Key result
Calcified aortic valve disease is an active process involving endothelial injury, lipid infiltration, chronic inflammation, matrix remodeling, and neovascularization.
Why the study?
CAVD is an active process and major cause of cardiovascular death, necessitating an updated understanding of its pathogenesis and therapeutic targets to guide future diagnosis and treatment.
Understanding the active molecular and immune mechanisms driving calcified aortic valve disease may help identify novel therapeutic targets to delay progression and reduce the need for surgical or transcatheter valve replacement.
Highlights potential targets for disease modification in calcified aortic valve disease; leaves open whether pathway modulation alters clinical outcomes.
Calcified aortic valve disease (CAVD) was previously regarded as a passive process associated with valve degeneration and calcium deposition. However, recent studies have shown that the occurrence of CAVD is an active process involving complex changes such as endothelial injury, chronic inflammation, matrix remodeling, and neovascularization. CAVD is the ectopic accumulation of calcium nodules on the surface of the aortic valve, which leads to aortic valve thickening, functional stenosis, and ultimately hemodynamic disorders. CAVD has become an important cause of death from cardiovascular disease. The discovery of therapeutic targets to delay or block the progression of CAVD and the clinical application of transcatheter aortic valve implantation (TAVI) provide new ideas for the prevention and treatment of CAVD. This article summarizes the pathogenesis of CAVD and provides insight into the future directions of CAVD diagnosis and treatment.
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Bian et al. (2021) conducted a review in Calcified aortic valve disease. Calcified aortic valve disease is an active process involving endothelial injury, lipid infiltration, chronic inflammation, matrix remodeling, and neovascularization.
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