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Microfluidics in Assessing Platelet Function
Published on: November 8, 2024
Smoking at least 10 cigarettes per day increases platelet inhibition by clopidogrel in patients with
Young-Hoon Jeong1, Jung-Hyun Cho, Min-Kyung Kang
1Division of Cardiology, Department of Internal Medicine, Gyeongsang National University Hospital, 90 Chiram-dong, Jinju, 660-702, Gyeongsangnam-do, South Korea. goodoctor@naver.com
Insights
Cigarette smoking (CS) significantly enhances clopidogrel
Area of Science:
- Cardiology
- Pharmacology
- Thrombosis
Background:
- Emerging data suggest cigarette smoking (CS) may reduce cardiovascular event risk in ST-segment-elevation myocardial infarction (STEMI) patients.
- The mechanism may involve CS affecting clopidogrel metabolism, but the dose-response relationship with clopidogrel's antiplatelet effect is unclear.
Purpose of the Study:
- To investigate the association between the extent of cigarette smoking (CS) and clopidogrel-induced platelet inhibition.
- To determine if smoking status influences platelet reactivity in healthy subjects and STEMI patients treated with clopidogrel.
Main Methods:
- Assessed inhibition of platelet aggregation (IPA) in 20 healthy subjects after a 600-mg clopidogrel load.
- Evaluated on-clopidogrel platelet reactivity (PR) using aggregometry and VerifyNow P2Y(12) in 138 STEMI patients, stratified by smoking status.
Main Results:
- In healthy subjects, smoking ≥10 cigarettes/day correlated with higher IPA.
- STEMI patients smoking ≥10 cigarettes/day showed significantly lower PR (5 & 20 μmol/L ADP) and P2Y(12) reaction units compared to non-smokers.
- Heavy smoking (≥10 cigarettes/day) was the sole predictor of low on-clopidogrel PR in multivariate analysis.
Conclusions:
- Cigarette smoking appears to augment the antiplatelet response to clopidogrel in both healthy individuals and STEMI patients.
- Smoking 10 or more cigarettes daily significantly reduces platelet reactivity to clopidogrel in these populations.
Background:
Recent data suggest that cigarette smoking (CS) might decrease the risk of cardiovascular events in patients with ST-segment-elevation myocardial infarction (STEMI) or established cardiovascular disease. Although it may be related to the effect of CS on the metabolism of clopidogrel, the association between the extent of CS and clopidogrel-induced platelet inhibition has not been well defined.
Patients And Methods:
We tested the association between smoking status and inhibition of platelet aggregation (IPA) in response to a clopidogrel loading of 600-mg in 20 healthy subjects. We then enrolled 138 consecutive STEMI patients treated with primary coronary stenting. On-clopidogrel platelet reactivity (PR) was assessed with conventional aggregometry and the VerifyNow P2Y(12) assay, according to smoking status.
Results:
After 6 hours post-loading in healthy subjects, CS patients on ≥10 cigarettes/day showed a significantly higher value of 5 μmol/L ADP-stimulated IPA (P=0.006), and had a trend toward a greater value of 20 μmol/L ADP-stimulated IPA (P=0.093) compared with non-smokers. In STEMI patients, there was no difference in PR between non-smokers (n=66) and CS patients<10 cigarettes/day (n=16). CS patients on ≥10 cigarettes/day (n=56) demonstrated lower PR with 5 and 20 μmol/L ADP (40.9±16.1% versus 46.6±11.7%, P=0.028, and 53.8±16.6% versus 59.2±12.2%, P=0.040, respectively) and lower P2Y(12) reaction units (204±85 versus 270±69, P<0.001) than non-smokers. On multivariate analyses, CS≥10 cigarettes/day was the only predictor of low on-clopidogrel PR (≤33%; the lowest quartile of 5 μmol/L ADP-induced PR; odds ratio 4.651, 95% confidence interval 1.181-18.519, P=0.028).
Conclusion:
CS seems to increase antiplatelet response to clopidogrel in healthy volunteers and STEMI patients. Smoking 10 or more cigarettes/day can significantly decrease on-clopidogrel platelet reactivity in these populations.
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