Hypertension is a known risk factor for aortic valve stenosis. The elevated blood pressure increases the transvalvular load and can elicit inflammation and extra-cellular matrix (ECM) remodeling. Elevated cyclic pressure and the vasoactive agent angiotensin II (Ang II) have both been shown to promote collagen synthesis, one of the early hallmarks of aortic sclerosis [1,2]. In the current study, it was hypothesized that the increased collagen production induced by either elevated pressure conditions or the presence of Ang II would affect the mechanical properties of the tissue by increasing stiffness.

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