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Calcific aortic stenosis (AS) is characterised by an initial inflammatory phase, with endothelial damage, lipoprotein infiltration and oxidative stress. This stage is followed by a disorganisation of the extracellular matrix with an overproduction of collagen fibres and a mineralisation phase in which valvular interstitial cells differentiate into an osteoblast-like cell type, leading to microcalcification analogue to skeletal bone formation. This self-perpetuating cycle of progressive fibrocalcific remodelling leads to macrocalcification, increases valve rigidity and therefore narrows the effective orifice area, increasing left ventricular afterload and ultimately provoking myocardial damage and symptoms (figure 1).1 Valvular fibrosis, although understudied, appears to play a major role in younger, bicuspid valve and female patients and is one of the reasons sex-specific thresholds are used to define severe AS by CT aortic valve calcification (CT-AVC) quantification (2000 Agatston units (AU) for men and 1200 AU for women).2 The pathogenic model depicted in figure 1 is not necessarily followed in a serial fashion, and although the advance of the disease is inexorable, the rate of AS progression remains largely unpredictable. However, some markers of rapid progression have been described, such as systolic hypertension,3 bicuspid morphology4 and metabolic syndrome.5
Contributors EG drafted the first version of the editorial. M-AC revised the draft of the editorial.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.
Patient consent for publication Not required.
Provenance and peer review Commissioned; internally peer reviewed.
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