Increased platelet activation following mechanical aortic valve replacement: evidence for the need for anti-platelet therapy?
Ira Goldsmith1,2, Gregory YH Lip2, Andrew D Blann2, Ramesh L Patel1
1Department of Cardio-thoracic Surgery, Walsgrave Hospital, Coventry &
2
Haemostasis, Thrombosis and Vascular Biology Unit, University Department of Medicine, City Hospital, Dudley Road, Birmingham, EnglandBackground: Following aortic valve replacement (AVR) there is increased risk of thromboembolism which may in part be due to an increase in platelet activation.
Methods: We studied indices of platelet activation, endothelial dysfunction and coagulation in 31 patients (20 males, mean age 68.2 years) who underwent AVR. Samples were taken from a peripheral vein prior to and at least 3 months following surgery. We measured levels of the soluble adhesion molecule P selectin (sP-sel, ng/ml, an index of platelet activation), von Willibrand factor (vWf, g/l marker of endothelial dysfunction) and plasma fibrinogen (IU/dl) by ELISA methods.
Results: expressed as mean (standard error)
|
Index |
Bioprosthesis |
P |
Mechanical |
P |
|||
|
SP-sel |
96.4 (11) |
98.5 (9) |
NS |
87 (13) |
102.6 (19) |
0.018 |
|
|
Fibrinogen |
3.8 (0.1) |
3.8 (0.1) |
NS |
3.4 (0.2) |
3.1 (1) |
NS |
|
|
vWf |
130 (6) |
138 (8) |
NS |
116.4 (10) |
121 (8) |
NS |
|
There were no differences in the levels of markers of endothelial dysfunction or fibrinogen following AVR in either groups. However, there was a significant increase in the level of sP-sel suggesting increased platelet activation in patients receiving mechanical AVR despite warfarin therapy. This was not observed in patients receiving bioprosthetic AVR.
Conclusion: Mechanical AVR is associated with increased platelet activation. This may contribute to the increased risk of thromboembolism in such patients compared with those with bioprosthesis. This has implications for thromboprophylaxis with the need for antiplatelet and anticoagulant therapy in patients with mechanical valves.
