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In this study, we evaluate the relationships between aspirin nonresponsiveness and the cyclooxygenase-1 (Cox-1) gene C50T polymorphism in stable coronary artery disease (CAD) in Tunisian patients. One hundred twenty-five stable CAD patients were included. The Cox-1 gene C50T polymorphism was determined by the polymerase chain reaction/restriction fragment length polymorphism method. Aspirin response was evaluated by measuring the collagen epinephrine closer time and the urinary dehydro-thromboxane B2 excretion. According to the collagen epinephrine closer time values, the frequency of the -50T allele was not significantly different in bad responders when compared with good responders (36.8% vs. 15.7%; p=0.1). Similarly, the presence of the -50T mutant allele was not statistically different comparing bad and good responders according to the urinary 11-dehydro-thromboxane B2 excretion concentration (60% vs. 40%; p=0.43). Our study did not demonstrate any association between the Cox-1 gene C50T polymorphism and aspirin nonresponsiveness status in stable CAD patients.

Background: Various genetic polymorphisms have been proposed to explain the persistent platelet hyperactivity (HPR) under aspirin treatment. PlA polymorphism of platelet GPIIIa receptor has been largely studied. However, its influence on platelet sensitivity to aspirin remains controversial., Objectives: The aim of this prospective study is to investigate whether this PlA polymorphism is associated with a greater prevalence of HPR in stable coronary artery disease patients Material and Methods: 188 stable coronary artery disease patients were included. Platelet aspirin inhibitory effect was determined with PFA-100 using Collagen/Epinephrine closure time (CEPI-CT). A CEPI-CT<160sec was defining the HPR status. GPIIIa PlA polymorphism was established using polymerase chain reaction and classical restriction fragments length polymorphism., Results: The observed frequencies of different genotypes were not different from those predicted by the Hardy-Weinberg equilibrium: PlA1/lA1 (55.3%), PlA1/PlA2 (39.4%) and PlA2/PlA2 (5.3%). HPR patients with inadequate aspirin inhibition were significantly more often homozygous PlA1/A1 (65.4% vs. 47.7%, p=0.015). After multivariate analysis, PlA1/A1 genotype was the only independent risk factor for persistent HPR (OR: 2.07; 95% CI [1.14 to 3.76; p=0.016)., Conclusion: In CAD patients receiving daily low dose of aspirin, there is a significant and independent association between the expression of GPIIIa PlA1 allele and the occurrence of persistent HPR detected with PFA-100., (Copyright 2009 Elsevier Ltd. All rights reserved.)