Calcific Aortic Valve Stenosis and Atherosclerotic Calcification.
Curr Atheroscler Rep
; 22(2): 2, 2020 01 07.
Article
en En
| MEDLINE
| ID: mdl-31912380
ABSTRACT
PURPOSE OF REVIEW This review summarizes the pathophysiology of calcific aortic valve stenosis (CAVS) and surveys relevant clinical data and basic research that explain how CAVS arises. RECENT FINDINGS:
Lipoprotein(a) [Lp(a)], lipoprotein-associated phospholipase A2 (Lp-PLA2), oxidized phospholipids (OxPL), autotaxin, and genetic driving forces such as mutations in LPA gene and NOTCH gene seem to play a major role in the development of CAVS. These factors might well become targets of medical therapy in the coming years. CVAS seems to be a multifactorial disease that has much in common with coronary artery disease, mainly regarding lipidic accumulation and calcium deposition. No clinical trials conducted to date have managed to answer the key question of whether Lp(a) lowering and anti-calcific therapies confer a benefit in terms of reducing incidence or progression of CAVS, although additional outcome trials are ongoing.Palabras clave
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Válvula Aórtica
/
Estenosis de la Válvula Aórtica
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Calcinosis
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Calcificación Vascular
Límite:
Animals
/
Humans
Idioma:
En
Revista:
Curr Atheroscler Rep
Asunto de la revista:
ANGIOLOGIA
Año:
2020
Tipo del documento:
Article
País de afiliación:
Brasil