Calcific Aortic Valve Stenosis and Atherosclerotic Calcification.

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.

journal_name

Curr Atheroscler Rep

authors

de Oliveira Sá MPB,Cavalcanti LRP,Perazzo ÁM,Gomes RAF,Clavel MA,Pibarot P,Biondi-Zoccai G,Zhigalov K,Weymann A,Ruhparwar A,Lima RC

doi

10.1007/s11883-020-0821-7

subject

Has Abstract

pub_date

2020-01-07 00:00:00

pages

2

issue

2

eissn

1523-3804

issn

1534-6242

pii

10.1007/s11883-020-0821-7

journal_volume

22

pub_type

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