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Calcific Aortic Valve Stenosis and Atherosclerotic Calcification

  • Evidence-Based Medicine, Clinical Trials and Their Interpretations (L. Roever, Section Editor)
  • Published:
Current Atherosclerosis Reports Aims and scope Submit manuscript

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.

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Correspondence to Michel Pompeu Barros de Oliveira Sá.

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All reported studies/experiments with human or animal subjects performed by the authors have been previously published and complied with all applicable ethical standards (including the Helsinki Declaration and its amendments, institutional/national research committee standards, and international/national/institutional guidelines).

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This article is part of the Topical Collection on Evidence-Based Medicine, Clinical Trials and Their Interpretations

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de Oliveira Sá, M.P.B., Cavalcanti, L.R.P., Perazzo, Á.M. et al. Calcific Aortic Valve Stenosis and Atherosclerotic Calcification. Curr Atheroscler Rep 22, 2 (2020). https://doi.org/10.1007/s11883-020-0821-7

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  • DOI: https://doi.org/10.1007/s11883-020-0821-7

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