AI Article Synopsis
- The study investigates how genetic variations, particularly in the P2RY12 gene, affect the response to clopidogrel in patients with coronary heart disease (CHD).
- It involves 539 patients, testing their platelet response after clopidogrel treatment and analyzing specific SNPs (single nucleotide polymorphisms) to see their impact on resistance to the drug.
- Results show that certain genetic variants, especially CYP2C19*2 and P2RY12 rs6809699, significantly increase the risk of clopidogrel resistance, highlighting the importance of genetic testing in optimizing treatment for CHD patients.
Article Abstract
Backgrounds: Remarkable interindividual variability in clopidogrel response is observed, genetic polymorphisms in P2RY12 and its signal pathway is supposed to affect clopidogrel response in CHD patients.
Methods: 539 CHD patients treated with clopidogrel were recruited. The platelet reaction index (PRI) indicated by VASP-P level were detected in 12-24 h after clopidogrel loading dose or within 5-7 days after initiation of maintain dose clopidogrel. A total of 13 SNPs in relevant genes were genotyped in sample A (239 CHD patients). The SNPs which have significant differences in PRI will be validated in another sample (sample B, 300 CHD patients).
Results: CYP2C19*2 increased the risk of clopidogrel resistance significantly. When CYP2C19*2 and CYP2C19*3 were considered, CYP2C19 loss of function (LOF) alleles were associated with more obviously increased the risk of clopidogrel resistance; P2RY12 rs6809699C > A polymorphism was also associated with increased risk of clopidogrel resistance (AA vs CC: P = 0.0398). This difference still existed after stratification by CYP2C19 genotypes. It was also validated in sample B. The association was also still significant even in the case of stratification by CYP2C19 genotypes in all patients (sample A + B).
Conclusion: Our data suggest that P2RY12 rs6809699 is associated with clopidogrel resistance in CHD patients. Meanwhile, the rs6809699 AA genotype can increase on-treatment platelet activity independent of CYP2C19 LOF polymorphisms.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9801627 | PMC |
| http://dx.doi.org/10.1186/s12872-022-02988-w | DOI Listing |
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