Aortic valve calcification is a degenerative disease with high prevalence, especially amongst the elderly, and is a major cause of morbidity and mortality. Ex vivo experiments has shown that aortic valve leaflets are sensitive to their mechanical environment in a magnitude dependent manner. Fluid shear stresses, specifically, has been shown to affect inflammatory and remodeling responses relevant to aortic valve calcification [1,2]. Consequently, it has been proposed that the phenomenon of diseased calcium nodules developing exclusively on the aortic surface as opposed to the ventricular surface is due to the exposure of the aortic surface to disturbed shear stresses, whereas undisturbed shear stresses on the ventricular surface do not trigger calcification [3,4]. Additionally, it has been observed that the non-coronary leaflet of the AV is more susceptible to calcification, which is hypothesized to be due to reduced shear stresses from the lack of diastolic coronary flow [5].

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