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Relationship between the serum sCD40L level and aspirin-resistant platelet aggregation in patients with stable
Burak Pamukcu1, Huseyin Oflaz, Imran Onur
1Department of Cardiology, Istanbul Faculty of Medicine, Istanbul University, Istanbul, Turkey. bpamukcu@gmail.com
Insights
Soluble CD40 ligand (sCD40L) levels did not differ between aspirin-resistant and aspirin-sensitive patients with coronary artery disease. Further research is needed to clarify the link between aspirin resistance and sCD40L in cardiovascular events.
Area of Science:
- Cardiovascular Medicine
- Inflammation Research
- Thrombosis and Hemostasis
Background:
- Inflammation plays a critical role in atherosclerosis and its thrombotic complications.
- Elevated serum soluble CD40 ligand (sCD40L) is implicated in platelet activation.
Purpose of the Study:
- To investigate the relationship between serum sCD40L levels and aspirin-resistant platelet aggregation in patients with coronary atherosclerosis.
Main Methods:
- 167 patients with stable coronary artery disease were assessed.
- Platelet function was evaluated using the Platelet Function Analyzer 100 (PFA-100) with collagen/epinephrine and collagen/adenosine diphosphate cartridges.
- Aspirin resistance was defined as a closure time <186 seconds with collagen/epinephrine cartridges despite aspirin therapy.
- Serum sCD40L levels were quantified using ELISA.
Main Results:
- 34.1% of patients exhibited aspirin resistance.
- Mean serum sCD40L levels were 166 pg/ml in aspirin-resistant patients and 152 pg/ml in aspirin-sensitive patients (p=0.582).
- No significant difference in sCD40L levels was observed between the two groups.
Conclusions:
- Serum sCD40L levels are comparable in patients with aspirin-resistant and aspirin-sensitive platelet aggregation.
- Further studies are warranted to elucidate the complex relationship between aspirin resistance, sCD40L, and cardiovascular risk.
Background:
Current evidence supports the central role of inflammation in all phases of the atherosclerotic process, including its thrombotic complications. Increased serum sCD40L may trigger platelet activation, so the aim of the present study was to determine the relation between sCD40L levels and aspirin-resistant platelet aggregation in patients with coronary atherosclerosis.
Methods And Results:
A total of 167 consecutive patients (39-85 years old, 35.9% women) with stable coronary artery disease was enrolled in the study. Platelet function was evaluated by a Platelet Function Analyzer 100 device (PFA-100) with collagen and epinephrine (Col/Epi) and collagen and adenosine diphosphate (ADP) (Col/ADP) cartridges. Aspirin resistance was defined as a closure time (CT) <186 s with Col/Epi cartridges, despite regular aspirin therapy. Serum sCD40L level was determined quantitatively with an ELISA method. Fifty-seven (34.1%) patients had aspirin resistance according to the PFA-100. Mean CT measured with the Col/ADP cartridges was 83+/-18 s (65-101 s). Mean serum sCD40L was 157 pg/ml (6-700 pg/ml) in the entire cohort. Patients with aspirin resistance had a mean serum sCD40L level of 166 pg/ml and patients with aspirin-sensitive platelet aggregation had an sCD40L level of 152 pg/ml (p=0.582).
Conclusion:
The sCD40L level is similar in patients with aspirin-resistant and aspirin-sensitive platelet aggregation according to the PFA-100. There is still need for further studies to elucidate the relationship between aspirin-resistant platelet aggregation and sCD40L, which is now known to be prothrombotic, proinflammatory and to be a risk factor for cardiovascular events.
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