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Relationship between Inflammation and Aspirin and Clopidogrel Antiplatelet Responses in Acute Ischemic Stroke
Zohara Sternberg1, Trevor Chichelli1, Daniel Sternberg1
1Department of Neurology, Stroke Center, Buffalo Medical Center, Buffalo, New York.
Insights
Clopidogrel reduced inflammatory markers like P-selectin and MMP-9 in ischemic stroke patients, with effects varying by aspirin dose and measurement method. This highlights clopidogrel's anti-inflammatory role.
Area of Science:
- Cardiovascular Medicine
- Neuroscience
- Pharmacology
Background:
- Ischemic stroke involves inflammation and thrombosis.
- Antiplatelet agents like aspirin (ASA) and clopidogrel are crucial in stroke management.
- Assessing antiplatelet response and its impact on inflammatory markers is vital.
Purpose of the Study:
- To measure serum levels of inflammatory markers (P-selectin, CD40L, MMP-9, ICAM-1, IL-6) in ischemic stroke patients.
- To correlate these levels with antiplatelet responses to aspirin and clopidogrel.
- To evaluate the effectiveness of three point-of-care platelet function instruments (TEG, ACU, IMP).
Main Methods:
- Serum inflammatory markers were measured in 51 ischemic stroke patients using ELISA.
- Measurements were taken at baseline (on ASA), and post-clopidogrel administration (loading and maintenance doses).
- Platelet function was assessed using thromboelastograph (TEG), Accumetrics (ACU), and impedance aggregometry (IMP).
Main Results:
- Clopidogrel administration reduced serum levels of P-selectin, CD40L, and MMP-9.
- No significant changes were observed in ICAM-1 and IL-6 levels.
- Lower baseline aspirin dose (81 mg) correlated with greater reductions in inflammatory markers post-clopidogrel compared to higher doses (325 mg).
- TEG correlated with aspirin response, while ACU and IMP correlated with clopidogrel response.
Conclusions:
- Clopidogrel demonstrates both platelet-dependent and independent anti-inflammatory effects in ischemic stroke patients.
- The relationship between platelet function and inflammation is influenced by the platelet function analyzer used, the specific antiplatelet agent, the inflammatory marker, and timing of measurement.
Objective:
We measured serum levels of proinflammatory/prothrombotic markers P-selectin, CD40L, matrix metalloproteinase 9 (MMP-9), intracellular adhesion molecule 1 (ICAM-1), and interleukin (IL)-6 in ischemic stroke patients, correlating their levels with the results of aspirin (ASA) and clopidogrel antiplatelet responses, using 3 "point of care" platelet function instruments, thromboelastograph (TEG), Accumetrics (ACU), and impedance aggregometer (IMP).
Methods:
Patients on chronic ASA regimen at the time of stroke were switched to 300 mg clopidogrel loading dose and 75 mg clopidogrel maintenance dose. Serum levels of the aforementioned inflammatory mediators were measured in 51 patients at baseline (on ASA regimen), and at 26 ± 5 hours and 64 ± 18 hours postclopidogrel administration by enzyme-linked immunosorbent assay.
Results:
P-selectin, CD40L, and MMP-9 serum levels were reduced; ICAM-1 and IL-6 serum levels showed no difference postclopidogrel administration relative to baseline. Patients' stratification based on ASA dose showed more significant reductions in P-selectin, CD40L, and MMP-9 serum levels postclopidogrel administration in patients who were on baseline 81 mg ASA, as compared to patients on 325 mg ASA. Measurement with TEG was sensitive for correlating ASA antiplatelet responses to serum levels of inflammatory markers, whereas measurements with ACU and IMP were sensitive for correlating clopidogrel antiplatelet responses to serum levels of inflammatory markers.
Conclusion:
Clopidogrel exerts both platelet-dependent and platelet-independent anti-inflammatory effects. The association between platelet function and inflammation depends on the platelet function analyzer, the type of antiplatelet agent, the nature of the inflammatory marker, and the time of measurement relative to the time of drug administration.
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