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Published on: October 22, 2020
Altered platelet reactivity, coagulation, endothelial and inflammatory markers early after smoking cessation verified
Bogumił Ramotowski1, Anetta Undas2, Andrzej Budaj3
1Department of Cardiology, Centre of Postgraduate Medical Education, Warsaw, Poland. bramotowski@cmkp.edu.pl.
Insights
Smoking cessation after coronary artery interventions (PCI) increased platelet reactivity and decreased P-selectin levels. This suggests a potentially higher risk of thrombotic complications in patients who quit smoking post-PCI.
Area of Science:
- Cardiovascular Medicine
- Thrombosis and Hemostasis
- Interventional Cardiology
Background:
- Cigarette smoking is a major risk factor for coronary artery disease (CAD).
- Limited understanding exists regarding early changes in prothrombotic state and platelet reactivity after smoking cessation in patients undergoing percutaneous coronary interventions (PCI).
Purpose of the Study:
- To investigate alterations in platelet reactivity, coagulation, and related biomarkers in clopidogrel-treated CAD patients post-PCI before and after smoking cessation.
- To assess changes in platelet, endothelial, inflammatory, and coagulation activation markers.
Main Methods:
- Recruited 117 smoking patients (≥18 years) at least 30 days post-PCI, encouraging smoking cessation.
- Measured platelet reactivity (VerifyNow), thrombomodulin, P-selectin, platelet factor 4 (CXCL4/PF4), citrullinated histone H3 (H3cit), and cotinine at baseline and 30 days.
- Assessed smoking cessation by cotinine levels (<50 ng/ml).
Main Results:
- 84 patients (72%) completed follow-up; 30 (35.7%) successfully quit smoking.
- Smoking quitters showed a significantly larger increase in platelet reactivity (Δ PRU: 19 vs. -6, p=0.018).
- A significant decrease in P-selectin concentration was observed in quitters (-11.82 ng/ml vs. 7.19 ng/ml, p=0.005).
- Positive correlations found between cotinine levels and P-selectin (r=0.23, p=0.045) and CXCL4 (r=0.27, p=0.02).
Conclusions:
- Smoking cessation in CAD patients post-PCI is associated with increased platelet reactivity and reduced P-selectin levels.
- These findings suggest a potential paradoxical increase in thrombotic complication risk among patients who stop smoking after PCI.
Background/Introduction:
Cigarette smoking is a potent modifiable risk factor for coronary artery disease (CAD). However, little is known about alterations to prothrombotic state and platelet reactivity early after smoking cessation following percutaneous coronary interventions (PCI).
Purpose:
We investigated alterations to platelet reactivity, coagulation and markers of platelet, endothelial, inflammatory and coagulation activation in clopidogrel-treated patients with CAD after PCI before and after smoking cessation.
Methods:
Smoking patients aged 18 years or older at least 30 days after PCI were recruited and encouraged to quit the habit. At baseline and at 30 days, we measured platelet reactivity with VerifyNow system, thrombomodulin, P-selectin, platelet factor 4 (CXCL4/PF4), citrullinated histone H3 (H3cit) and cotinine level.
Results:
Among 117 patients, 84 patients (72%) at a median age of 60.5 years (40 [interquartile range 30-47] pack-years) completed a 30-day follow-up. At day 30, 30 (35.7%) patients stopped smoking with cotinine level < 50 ng/ml. Baseline characteristics were similar in both groups. In smoking quitters a change in platelet reactivity was larger (Δ platelet reactivity units (PRU) 19 [2, 43] vs. -6 [-32, 37], p = 0.018), along with a change in P-selectin concentration (-11.82 [-23.62, 1.34] vs. 7.19 [-14.24, 17.19] ng/ml, p = 0.005). Positive correlations was noticed between cotinine and both P-selectin ( r = 0.23, p = 0.045) and CXCL4 (r = 0.27, p = 0.02).
Conclusion:
After smoking cessation in CAD patients following PCI an increase in platelet reactivity and a decrease in P-selectin levels were observed. The risk of thrombotic complications post PCI might be paradoxically enhanced among patients who stopped smoking.
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