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Performing basic translational research to elucidate the underlying mechanisms driving calcific aortic valve disease (CAVD) pathogenesis is a critical step for the development of early intervention strategies. CAVD is a significant worldwide healthcare burden that is increased in ageing populations, and currently no therapies exist to delay or prevent its onset and progression. In their Heart paper, Gomez-Stallons et al histologically present the progression of calcification and associated matrix changes in tissues obtained from postmortem valves with no prior diagnosis of aortic valve stenosis (AS) and patients with AS.1 This is an important study that validates mineral and extracellular matrix composition changes accompanying CAVD progression.2 An intriguing finding was that valves without clinical AS from people over 50 years all had some form of calcification present. Clinically, only 5% of people over the age of 70 years experience CAVD that results in valvular dysfunction necessitating valve replacement. This raises a crucial unanswered question: what causes some people to develop AS while in others the disease does not progress past microcalcification? Future work that elucidates these early mechanisms will be the first step in developing targeted, precision-based medicine approaches that can identify, follow and treat high-risk patients. The findings of this research provide the initial support for more in-depth work that longitudinally studies clinical, molecular, genetic and haemodynamic properties in individuals at high risk for AS.
Future investigations should consider two important factors to help accelerate CAVD mechanistic discovery: terminology standardisation and optimised tissue utilisation. Standardised nomenclature of anatomical features and …
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