BACKGROUND: In a recent study by Desai et al., clopidogrel was significantly more effective at reducing the rate of 30-day adverse clinical events in patients with ST-segment elevation myocardial infarction (STEMI) who smoked ≥ 10 cigarettes/day. However, the association between the amount of cigarette smoking (CS) and clopidogrel-induced platelet inhibition in STEMI patients has not been fully established.
METHOD: We enrolled 138 consecutive STEMI patients treated with primary coronary stenting, and pre-discharge platelet reactivity was assessed with conventional aggregometry and the VerifyNow P2Y12 assay.
RESULT: There was no difference of residual platelet reactivity between non-smoker (n = 66) and CS patients < 1/2 pack/day (n = 16). CS patients ≥ 1/2 pack/day (n = 56) demonstrated lower platelet reactivity with 5 and 20 ųmol/l ADP (40.9 ± 16.1% vs. 46.6 ± 11.7%, p = 0.028 and 53.8 ± 16.6% vs. 59.2 ± 12.2%, p = 0.040, respectively) and lower PRU (204 ± 85 vs. 270 ± 69, p < 0.001) than non-smoker. On multivariate analyses including values with p < 0.2 in univariate analysis, CS was the only predictor of low post-clopidogrel platelet reactivity (≤ 33%; the lowest quartile of 5
ųmol/l ADP-induced platelet reactivity) (odds ratio 4.926, 95% confidence interval 1.300 to 18.868, p = 0.019).
CONCLUSION: This study demonstrated a positive association between the amount of CS and clopidogrel-induced platelet inhibitory effect in STEMI patients undergoing primary coronary stenting. CS < 0.5 pack/day did not enhance sufficiently platelet inhibition by clopidogrel, whereas patients who smoked ≥ 0.5 pack/day showed intensified clopidogrel-induced platelet inhibition after coronary stenting.
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