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. Whether this increased procedural risk applies to other coronary interventions is unknown. We investigated the role of A1/A2 polymorphism as a putative risk factor. Methods We genotyped 1000 consecutive patients with angiographically confirmed 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, myocardial infarction, and death. Findings The composite endpoint occurred in 41 (6·3%) patients. There was no evidence that the A2 allele was associated with excess procedural risk (relative risk 1·36 [95% CI 0·70–2·70], p=0·37). Nor, in subgroup analyses, did 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 over-represented in any subgroup, including those with acute coronary syndromes, early disease manifestation (age <40 years), and histories of myocardial infarction. Interpretation A1/A2 polymorphism is not a major risk factor for 30-day adverse events that complicate coronary angioplasty, directional coronary atherectomy, or stenting. Furthermore, A1/A2 polymorphism has no apparent impact on more chronic processes such as atherogenesis of the coronary arteries.