The Impact of Single Nucleotide Polymorphisms and Other Mechanisms on Aspirin Resistance

Atherosclerosis and ischemic events play a pivotal role in the pathogenesis of several cardiovascular diseases (CVD). The primary aim of preventing recurrent thrombosis in patients who underwent cardiovascular surgery is the antiplatelet agent administration. Nevertheless, despite the aspirin therapy or double (aspirin plus clopidogrel) therapy, the effectiveness of antithrombotic treatment remains controversial. In recent years, we have learned that some percentage of patients still demonstrate no clinical response to aspirin treatment and may experience a vascular complication. This article provides an overview of recent scientific studies that have focused on experimental detection and genotyping of single nucleotide polymorphisms (SNPs) in patients, involving the main therapeutic target genes: cyclooxygenase COX-1 and COX-2, guanylate cyclase GUCY1A3, the glycoprotein complex GPIIb-IIIa, and the platelet receptor protein PEAR1." The aspirin resistance (AR) ranges considerably from 0 % to 66% in patients with ischemic heart disease (IHD) and relatively healthy people (control group). SNP distribution analysis has been proposed to explain the inadequate high platelet reactivity (HPR) among patients with IHD under aspirin treatment. Various SNPs have been proposed to explain the development of CVD and the persistent HPR under aspirin treatment widely used in the prevention of recurrent cardiovascular thrombotic events. Meanwhile, the efficacy of aspirin therapy in secondary thrombosis prevention in patients with IHD is not strongly associated with known SNP. The inconsistent results of different AR clinical trials are likely due to the design of the experiments and methodological and quantitative issues; therefore, careful interpretation of the SNP genotyping results is necessary.