Background: Smoking is associated with increased platelet reactivity and reduced response to aspirin treatment. On the contrary smoking is associated with faster conversion of clopidogrel to its active metabolite via the CYP P450 and therefore increased platelets responsiveness to clopidogrel. The effect of smoking on responsiveness to prasugrel is unknown.
Methods: The study comprised 195 consecutive patients with ST-elevation myocardial infarction (STEMI), who underwent PPCI within 12 hours of symptoms onset. Patients older than 75 years,with a history of cerebro-vascular event and\or weight < 60 kg were excluded from the study. Seventy four patients were treated with high dose clopidogrel (600\150 mg) and 121 with prasugrel (60\10 mg). ADP- induced platelet aggregation (PA) was determined 72 hours post loading dose . Suboptimal response to thienopyridine was defined as ADP-PA > 50%.
Results: Among clopidogrel treated patients smoking was associated with numerically lower PA (36.8±13 vs. 40±16%, p=0.3). In contrast among prasugrel treated patients smokers tended to have higher PA (32.9±16 vs. 27.7±18, p=0.1).
Interestingly, while among non-smokers (N=80) prasugrel as compared with clopidogrel treatment was associated with significantly lower PA (27.7±18 vs. 40±16%, p<0.002), among smokers (N=115) there was no significant difference in PA between prasugrel and clopidogrel treated patients (32.9±16 vs. 36.8±13%, p=0.2). Accordingly, while among non-smokers prasugrel compared with clopidogrel treated patients were less likely to demonstrate suboptimal response (7.3% vs. 23%, p=0.06), the rate of smokers showing suboptimal response was similar regardless of the thienopyridine which was administered (10% vs. 14%, p=0.5).
Conclusions: Smoking has differential effect on PA in STEMI patients treated with different thienopyridines.
