F1000Res
The impact of smoking status on clopidogrel responsiveness in patients with coronary artery disease who undergo percutaneous coronary intervention
By Aldallal AAR, Mohammad BI, Rgeeb AN and 2 others.
Abstract
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.




