COX-1, COX-2 and CYP2C19 variations may be related to cardiovascular events due to acetylsalicylic acid resistance

• Published in: Molecular biology reports 2022-04, Vol.49 (4), p.3007-3014
• Main Authors: Kirac, Deniz, Yaman, Aysun Erdem, Doran, Tansu, Mihmanli, Mujgan, Keles, Elif Cigdem
• Format: Article
• Language: English
• Subjects: Acetylsalicylic acid; Alleles; Animal Anatomy; Animal Biochemistry; Aspirin; Aspirin - pharmacology; Biomedical and Life Sciences; Clopidogrel; Cyclooxygenase 2 - genetics; Cyclooxygenase-1; Cyclooxygenase-2; Cytochrome P-450 CYP2C19 - genetics; Cytochrome P-450 CYP2C9 - genetics; Genotype; Genotype & phenotype; Genotypes; Histology; Humans; Implants; Life Sciences; Morphology; Original Article; Platelet aggregation; Platelet Aggregation Inhibitors - pharmacology; Polymerase chain reaction; Stents; Stents - adverse effects; Thrombosis; Thrombosis - genetics; Ticlopidine; Variation
• ISSN: 0301-4851; 1573-4978
• DOI: 10.1007/s11033-022-07124-7

Background In some stent implanted patients, cardiovascular events (CE) may occur. Acetylsalicylic acid (ASA) is routinely administered to these patients in order to prevent the occurrence of CE. CE may be related to gene variations which cause ASA resistance (AR). Therefore, it was aimed to investigate the relationship between COX-1 , COX-2 , CYP2C9 and CYP2C19 variations with CE due to AR. Materials and results Seventy-four stent implanted patients, using 100 mg of ASA per day during five years were enrolled into the study. Following stent implantation, thirty-eight patients who had a CE within five years due to AR and 36 patients without CE were enrolled in patient and control group, respectively. AR was confirmed by platelet aggregation testing. After DNA isolation from blood; COX-1 , COX-2 , CYP2C19 and CYP2C9 variations were investigated with real-time polymerase chain reaction. At the end of this study, heterozygous genotype of COX-1 was found statistically high in patients whereas heterozygous genotype of CYP2C19*1 7 was found statistically high in controls. The presence of C and G allele in COX-1 and COX-2 were found statistically high in patients, respectively. The presence of T allele in CYP2C19*17 was found statistically high in controls. Heterozygous genotype of COX-1 variation was found statistically high in patients who have AR. Additionally heterozygous genotype of CYP2C19*17 was found statistically high in patients who have low thrombosis risk. Conclusions COX-1 and COX-2 gene mutations may increase the risk of CE due to AR whereas CYP2C19*17 may have a protective effect in this process.