Summary
Aortic valve stenosis (AS) increasingly afflicts our aging population. However, the
pathobiology of the disease is still poorly understood and there is no effective pharmacotherapy
for treating those at risk for clinical progression. The progression of AS involves
complex inflammatory and fibroproliferative processes that resemble to some extent
atherosclerosis. Accumulating evidence indicates that several coagulation proteins
and its inhibitors, including tissue factor, tissue factor pathway inhibitor, prothrombin,
factor XIII, von Willebrand factor, display increased expression within aortic stenotic
valves, predominantly on macrophages and myofibroblasts around calcified areas. Systemic
impaired fibrinolysis, along with increased plasma and valvular expression of plasminogen
activator inhibitor-1, has also been observed in patients with AS in association with
the severity of the disease. There is an extensive cross-talk between inflammation
and coagulation in stenotic valve tissue which contributes to the calcification and
mineralisation of the aortic valve leaflets. This review summarises the available
data on blood coagulation and fibrinolysis in AS with the emphasis on their interactions
with inflammation and calcification.
Keywords
Aortic stenosis - blood coagulation - fibrinolysis - fibrin - tissue factor