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onrheumatic aortic stenosis has assumed center stage in contemporary cardiology because of the aging of the population and the prodigious advances in percutaneous approaches to its treatment. Many refer to this disease dismissively as "degenerative". That term implies an inevitable, ineluctably progressive, and inherent process that defies slowing or regressing. Use of the term degenerative cloaks our ignorance regarding mechanisms, much as do the designations idiopathic cardiomyopathy or essential hypertension. Yet, in step with the remarkable advances in addressing the mechanical aspects of aortic stenosis, researchers continue to stride toward better mechanistic understanding of the pathophysiology of this condition. Rather than "degenerative" aortic stenosis, we advocate use of the terms fibrocalcific or sclerocalcific aortic valve disease: nomenclature that captures the hardening of the valve tissue and its mineralization. We now recognize a number of active biological mechanisms that pave the pathway to alterations in the structure and function of the aortic valve (Figure
Aïkawa et al. (Mon,) studied this question.
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