Aortic valve stenosis (AS) is a common
heart valve disease in the elderly population, and its pathogenesis remains an interesting area of research. The degeneration of the aortic valve leaflets gradually progresses to valve
sclerosis. The advanced phase is marked by the presence of extracellular
fibrosis and calcification. Turbulent, accelerated blood flow generated by the stenotic valve causes excessive damage to the aortic wall. Elevated shear stress due to AS leads to the degradation of high-molecular weight multimers of
von Willebrand factor, which may involve
bleeding in the mucosal tissues. Conversely, elevated shear stress has been associated with the release of
thrombin and the activation of platelets, even in individuals with acquired von Willebrand syndrome. Moreover, turbulent blood flow in the aorta may activate the endothelium and promote platelet adhesion and activation on the aortic valve surface. Platelets release a wide range of mediators, including
lysophosphatidic acid, which have pro-osteogenic effects in AS. All of these interactions result in blood coagulation, fibrinolysis, and the
hemostatic process. This review summarizes the current knowledge on high shear stress-induced
hemostatic disorders, the influence of AS on platelets and antiplatelet
therapy.