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Calcific Aortic Valve Stenosis and Atherosclerotic Calcification. 2020
Michel Pompeu Barros de Oliveira Sá, and
Luiz Rafael P Cavalcanti, and
Álvaro M Perazzo, and
Rafael A F Gomes, and
Marie-Annick Clavel, and
Philippe Pibarot, and
Giuseppe Biondi-Zoccai, and
Konstantin Zhigalov, and
Alexander Weymann, and
Arjang Ruhparwar, and
Ricardo Carvalho Lima
Division of Cardiovascular Surgery of Pronto Socorro Cardiológico de Pernambuco, PROCAPE, Av. Eng. Domingos Ferreira n°4172. Edf. Paquetá, apt° 405, Recife, Pernambuco, 51021-040, Brazil. michel_pompeu@yahoo.com.br.
This review summarizes the pathophysiology of calcific aortic valve stenosis (CAVS) and surveys relevant clinical data and basic research that explain how CAVS arises. 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.
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