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Published on: February 4, 2021
Calcific Aortic Valve Stenosis and Atherosclerotic Calcification
Michel Pompeu Barros de Oliveira Sá1,2,3, Luiz Rafael P Cavalcanti4,5, Álvaro M Perazzo4,5
1Division 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.
Calcific aortic valve stenosis (CAVS) involves lipid buildup and calcium deposits, similar to coronary artery disease. Emerging research highlights key factors like Lipoprotein(a) [Lp(a)] as potential therapeutic targets.
Area of Science:
- Cardiovascular Medicine
- Pathophysiology
- Biochemistry
Background:
- Calcific aortic valve stenosis (CAVS) is a progressive disease.
- Understanding CAVS pathophysiology is crucial for developing effective treatments.
Purpose of the Study:
- To review the pathophysiology of CAVS.
- To survey clinical data and basic research on CAVS development.
Main Methods:
- Literature review of clinical trials and basic research.
- Analysis of etiological factors in CAVS.
Main Results:
- Lipid accumulation and calcium deposition are key features of CAVS.
- Factors like Lipoprotein(a) [Lp(a)], Lp-PLA2, OxPL, autotaxin, and genetic mutations (LPA, NOTCH) are implicated.
- CAVS shares similarities with coronary artery disease.
Conclusions:
- CAVS is a multifactorial disease with identified molecular and genetic drivers.
- These factors represent potential targets for future medical therapies.
- Further clinical trials are needed to evaluate the efficacy of Lp(a) lowering and anti-calcific therapies.
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