A1/A2 polymorphism of glycoprotein IIIa and association with excess procedural risk for coronary catheter interventions: a case-controlled study

Background A five-fold increase in risk of stent thrombosis in carriers of A1/A2 (Leu33Pro) polymorphism of glycoprotein IIIa has been described. Whet her this increased procedural risk applies to other coronary interventions is unknown. We investigated the role of A1/A2 polymorphism as a putative ri sk factor. Methods We genotyped 1000 consecutive patients with angiographically confir med coronary-artery disease and 1000 controls matched for age and sex. 653 of the 1000 patients received interventions (271 coronary angioplasty, 102 directional coronary atherectomy, and 280 stenting) and were assessed for a 30-day composite endpoint of need for target-vessel revascularisation, myo cardial infarction, and death. Findings The composite endpoint occurred in 41 (6.3%) patients. There was n o evidence that the A2 allele was associated with excess procedural risk (r elative risk 1.36 [95% CI 0.70-2.70], p=0.37). Nor, in subgroup analyses, d id A2 predict events that complicated coronary angioplasty (1.17 [0.40-2.70 ]), directional coronary atherectomy (1.50 [0.30-8.70]), or stenting (1.45 [0.60-3.50]). Neither heterozygotes (A1/A2) nor homozygotes (A2/A2) were ov er-represented in any subgroup, including those with acute coronary syndrom es, early disease manifestation (age <40 years), and histories of myocardia l infarction. Interpretation A1/A2 polymorphism is not a major risk factor for 30-day adv erse events that complicate coronary angioplasty, directional coronary athe rectomy, or stenting. Furthermore, A1/A2 polymorphism has no apparent impac t on more chronic processes such as atherogenesis of the coronary arteries.