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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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The role of elevated lipoprotein(a) in aortic valve disease: a systematic review

P Wambua1, M Wahinya2, Z Khan3

  • 1Tigoni Level IV Hospital, Kiambu, Kenya.

Frontiers in Cardiovascular Medicine
|October 29, 2025
PubMed

Insights

Elevated Lipoprotein(a) [Lp(a)] is a significant risk factor for calcific aortic valve stenosis (CAVS). Lp(a) levels and genetic factors influence CAVS risk, suggesting potential for early screening and targeted therapies.

Area of Science:

  • Cardiology
  • Genetics
  • Public Health

Background:

  • Calcific aortic valve stenosis (CAVS) is a prevalent valvular heart disease.
  • Aortic sclerosis (ASc) and stenosis (AS) involve leaflet thickening, inflammation, lipid deposition, and calcification.
  • Lipoprotein(a) [Lp(a)] is increasingly recognized for its pro-atherogenic, pro-inflammatory, and pro-calcific roles in CAVS.

Purpose of the Study:

  • To systematically review the evidence on the association between Lipoprotein(a) [Lp(a)] and calcific aortic valve stenosis (CAVS).
  • To explore the role of Lp(a) levels and genetic variants in CAVS pathogenesis and risk stratification.
  • To identify potential therapeutic implications of targeting Lp(a) in CAVS.

Main Methods:

  • A systematic literature search was performed across multiple databases (PubMed, Cochrane Library, etc.) following PRISMA guidelines.
  • Included studies were observational designs (case-control, cohort, cross-sectional) and randomized trials.
  • Study quality was assessed using the Newcastle-Ottawa Scale (NOS).

Main Results:

  • Eighteen studies with 153,192 participants were included; no RCTs were found.
  • Elevated Lp(a) levels showed a consistent, dose-dependent association with increased risk of AS and aortic valve calcification (AVC).
  • Genetic variant rs10455872 was a significant risk allele; racial variability in Lp(a) levels and AVC prevalence was observed.

Conclusions:

  • Lipoprotein(a) [Lp(a)] is an independent risk factor for CAVS, influenced by concentration and genetics.
  • Emerging Lp(a)-lowering therapies offer potential for mitigating CAVS progression.
  • Further randomized trials are necessary to confirm the benefit of Lp(a) reduction in CAVS.
Abstract

Keywords:
aortic sclerosisaortic stenosisaortic valve calcificationcardiovascular diseasegenetic polymorphismslipoprotein(a)targeted therapies

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