Abstract 480: Platelet Activation After Cardiac Surgery Increases Thrombogenicity After Valve Replacement and Contributes to “Aspirin-Resistance” After Coronary Artery Bypass Grafting
Introduction: Though platelet activation due to cardiopulmonary bypass is a general phenomenon in cardiac surgery, aspirin is routinely used only after coronary artery bypass grafting (CABG), but not after valve replacement. We hypothesized that increased platelet reactivity enhances the thromboembolic risk, especially early after valve replacement.
Methods: We investigated platelet function in patients undergoing mechanical aortic valve replacement (AVR) compared to those undergoing CABG (each group n = 15). In vitro aggregation (turbidimetry) and thromboxane formation (immunoassay) after stimulation with 1 mmol/L arachidonic acid were measured before and at days 5 and 10 after surgery. Oral aspirin was stopped at least 10 days before CABG and re-started at day 1 after CABG (100 mg/d).
Results: Before surgery, platelet aggregation and thromboxane formation in patients undergoing AVR were significantly higher compared to CABG. In AVR-patients, thromboxane further increased after surgery (twofold from days 5 to 10). Platelet thromboxane formation, but not aggregation, was moderately inhibited by oral aspirin after CABG, but this was not statistically significant. Platelet counts were always comparable in both groups.
Conclusion: The higher amount of arachidonic acid - induced platelet aggregation and thromboxane formation (before surgery) in patients suffering from aortic valve disease compared to patients with coronary heart disease may indicate a greater extent of platelet activity in the former. This study shows for the first time that platelet thromboxane formation significantly increases early after AVR, indicating increased platelet reactivity in these patients. But low-dose aspirin may not be sufficient to control platelet reactivity in AVR-patients when required, as suggested by its weak inhibition of thromboxane formation and its insufficient inhibition of aggregation in CABG-patients.