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Updated: May 3, 2026
Optimized Management of Endovascular Treatment for Acute Ischemic Stroke
Published on: January 18, 2018
[Clopidogrel cannot yet be exclusively for smokers]
1Universitair Medisch Centrum St Radboud, afd. Interne Geneeskunde en afd. Farmacologie-Toxicologie, Nijmegen.
Insights
Smoking may enhance the effectiveness of clopidogrel, a P2Y12 receptor antagonist, in preventing cardiovascular events. Further research is needed to confirm this effect and assess bleeding risks in smokers.
Area of Science:
- Cardiology
- Pharmacology
- Clinical Trials
Background:
- Dual antiplatelet therapy (DAPT) with aspirin and a P2Y12 inhibitor is standard for acute coronary syndromes and stenting.
- Recent meta-analyses suggest enhanced clopidogrel efficacy in smokers.
Purpose of the Study:
- To explore the potential impact of smoking on clopidogrel's efficacy and safety.
- To investigate the mechanism behind potentially increased clopidogrel effectiveness in smokers.
Main Methods:
- Review of existing meta-analyses on clopidogrel efficacy in smokers versus non-smokers.
- Hypothesized mechanism involving smoking-induced cytochrome P450 1A2 activity.
Main Results:
- Meta-analyses indicate a more pronounced reduction in cardiovascular events with clopidogrel among smokers.
- Smoking may accelerate the conversion of clopidogrel to its active metabolite via CYP1A2 induction.
Conclusions:
- Observed enhanced clopidogrel efficacy in smokers warrants further investigation.
- Prospective trials are necessary to validate these findings and evaluate bleeding risks associated with smoking and clopidogrel therapy.
Abstract:
Dual antiplatelet therapy with acetylsalicylic acid and a P2Y12 receptor antagonist is the cornerstone of treatment in patients with acute coronary syndromes and patients undergoing coronary stenting. Two recent meta-analyses concluded that the efficacy of the P2Y12 receptor antagonist clopidogrel in reducing cardiovascular events is more pronounced in smokers than in non-smokers. Most probably, this is due to induction of cytochrome p450 1A2 by smoking, which accelerates conversion of clopidogrel to its active metabolite. These observations are of great interest. However, before these observations can be used to guide treatment in the clinical arena, the effect of smoking should be studied in prospective clinical trials, investigating not only its modulation of the efficacy but also of the bleeding complications of clopidogrel.
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