The Impact of Smoking on Post-Clopidogrel Platelet Reactivity in Patients With Acute Myocardial Infarction

Abstract

Background and ObjectivesSmoking increases inhibition of clopidogrel-induced platelet reactivity in patients undergoing elective coronary stenting. However, an association between pre-admission smoking (PS) and post-clopidogrel platelet reactivity in patients with acute myocardial infarction (AMI) has not been determined.Subjects and MethodsStudy cohorts were recruited from a pool of patients at our hospital who were undergoing coronary stenting for AMI (n=134). Immediately after arrival at the emergency room (ER), all patients received a 600 mg loading dose of clopidogrel followed by a maintenance dose of 75 mg/day. Platelet aggregation was measured with light transmittance aggregometry (LTA) after addition of 5 or 20 µmol/L adenosine diphosphate (ADP).ResultsMaximal platelet aggregation (Aggmax) was lower in PS patients after 5 µmol/L ADP (43.6±15.7% vs. 48.4±12.5%, p=0.096) and 20 µmol/L ADP stimuli (56.2±15.6% vs. 61.3±11.6%, p=0.073) compared with non-smoking (NS) patients. However, there were no differences in 5 µmol/L (42.6±16.3% vs. 43.8±15.6%, p=0.776) and 20 µmol/L ADP-induced Aggmax (54.8±14.3% vs. 56.5±15.9%, p=0.692) between PS patients <0.5 pack/day and ≥0.5 pack/day. Although more PS patients met the criteria for low post-clopidogrel platelet reactivity (LPPR) (≤37%; the lowest quartile of 5 µmol/L ADP-induced Aggmax) than NS patients (30.9% vs. 13.5%, p=0.048), advancing age was the only independent predictor of LPPR {odds ratio (OR) 0.960, 95% confidence interval (CI) 0.929 to 0.993, p=0.019}.ConclusionPS is significantly not associated with decreased residual platelet reactivity in AMI patients.

The impact of smoking on clinical efficacy and pharmacodynamic effects of clopidogrel: a systematic review and meta-analysis

“…The other five independent studies (n=3501) from two articles observed no significant interaction between smoking and OPR 21 45. Pooled data for the 12 studies suggested a significantly lower OPR in current smokers, but there was significant inter-study heterogeneity (pooled SMD=−0.30; 95% CI −0.46 to −0.15; I 2 =76.2%, p=0.000; figure 3).…”

“…The findings were robust when fixed-effects model was used (pooled SMD=−0.20; 95% CI −0.27 to −0.13; I 2 =76.2%, p=0.000). Also, a sensitivity analysis was performed for laboratory studies by restricting to the seven studies in which former smokers were excluded or analysed separately 19 20 22 35 36 39 45. The results suggested a significant more evident difference in OPR between current and never smokers (pooled SMD=−0.58; 95% CI −0.75 to −0.41; figure 5).…”

Factors related to on-treatment platelet aggregation assessed by multiple electrode aggregometry in percutaneous coronary intervention patients on clopidogrel and aspirin

“…It is interesting how variably the risk factors of HPR have been described in the literature. The least controversy is associated with age [ 25 – 27 ], diabetes mellitus [ 28 – 31 ] and smoking. Active smoking has been found to be an independent predictor of better clopidogrel response, explained by the drug’s pharmacodynamics [ 32 – 36 ], the so-called “smoker’s paradox”.…”

Coronary artery calcium scoring and its impact on the clinical practice in the era of multidetector CT

“…The pharmacological effect of clopidogrel can be monitored by measurement of residual platelet aggregation, which can vary according to subject [97]. Drosch et al [98] investigated the possible cause of low clopidogrel-responders.…”