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Microfluidics in Assessing Platelet Function
Published on: November 8, 2024
Effect of cigarette smoking on platelet aggregation
Burak Pamukcu1, Huseyin Oflaz, Imran Onur
1Istanbul University, Istanbul Faculty of Medicine, Department of Cardiology, Istanbul, Turkey. bpamukcu@gmail.com
Insights
Cigarette smoking significantly increases platelet aggregation in patients with ischemic coronary heart disease (CHD), even with aspirin therapy. Quitting smoking is crucial for these patients to improve cardiovascular health.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Clinical Research
Background:
- Cigarette smoking is a known risk factor for atherothrombotic cardiovascular events.
- Its impact on platelet function in patients with ischemic coronary heart disease (CHD) requires further investigation.
Purpose of the Study:
- To investigate the effect of cigarette smoking on platelet function in patients with ischemic CHD undergoing aspirin therapy.
- To assess whether smoking influences aspirin responsiveness in this patient group.
Main Methods:
- Twenty smokers and 20 non-smokers with stable ischemic CHD on aspirin therapy were enrolled.
- Platelet function was assessed using the Platelet Function Analyzer (PFA)-100 before and after smoking the first cigarette.
- Aspirin non-responsiveness was defined as a closure time (CT) < 186 seconds.
Main Results:
- Cigarette smoking significantly increased platelet activity (P = .004).
- Smoking led to shorter CTs in all patients, converting more participants into aspirin non-responders (P = .004).
- No significant demographic, hematological, or biochemical differences were found between aspirin responders and non-responders.
Conclusions:
- Cigarette smoking enhances platelet aggregation in ischemic CHD patients, potentially in an aspirin non-responsive manner.
- These findings underscore the critical importance of smoking cessation for patients with CHD to mitigate cardiovascular risk.
Background:
Cigarette smoking may increase platelet aggregation and cause atherothrombotic cardiovascular events. We aimed to investigate the impact of cigarette smoking on platelet function in patients with ischemic coronary heart disease (CHD).
Methods:
Twenty patients with ischemic stable CHD under aspirin therapy (300 mg/d), who continue to smoking despite all warnings, and 20 nonsmokers with CHD are enrolled in the study. Platelet function is studied at the morning, before and 15 minutes after the first cigarette, by the Platelet Function Analyzer (PFA)-100, with collagen and epinephrine and collagen and adenosine diphosphate cartridges. Post aspirin platelet hyperactivity is defined as having a closure time (CT) shorter than 186 seconds despite regular aspirin intake. Serial CT measurements are analyzed by paired samples t test.
Results:
Persistent platelet activity was present in 4 smoker (20%) and 3 nonsmoker (15%) patients at the beginning. Platelet activity measured by the PFA-100 is been increased significantly after cigarette smoking (P = .004). Shorter CTs were determined after smoking in all patients with and without baseline persistent platelet activity, and 4 more participants became aspirin nonresponder (P = .004). No significant differences in demographic, hematological, and biochemical parameters were determined between aspirin responders and nonresponders.
Conclusions:
We determined that cigarette smoking may increase platelet aggregation in patients with ischemic CHD in an aspirin nonresponsive manner. Our results emphasize the importance of quitting cigarette smoking in patients with CHD.
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