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Updated: Oct 24, 2025

Investigating Aortic Valve Calcification via Isolation and Culture of T Lymphocytes using Feeder Cells from Irradiated Buffy Coat
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The current landscape of lipoprotein(a) in calcific aortic valvular disease

Grace Hsieh1, Theresa Rizk2, Adam N Berman1

  • 1Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.

Current Opinion in Cardiology
|August 16, 2021
PubMed

Insights

Lipoprotein (a) drives calcific aortic stenosis (CAVS) by carrying oxidized phospholipids, leading to inflammation and valve calcification. Therapies targeting lipoprotein (a) show promise for halting CAVS progression.

Area of Science:

  • Cardiology
  • Biochemistry
  • Genetics

Background:

  • Calcific aortic stenosis (CAVS) is a prevalent valvular heart disease in aging populations.
  • Current treatments for severe aortic stenosis (AS) involve valve replacement.
  • Lipoprotein (a) [Lp(a)] is increasingly recognized as a significant factor in CAVS.

Purpose of the Study:

  • To review the pathophysiology of CAVS linked to Lp(a).
  • To summarize emerging therapies targeting Lp(a) for CAVS.
  • To explore Lp(a) as a therapeutic target for AS.

Main Methods:

  • Review of recent pathophysiologic, epidemiological, and genetic studies.
  • Analysis of Lp(a)'s role in valvular calcification.
  • Evaluation of ongoing Lp(a)-lowering therapy studies.

Main Results:

  • Lp(a) acts as a key carrier of pro-calcifying oxidized phospholipids (OxPL).
  • OxPL metabolism promotes inflammation, valvular thickening, and mineralization.
  • Lp(a) is identified as a causal mediator of calcific aortic valvular disease (CAVD).

Conclusions:

  • Lp(a) plays a critical, rate-limiting role in CAVS progression.
  • Lp(a)-lowering therapies offer potential novel pharmacotherapies for AS.
  • Targeting Lp(a) may significantly impact the clinical management of CAVD.
Abstract

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