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 Repjournal_title
Current atherosclerosis reportsauthors
de Oliveira Sá MPB,Cavalcanti LRP,Perazzo ÁM,Gomes RAF,Clavel MA,Pibarot P,Biondi-Zoccai G,Zhigalov K,Weymann A,Ruhparwar A,Lima RCdoi
10.1007/s11883-020-0821-7subject
Has Abstractpub_date
2020-01-07 00:00:00pages
2issue
2eissn
1523-3804issn
1534-6242pii
10.1007/s11883-020-0821-7journal_volume
22pub_type
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