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. Summary: 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.

Calcific Aortic Valve Stenosis and Atherosclerotic Calcification / de Oliveira Sa, M. P. B.; Cavalcanti, L. R. P.; Perazzo, A. M.; Gomes, R. A. F.; Clavel, M. -A.; Pibarot, P.; Biondi-Zoccai, G.; Zhigalov, K.; Weymann, A.; Ruhparwar, A.; Lima, R. C.. - In: CURRENT ATHEROSCLEROSIS REPORTS. - ISSN 1523-3804. - 22:2(2020), p. 2. [10.1007/s11883-020-0821-7]

Calcific Aortic Valve Stenosis and Atherosclerotic Calcification

Biondi-Zoccai G.;
2020

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. Summary: 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.
2020
Aortic valve stenosis; Atherosclerosis; Calcific aortic stenosis; Vascular calcification; 1-Alkyl-2-acetylglycerophosphocholine Esterase; Animals; Aortic Valve; Aortic Valve Stenosis; Calcinosis; Coronary Artery Disease; Disease Progression; Humans; Lipoprotein(a); Mutation; Phospholipids; Phosphoric Diester Hydrolases; Receptor, Notch1; Vascular Calcification
01 Pubblicazione su rivista::01a Articolo in rivista
Calcific Aortic Valve Stenosis and Atherosclerotic Calcification / de Oliveira Sa, M. P. B.; Cavalcanti, L. R. P.; Perazzo, A. M.; Gomes, R. A. F.; Clavel, M. -A.; Pibarot, P.; Biondi-Zoccai, G.; Zhigalov, K.; Weymann, A.; Ruhparwar, A.; Lima, R. C.. - In: CURRENT ATHEROSCLEROSIS REPORTS. - ISSN 1523-3804. - 22:2(2020), p. 2. [10.1007/s11883-020-0821-7]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1474512
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