OS 34-05 HIGH ON-TREATMENT PLATELET REACTIVITY WAS ASSOCIATED WITH SMOKING IN CLOPIDOGREL-TREATED PATIENTS. (September 2016)

• Record Type: Journal Article
• Authors: Wang, Xingyu; Liu, Xin; Zhang, Wei; Meng, Xianmin; Liu, Lisheng
• Is Part Of: Journal of hypertension. Volume 34:(2016) Supplement 1
• Publication Date: 2016-09
• Subjects: Hypertension -- Periodicals; Hypertension -- Periodicals; 616.132005
• DOI: 10.1097/01.hjh.0000501018.68966.56
• Languages: English
• ISSNs: 1473-5598

Abstract

Abstract : Objective: High on-treatment platelet reactivity (HTPR) was associated with an increased risk of ischemic events in clopidogrel-treated patients. Cigarette smoking was considered as an inducer of CYP1A2, and may theoretically enhance the biological effects and clinical efficacy of clopidogrel through facilitating the conversion of clopidogrel into its active metabolite. The purpose of this study was to examine the effect of cigarette smoking on the platelet response to clopidogrel. Design and Method: A total of 713 patients undergoing percutaneous coronary intervention were selected from Beijing Shijingshan Hospital and assigned to treatment with a loading 300 mg dose of clopidogrel. All patients are Han ethnicity from local community in Beijing. ADP-induced platelet aggregation inhibition was measured by thrombelastography (TEG). Results: For both previous smokers and nonsmokers, significantly lower ADP-induced platelet aggregation inhibition were found compared withcurrent smokers (69.16 ± 26.57 vs. 75.92 ± 22.76, p = 0.017 and 65.55 ± 23.85 vs. 75.92 ± 22.76, p = 0.006, respectively). Yet, previous smokers had higher ADP-induced platelet inhibition than nonsmokers, but the difference was not significant ( p = 0.996). During clopidogrel therapy, ADP-induced platelet aggregation inhibition trended higher in current smokers whose length of smoking was more than or equal to 25 years than whose length of smoking was less than 25 ( p = 0.045). Similarly, current smokers of 11–20 and > 20 cigarettes per day displayed greater platelet inhibition compared with nonsmokers (75.68 ± 23.30 vs. 65.55 ± 23.85, p = 0.027 and 77.22 ± 22.23 vs. 65.55 ± 23.85, p = 0.035, respectively). In a multivariate logistics regression analysis, cigarette smoking was an independent influencing variable for high on-treatment platelet inhibition (OR = 1.550, p = 0.004). Conclusions: In our study, cigarette smoking was positively associated with enhanced response to clopidogrel. The study also demonstrated that the length of smoking and amount of cigarettes smoked appeared to affect the response to clopidogrel in Chinese patients undergoing percutaneous coronary intervention.