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Common Polymorphisms within Genes Encoding Platelet Receptors: Still a Way to Go?

in the Chinese population than in individuals of Caucasian origin. The average frequency of the ITGA2 gene 807T allele was 40.77% in Caucasian patients with aspirin insensitivity, and as high as 58.58% in the Chinese patients. This ethnicity-specific effect suggests that different genetic backgrounds may account for this discrepancy or that different populations may have different linkage disequilibrium patterns due to their evolutionary history [8] . In the latest issue of Cardiology , Zhang et al. [9] present the results of a study that aimed to assess the impact of the ITGA2 common SNP on platelet aggregation in patients with acute coronary syndrome (ACS) who received a loading dose of dual antiplatelet treatment while undergoing invasive therapy. They found that, 24 h after the administration of aspirin and clopidogrel, the baseline platelet aggregation value in the minor allele homozygote group (i.e. TT) was higher than in the major allele group (i.e. CC) when induced by arachidonic acid and by ADP. Moreover, they observed a more significant reduction in the platelet aggregation rate in the TC and CC groups after dual antiplatelet therapy after stimulation with ADP. They concluded that patients carrying the CC genotype may be more sensitive to antiplatelet treatment than those with the T allele, particularly those with the TT genotype. How do we interpret these results in the context of the earlier literature? The functional role of the C807T ITGA2 polymorphism in modulating the response to dual antiplatelet therapy in patients with coronary artery disease or ACS has been hypothesized in previous studies. In a study on patients on dual antiplatelet treatment who underwent perGlycoprotein (GP) Ia is encoded by the ITGA2 gene on chromosome 5, and, together with GP IIa, forms a major collagen receptor on platelets, namely GP Ia/IIa (integrin a2b1, CD49b/CD29). Several single-nucleotide polymorphisms (SNP) have been described in the cDNA coding for the GP Ia subunit, and the most important common SNP may be C807T [1] . Three different genotypes of the C807T dimorphism have been associated with varying expression of GP Ia/IIa on platelets; the highest numbers of the receptor are characteristic for the TT genotype, intermediate numbers for the TC and lowest numbers for the CC genotypes [2] . Differences in receptor density correlate directly with the rate of platelet attachment to type I collagen in whole blood under flow conditions and the risk of premature myocardial infarction and other thrombotic events [1, 3, 4] . In the literature, reports on the role of ITGA2 polymorphisms in platelet function and sensitivity to dual antiplatelet therapy are scarce. Clopidogrel is a prodrug, and, to date, most studies have focused on an association with genetic polymorphisms within genes encoding metabolizing enzymes [5] . However, previous reports have shown that platelet aggregation induced by different agonists, including adenosine diphosphate (ADP) or thrombin, was increased in ITGA2 807T-allele carriers [6] . Moreover, the active GP Ia/IIa receptor initiates the arachidonic acid pathway and the release of thromboxane A2 [7] . The latest meta-analysis demonstrated the contributory role of the ITGA2 genetic polymorphism in the susceptibility to aspirin insensitivity, with a greater effect Received: August 17, 2015 Accepted: August 17, 2015 Published online: October 6, 2015