LAUSR

“Aspirin resistance” is a poor pharmacological termwhich should be used when aspirin is unable to hit its molecular target – the platelet cyclooxygenase (COX)-1. However, this type of resistance is rare and in the range of 1% or less [1–2]. This term frequentlymixed upwith clinical treatment failure in an inappropriate way [3]. Therefore, patients with poor aspirin response should not be considered resistant or nonresistant. Using “aspirin treatment failure” may be more appropriate. We thank Moris et al. for their interest in their letter regarding our study [4]. Considering that aspirin treatment failure is related to clinical outcome in ischemic stroke patients treated with clopidogrel and aspirin, we think their suggestion that evaluating the effect of aspirin treatment failure on adverse clinical events (nonfatal ischemic stroke, myocardial infarction, or vascular death) is meaningful. Aspirin treatment failure should bedefined anddiagnosed according to the results of laboratory tests or the occurrence of an atherothrombotic ischaemic event [5], which is same as clopidogrel poor response. Aspirin treatment failure is one of the factors that contribute to adverse clinical event (nonfatal ischemic stroke, myocardial infarction, or vascular death). However, there are different clinical determinants, not only aspirin (e.g. nicotine). In our study, the variables (age, sex, smoking, hypertension, hyperlipidemia, diabetes, previous MI, previous TIA, chronic heart disease, aspirin, statins, PPI, CCB, stent) were adjusted in the multivariate logistic regression model and Cox regressionmodel to evaluate the effects of CYP2C19 gene polymorphisms on risk of adverse clinical event. We really agree with Moris's viewpoint that the response to clopidogrel may be influenced by pharmacokinetic variables such as absorption (ABCB1 C1236T, G2677T/A, C3435T), metabolism (e.g. CYP2C19, CYP2C9, CYP3A4, CYP3A5), bioactivation (PON1), and platelet receptors (P2RY12, P2Y1). Genetic polymorphisms of CYP isoenzymes play a role in high on-treatment platelet reactivity. The most important impact comes from CYP2C19 polymorphisms [6]. Therefore, we focused on CYP2C19 polymorphism in current study. However we will consider further research on the relationship between other genetic polymorphisms and the response to clopidogrel.