Effect of aortic valve stenosis on haemostasis is independent from vascular atherosclerotic burden

Abstract

Objective The aim of study was to assess whether activation of blood coagulation and platelets is enhanced in aortic stenosis (AS) and if so, to determine factors that might modulate these processes. Patients/Methods Seventy-five patients with AS (48 males, 27 females, aged 65 ± 10 years) were enrolled in the study. A control group comprised 75 age- and sex-matched subjects. We determined markers of thrombin generation (thrombin–antithrombin complex [TAT], prothrombin fragment 1 + 2 [F1 + 2]), platelet activation (soluble CD40 ligand [sCD40L], beta-thromboglobulin [beta-TG], P-selectin) in peripheral blood plasma. The extent of atherosclerosis in the carotid and coronary arteries was assessed as a potential confounding factor. Results Mean concentrations of thrombin and platelet markers were higher approximately two-fold in the AS group than in controls ( p < 0.005 for all comparisons). Maximal gradient was positively associated with TAT ( r = 0.61, p < 0.001), F1 + 2 ( r = 0.60, p < 0.001), sCD40L ( r = 0.52, p < 0.01) and beta-TG ( r = 0.70, p < 0.001). Aortic valve area (AVA) negatively associated only with one platelet marker, beta-TG ( r = −0.30, p < 0.05). The presence of concomitant atherosclerotic plaque in the carotid (in 65% of patients) or coronary arteries (in 43% of patients) did not influence thrombin generation and platelet activation in patients with AS. Conclusions AS predisposes to prothrombotic state. Maximal gradient as an index of turbulent flow associated with activation of coagulation and platelets. In contrast, the small aortic valve area was not closely related to these parameters.