Age Differences in Aortic Stenosis—Graphic Abstract

Aortic valve disease typically begins with thickening which occurs from an increase in the extracellular matrix of the fibrosa, followed by progressive sclerosis in the third and fourth decades at sites of mechanical stress, usually on the ventriculoaortic junction. Early calcification occurs in the fifth and sixth decades, becoming severe in the seventh and eighth decades. The pathogenesis of aortic stenosis (AS) shares key mechanisms with atherosclerosis, involving endothelial damage, lipoprotein deposition, excessive proteoglycan synthesis, inflammation, oxidative stress, and myofibroblast differentiation in the early stages, with mineral deposition and valvular interstitial cell (VIC) differentiation occurring in the later stages. There are three main etiologies of AS: degenerative tricuspid, congenital (i.e., bicuspid and unicuspid), and post-rheumatic. Congenital and post-rheumatic AS often present symptoms at earlier ages: bicuspid AS typically manifests between ages 50–70, unicuspid AS at 20–30 years (acommissural type) or 50–60 years (unicommissural type), and post-rheumatic AS between 20–40 years, although this reflects the general age range of rheumatic heart disease.

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Age Differences in Aortic Stenosis: https://doi.org/10.31083/RCM28185

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Prognostic Effects of Operation Age for Pediatric Patients with Supravalvar Aortic Stenosis: https://doi.org/10.31083/j.rcm2510384