of the study was to investigate the potential importance of PI A2 [Pro 33] allele as a risk factor for acute coronary syndromes. the study included 90 patients [aged 45 +/- 7 years], with angiographically documented CAD, 39 patients with acute myocardial infarction [MI] 3 with non-Q wave MI, and 48 with unstable angina. Patients underwent complete clinical, ECG, and enzymatic assessment, in addition to coronary angiography. Patients were compared to 48 age- and sex-matched controls. PI Al allele was assessed with the aid of polymerase chain reaction for all patients and controls. The PI A2 allele was present in 24 patients [26.7%] II with acute MI [28.2%] and 13 with unstable angina [27.1%], [P > 0.05]. Yet, it was present in 10 controls [20.8%, P > 0.05]. PI A1/A2 polymorphism has no association to the extent of angiographic findings. This study demonstrated that PI A1/A2 polymorphism might be associated with an increased risk for acute coronary syndromes. Patients who possess PI A2 allele may be at increased risk of coronary thrombotic events. The attractive possibility remains that such polymorphism might identify a subset of individuals who would respond better to a particular therapy