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Haemodynamic studies have shown that diseased cardiac valves, whether stenosed or incompetent, create regions of increased turbulence and shear stresses that are large enough to damage the vascular endothelium and cellular blood elements, leading to abnormal haemorheology, platelet activation, and endothelial dysfunction.1 For example, the intensity of turbulence in patients with pure aortic stenosis (AS) may be 10 times greater than normal while the intensity of turbulence in patients with pure aortic regurgitation (AR) may be three times greater than normal1.
We hypothesised that patients with aortic valve disease may show abnormal haemorheology, platelet activation, and endothelial dysfunction, that may increase their risk of thromboembolism. These abnormalities may perhaps reflect haemodynamic changes resulting from AS or AR, in particular their respective severity. To test our hypothesis, we measured plasma concentrations of soluble P-selectin (sP-sel, a marker for platelet activation2), von Willebrand factor (vWf, a marker for endothelial cell dysfunction3) and fibrinogen (as an index of haemorheology and a clotting factor), in 61 patients with moderate to severe aortic valve disease in sinus rhythm.
We recruited consecutive patients attending outpatient clinics or admitted to our regional referral cardiothoracic unit with primary (native) aortic valve disease. We excluded patients with atrial fibrillation, patients on warfarin, statins or hormone replacement therapy, those with double valve disease (namely, mitral and aortic valve disease) and associated medical conditions known to influence the markers under investigation (including coronary artery …
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