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Updated: Aug 14, 2026

Investigating Aortic Valve Calcification via Isolation and Culture of T Lymphocytes using Feeder Cells from Irradiated Buffy Coat
04:30

Investigating Aortic Valve Calcification via Isolation and Culture of T Lymphocytes using Feeder Cells from Irradiated Buffy Coat

Published on: February 4, 2021

Lipids and lipoproteins in calcific aortic valve disease

Olcay Aksoy1, Yin Tintut1,2,3, Linda L Demer1,2,4

  • 1Department of Medicine.

Current Opinion in Lipidology
|August 13, 2026
PubMed

Insights

Lipoprotein(a) [Lp(a)] plays a key role in calcific aortic valve disease (CAVD), despite disappointing results from traditional lipid-lowering therapies. New diagnostic and therapeutic strategies targeting Lp(a) and other pathways are emerging for CAVD.

Area of Science:

  • Cardiovascular Medicine
  • Lipidology
  • Valvular Heart Disease

Background:

  • Lipids and lipoproteins are implicated in calcific atherosclerosis.
  • The role of lipids in calcific aortic valve disease (CAVD) is increasingly recognized, with links to hypercholesterolemia and lipoprotein(a) [Lp(a)].
  • Despite similarities with atherosclerosis, lipid-lowering therapies have shown disappointing results in CAVD.

Purpose of the Study:

  • To review current evidence on the role of lipids and lipoproteins in CAVD.
  • To discuss novel diagnostic and therapeutic approaches for CAVD.
  • To explore the mechanisms underlying lipid involvement in CAVD.

Main Methods:

  • Review of clinical and genetic studies linking lipids, particularly Lp(a), to CAVD.
  • Analysis of emerging diagnostic techniques, including lipid droplet visualization and antibody screening.
  • Evaluation of novel therapeutic strategies, such as Lp(a) lowering and SGLT2 inhibition.

Main Results:

  • Strong evidence supports the role of Lp(a) levels in CAVD.
  • Potential diagnostic advances include pH-sensitive probes for lipid droplets and natural antibodies to modified LDL.
  • Emerging therapies include Lp(a) lowering, SGLT2 inhibition, and soluble guanylate cyclase reactivation, though trial outcomes are mixed.

Conclusions:

  • Recent research clarifies the mechanisms of lipid and Lp(a) contribution to CAVD.
  • New diagnostic tools involve screening for natural antibodies and visualizing lipid deposits.
  • Novel therapeutic agents like oligonucleotides and nanoparticles are under investigation, with new clinical trials commencing.
Abstract

Keywords:
aortic stenosisaortic valvecalcificationcardiac valvelipidslipoprotein (a)lipoproteins

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