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Aspirin-induced platelet inhibition in patients undergoing cardiac surgery
Norbert Zimmermann1, Muhammed Kurt, Joachim Winter
1Federal Institute for Drugs and Medical Devices, Bonn, Germany. nzimmermann@bfarm.de
Insights
Platelet function is altered after cardiac surgery, potentially impairing aspirin
Area of Science:
- Cardiovascular Surgery
- Hematology
- Pharmacology
Background:
- Cardiac surgery, including coronary artery bypass grafting (CABG) and aortic valve replacement (AVR), can alter platelet function.
- Platelet aggregation may increase post-surgery, and response to aspirin can be insufficient, particularly after CABG.
Purpose of the Study:
- To investigate the antiplatelet effect of aspirin in patients undergoing CABG and AVR.
- To determine if platelet activation after cardiac surgery impairs aspirin's efficacy.
Main Methods:
- Compared aspirin's antiplatelet effect in 20 CABG patients and 20 AVR patients.
- Measured arachidonic acid-induced platelet aggregation and thromboxane formation pre- and post-surgery (days 1, 5, 10).
- Assessed in vitro aspirin inhibition of platelet function.
Main Results:
- Thromboxane formation increased significantly after AVR but not after CABG, despite aspirin treatment in CABG patients.
- In vitro aspirin inhibition of platelet function was attenuated post-surgery in both CABG and AVR groups.
- Platelet aggregation and thromboxane formation were higher pre-surgery in patients with aortic stenosis.
Conclusions:
- Thromboxane formation increases post-AVR, suggesting impaired platelet function.
- Aspirin's antiplatelet effect may be reduced after CABG due to increased platelet activity.
- Both CABG and AVR are associated with a post-operative in vitro "resistance" to aspirin's effects on platelets.
Abstract:
Platelet function and response to pharmacological inhibition are altered by cardiac surgery. For example, aggregation is increased early after aortic valve replacement (AVR) and platelet response to aspirin is often insufficient after coronary artery bypass grafting (CABG). We hypothesized that the effect of aspirin administration after cardiac surgery might be impaired due to platelet activation. Therefore, the antiplatelet effect of aspirin was compared in patients (n = 20 per group) after CABG and AVR surgery (bileaflet prosthesis). Arachidonic acid-induced aggregation (turbidimetry) and thromboxane formation (radioimmunoassay) were determined before and 1, 5, and 10 days after surgery. In CABG-patients, antiplatelet treatment had been discontinued 10 days before surgery. Oral aspirin was started on day 1 after CABG. AVR-patients did not receive oral aspirin. Before surgery, platelet aggregation and thromboxane formation were significantly higher in patients with aortic stenosis. After CABG, thromboxane formation was not significantly changed from control values before surgery (66 +/- 13% on day 10) despite oral aspirin treatment, whereas thromboxane formation in patients undergoing AVR significantly increased compared to values before surgery (216 +/- 29% on day 10). In both groups of patients, 100 micromol/l aspirin in vitro largely inhibited platelet function before surgery, with markedly attenuated effects after surgery. In conclusion, thromboxane formation increased after AVR but not after CABG. The antiplatelet effect of aspirin, therefore, may be impaired after CABG by increased platelet activity. An additional in vitro "resistance" of platelets was seen after both CABG and AVR.
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