Key result
Smoking is linked to ~4.4-fold higher odds of clopidogrel responsiveness after PCI.
Why the study?
The nature of the relationship between smoking status and clopidogrel responsiveness in patients with CAD undergoing PCI remains undefined and may be confounded by various factors.
Does smoking status improve clopidogrel responsiveness in patients with coronary artery disease undergoing percutaneous coronary intervention?
Observational (n=324)
No
Does smoking status improve clopidogrel responsiveness in patients with coronary artery disease undergoing percutaneous coronary intervention?
In an Iraqi cohort of CAD patients undergoing PCI, current smoking was associated with significantly increased pharmacodynamic clopidogrel responsiveness (the 'smoker's paradox'), though this finding is mechanistic and does not imply clinical benefit.
Smoking was associated with higher clopidogrel responsiveness; hypothesis-generating and should not yet change practice in CAD patients undergoing PCI.
Background The association between smoking and clopidogrel response has been stated in numerous studies, so the nature of this relationship remains undefined and may be confounded by methodological, hematological, and clinical factors. This study was designed to examine the relationship between smoking status and clopidogrel response between patients with coronary artery disease (CAD) who undergoing percutaneous coronary intervention (PCI). Methods In this observational analytical study, smoking status was assessed as the primary exposure variable, and responsiveness of clopidogrel was defined according to a predefined area-under-the-curve (AUC) threshold found using the Multiplate platelet function test. Patients were first classified according to smoking status (smokers vs non-smokers). Inside these groups, patients were further categorized as clopidogrel responder’s or non-responders. Baseline laboratory and clinical and features were compared between smokers and non-smokers, and a multivariable logistic regression model was tested to measure whether smoking status was independently related with responsiveness of clopidogrel after modification for main cardiovascular risk factors and hemoglobin level. Results Smokers confirmed a higher percentage of clopidogrel responders compared with non-smokers. Related to multivariable analysis, smoking status remained independently related with an increased likelihood of clopidogrel responsiveness, and level of hemoglobin similarly exhibited a significant positive relation with treatment responsiveness, whereas hypertension, age, BMI, and diabetes were not significant predicters. Conclusions Between patients undergoing PCI; smoking status was independently related with clopidogrel responsiveness; though, this result represents an observational association rather than sign of clinical benefit. The findings should be considered hypothesis-generating and justified further mechanistic and longitudinal study to explain the underlying elucidations for this design.
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Aldallal et al. (2026) conducted an observational in Coronary artery disease (CAD) (n=324). Smoking vs. Non-smokers was evaluated on Clopidogrel responsiveness (defined as Multiplate AUC < 50 U) (Adjusted OR 4.36, 95% CI 2.48-7.68, p=<0.001). Smoking was independently associated with a significantly higher likelihood of clopidogrel responsiveness (Adjusted OR 4.36) compared to non-smoking in patients with coronary artery disease undergoing percutaneous coronary intervention.
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