Calcified aortic stenosis (AS) is one of the most common valvular heart diseases worldwide, characterized by progressive fibrocalcific remodeling and thickening of the leaflets, which ultimately leads to obstruction of blood flow. Its pathobiology is an active and complicated process, involving endothelial cell dysfunction, lipoprotein deposition and oxidation, chronic inflammation, phenotypic transformation of valve interstitial cells, neovascularization, and intravalvular hemorrhage. To date, no targeted drug has been proven to slow down or prevent disease progression. Aortic valve replacement is still the optimal treatment of AS. This article reviews the etiology, diagnosis, and management of calcified aortic stenosis and proposes novel potential therapeutic targets.
Keyphrases
- aortic stenosis
- aortic valve replacement
- aortic valve
- transcatheter aortic valve replacement
- ejection fraction
- transcatheter aortic valve implantation
- left ventricular
- blood flow
- coronary artery disease
- oxidative stress
- endothelial cells
- induced apoptosis
- multiple sclerosis
- atrial fibrillation
- heart failure
- randomized controlled trial
- hydrogen peroxide
- mitral valve
- emergency department
- systematic review
- nitric oxide
- endoplasmic reticulum stress
- risk assessment
- combination therapy
- drug delivery
- drug induced
- human health
- cell proliferation
- signaling pathway
- diabetic retinopathy
- oral anticoagulants