Abstract

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.

Highlights

  • Valvular heart disease decreases activity tolerance of physical function and longevity

  • Calcified aortic valve disease (CAVD) is a common valvular disease that progresses from early valvular sclerosis without hemodynamic influence to severe calcified aortic valve stenosis requiring valve replacement [2]

  • Cardiovascular disease-related studies have shown that the incidence of all-cause death from cardiovascular disease caused by aortic valve sclerosis has increased by 35% [5]

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Summary

Pathogenesis and Molecular Immune Mechanism of Calcified Aortic Valve Disease

Specialty section: This article was submitted to Cardiovascular Biologics and Regenerative Medicine, a section of the journal Frontiers in Cardiovascular Medicine. Calcified aortic valve disease (CAVD) was previously regarded as a passive process associated with valve degeneration and calcium deposition. 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 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

INTRODUCTION
EPIDEMIOLOGY AND CLINICAL CHARACTERIZATION
AORTIC VALVE CALCIFICATION PROCESS
Endothelial Injury Caused by Mechanical Stress
Lipid Infiltration Triggers Chronic Inflammation
Matrix Remodeling and Fibrosis
CAVD TREATMENT
CONCLUSION
Findings
AUTHOR CONTRIBUTIONS
Full Text
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