Calcific Aortic Valve Disease
A Battle of the Sexes
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Despite the high prevalence and severe consequences of calcific aortic valve disease (CAVD), its pathogenesis remains relatively poorly understood. For many years, CAVD was considered a degenerative disease, where calcification was a consequence of normal aging. Although it is now widely accepted that CAVD is an active disease process,1 the erroneous degenerative label contributed to delayed progress in characterizing this condition. At present, our understanding of the mechanisms governing CAVD lags far behind our knowledge of atherosclerosis, a disease to which CAVD is frequently compared. Ultimately, our incomplete understanding of CAVD pathogenesis has profound consequences: other than surgical valve replacement, there remains no treatment to stop the onset or progression of CAVD.
Article, see p 681
Sex as an Important Biological Variable
Consistent with many other cardiovascular diseases, male sex closely follows advanced age as a risk factor for developing CAVD.2 During the past 5 years, there has been a surge in the appreciation of sex as a biological variable, with a report on the importance of sex-specific research reporting issued by the Institute of Medicine and National Academies,3 decisions by several journal publishers to require the reporting of the sex of all tissues and cells in papers, and the 2014 introduction of an National Institutes of Health policy requiring that sex as a biological variable be addressed as an aspect of rigor and reproducibility in National Institutes of Health grants. In the context of CAVD, there is scant information on sex-specific differences in valve biology or pathology. Although several studies have demonstrated higher prevalence of CAVD among men, investigations that explicitly focus on this issue have concentrated on sex differences in ventricular or vascular dysfunction caused by CAVD,4,5 rather than the valve itself. Moreover, the majority of in vitro valve investigations use valvular interstitial cell …