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Updated: Jun 3, 2026

Microfluidics in Assessing Platelet Function
Published on: November 8, 2024
Functional evaluation of platelet aspirin resistance after on-pump coronary bypass grafting using multiple
1Department of Cardiac Surgery, Academic City Hospital Ludwigshafen, Ludwigshafen, Germany. kammerei@klilu.de
Insights
Intravenous aspirin (ASA) administration in patients undergoing coronary artery bypass grafting (CABG) may improve platelet function and reduce aspirin resistance. This approach shows promise for enhancing antiplatelet therapy effectiveness after cardiac surgery.
Area of Science:
- Cardiovascular Surgery
- Pharmacology
- Hematology
Background:
- Early graft failure after coronary artery bypass grafting (CABG) is often linked to antiplatelet therapy, particularly acetylsalicylic acid (ASA).
- Patients undergoing on-pump cardiac surgery frequently exhibit impaired hemostasis due to various factors.
Purpose of the Study:
- To investigate the impact of intravenous ASA administration on platelet function in patients after CABG.
- To assess the effectiveness of intravenous ASA in overcoming aspirin resistance in this patient population.
Main Methods:
- Forty-two patients received oral ASA post-surgery, with intravenous ASA administered 6-8 days post-operation to ensure compliance.
- Platelet function was evaluated using a platelet function analyzer (PFA-100™) measuring closure time (CT) and aggregation (TPA, IPA) before and after ASA administration.
- Results were compared to 120 healthy individuals.
Main Results:
- Intravenous ASA significantly prolonged CEPI-CT and reduced arachidonic acid (AA) and collagen-induced impedance platelet aggregation (IPA) at 1 and 24 hours.
- Despite oral ASA, patients showed shorter PFA-100™ CEPI and CADP-CT, and greater ADP-TPA and IPA compared to controls.
- Intravenous ASA did not significantly affect CADP-CT or ADP-induced IPA.
Conclusions:
- Platelet tests for aspirin response (ASA-R/ASA-NR) were not comparable in this study.
- Patients after CABG exhibit increased platelet dysfunction.
- Intravenous ASA administration presents a potential strategy to mitigate laboratory resistance following CABG, warranting further clinical investigation.
Object:
The predominant mechanism of early graft failure after coronary artery bypass grafting (CABG) is associated with antiplatelet treatment using drugs such as acetylsalicylic acid (ASA). Impaired hemostasis of multiple etiologies is often present in patients undergoing on-pump cardiac surgery. We investigated the impact of intravenous ASA administration on platelet function in this setting.
Methods:
Forty-two patients were enrolled in the study. Patients received 100 mg oral ASA once daily, beginning in the early postoperative period. Noncompliance was eliminated by the administration of 300 mg ASA intravenously at 6-8 days post-operation. Blood was drawn immediately before, 1 h and 24 h after ASA administration.
Results:
A platelet function analyzer (PFA-100™) was used to evaluate closure time (CT), turbidimetric platelet aggregation (TPA) and impedance platelet aggregation (IPA) induced by arachidonic acid (AA), collagen and ADP and results were compared with the respective values from 120 healthy individuals. At 1 h and 24 h after administration, we found that intravenous ASA caused CEPI-CT to be significantly prolonged with a reduction of AA and collagen-induced IPA. Despite postoperative oral ASA administration for 6-8 days, PFA-100™ CEPI and CADP-CT were significantly shorter and ADP-TPA and IPA values induced by any agonist were significantly greater in patients than in controls. Intravenous ASA had no significant influence on CADP-CT or ADP-induced IPA (ADP-IPA).
Conclusion:
Platelet tests for diagnosing patients as aspirin responders (ASA-R) or aspirin non-responders (ASA-NR) were found to be not comparable. Patients after CABG show augmented platelet dysfunction. Intravenous ASA administration may indicate a promising approach to reduce laboratory resistance after CABG procedure. The reason for this is not clear and requires additional clinical studies.
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