Key result
Current smokers on clopidogrel had significantly lower P2Y12 reaction units and higher percent inhibition than nonsmokers (p<0.001), with similar effects seen for good versus poor CYP2C19 genotypes.
Why the study?
The study was conducted to explore the relationship between VerifyNow P2Y12 assay results, CYP2C19 polymorphisms, and smoking status in non-cardiogenic ischemic stroke patients receiving clopidogrel.
Do CYP2C19 polymorphisms and smoking status affect platelet responsiveness to clopidogrel in patients with non-cardiogenic ischemic stroke?
RCT (n=256)
open-label
randomized
Yes
Do CYP2C19 polymorphisms and smoking status affect platelet responsiveness to clopidogrel in patients with non-cardiogenic ischemic stroke?
Current smoking appears to enhance clopidogrel responsiveness, potentially overcoming the reduced antiplatelet efficacy typically associated with poor CYP2C19 metabolizer genotypes.
Answers are grounded in this paper and cite their sources.
Smoking associated with enhanced clopidogrel responsiveness across CYP2C19 genotypes; leaves open whether this interaction affects clinical outcomes in stroke.
The "comparison of triflusal and clopidogrel effects in secondary prevention of stroke based on cytochrome P450 2C19 (CYP2C19) genotyping (MAESTRO)" study was a prospective, multicenter, randomized, open-label, and blind genotype trial. We performed a subgroup analysis of the MAESTRO study to explore the relationship between VerifyNow P2Y12 assay with regard to CYP2C19 polymorphisms and smoking status in patients with non-cardiogenic ischemic stroke who underwent clopidogrel treatment. Methods: For the study, patients treated with clopidogrel and who underwent VerifyNow P2Y12 assay was selected from the MAESTRO study. Results: Of the 393 patients in 18 hospitals, 256 (65%) patients in 12 hospitals were entered for this subgroup analysis. P2Y12 reaction unit (PRU) was significantly lower and percent inhibition (% INH) was higher in the current smoking group than in the nonsmoking group (p<0.001). The same results were also observed in the good genotype group when compared with the poor genotype group (p<0.001). Among the groups, significant lower PRU and higher % INH was demonstrated in current smoking with good genotype group. However, there was no difference in PRU and % INH between current smoking with poor genotype group and nonsmoking with good genotype group, suggesting that clopidogrel activity was concurrently related to CYP2C19 polymorphisms and smoking status. Conclusions: Regarding secondary stroke prevention, patients who were current smokers and had a poor genotype for clopidogrel metabolism may benefit from clopidogrel treatment similar to that in patients who were nonsmokers and had a good genotype.
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Han et al. (2019) conducted an RCT in non-cardiogenic ischemic stroke (n=256). Clopidogrel vs. Compared by smoking status and CYP2C19 genotype was evaluated on P2Y12 reaction unit (PRU) and percent inhibition (% INH) (p=<0.001). Current smokers on clopidogrel had significantly lower P2Y12 reaction units and higher percent inhibition than nonsmokers (p<0.001), with similar effects seen for good versus poor CYP2C19 genotypes.
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