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Investigating Aortic Valve Calcification via Isolation and Culture of T Lymphocytes using Feeder Cells from Irradiated Buffy Coat
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Lipoprotein(a): Expanding our knowledge of aortic valve narrowing

Amer Youssef1, Justin R Clark2, Marlys L Koschinsky3

  • 1Robarts Research Institute, Canada.

Trends in Cardiovascular Medicine
|June 12, 2020
PubMed

Insights

Elevated lipoprotein(a) [Lp(a)] is a key risk factor for calcific aortic valve disease (CAVD), leading to aortic valve stenosis (AS). Therapies lowering Lp(a) may offer the first medical treatment to halt AS progression.

Area of Science:

  • Cardiovascular Medicine
  • Biochemistry
  • Genetics

Background:

  • Elevated lipoprotein(a) [Lp(a)] is a causal risk factor for atherosclerotic cardiovascular disease (ASCVD) and calcific aortic valve disease (CAVD).
  • Calcific aortic valve disease (CAVD) progresses to aortic valve stenosis (AS), affecting 2% of individuals over 65.
  • Current treatments for AS involve valve replacement; no medical therapies exist to halt its progression.

Purpose of the Study:

  • To explore the role of lipoprotein(a) [Lp(a)] in the pathogenesis of calcific aortic valve disease (CAVD) and aortic valve stenosis (AS).
  • To identify barriers in understanding Lp(a) 's molecular role in AS and the need for effective interventions.
  • To highlight the potential of novel therapies targeting Lp(a) for AS treatment.

Main Methods:

  • Literature review and synthesis of existing evidence on Lp(a) and CAVD.
  • Analysis of pathophysiological mechanisms linking Lp(a) to valve calcification.
  • Review of current therapeutic strategies and emerging treatments for AS.

Main Results:

  • Lp(a) exacerbates CAVD through endothelial dysfunction, foam cell formation, and inflammation.
  • Lp(a)-induced inflammation promotes valve thickening and mineralization via pro-osteogenic signaling.
  • Oxidized phospholipid content of Lp(a) facilitates pro-inflammatory effects in valve interstitial cells.

Conclusions:

  • Understanding Lp(a)'s molecular role in AS pathogenesis is crucial for developing targeted therapies.
  • The lack of appropriate animal models hinders the development of effective interventions.
  • Emerging therapies that lower Lp(a) present a promising first medical treatment to halt AS progression.

Keywords:
Aortic stenosisCalcific aortic valve diseaseLipoprotein(a)Oxidized phospholipids

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