Calcific aortic valve disease (CAVD) is the most prevalent heart valve disease in the U.S. and is characterized by the formation of calcific lesions within the valve leaflets [1]. The emerging hemodynamic theory of CAVD pathogenesis assumes a link between gradual hemodynamic alterations caused by the growing lesions and further disease progression [2–5]. In order to test this hypothesis, it is necessary to quantify the hemodynamic changes experienced downstream of a calcifying valve.

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