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  1. Home
  3. Lipoprotein(a) And Long-term Plaque Progression, Low-density Plaque, And Pericoronary Inflammation.
  1. Home
  3. Lipoprotein(a) And Long-term Plaque Progression, Low-density Plaque, And Pericoronary Inflammation.

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Lipoprotein(a) and Long-Term Plaque Progression, Low-Density Plaque, and Pericoronary Inflammation.

Nick S Nurmohamed1,2,3, Emilie L Gaillard1,2, Shant Malkasian4

  • 1Department of Cardiology, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands.

JAMA Cardiology
|July 17, 2024

View abstract on PubMed

Summary
This summary is machine-generated.

Higher Lipoprotein(a) (Lp[a]) levels are linked to increased coronary plaque progression and inflammation over 10 years. This suggests Lp(a) significantly impacts the development of high-risk, rupture-prone plaques in cardiovascular disease.

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Area of Science:

  • Cardiology
  • Biomarkers
  • Imaging

Background:

  • Lipoprotein(a) (Lp[a]) is a known causal risk factor for cardiovascular disease.
  • Long-term effects of Lp(a) on coronary plaque phenotype and inflammation are not well understood.

Purpose of the Study:

  • To investigate the association between Lp(a) levels and long-term coronary artery plaque progression.
  • To assess the relationship of Lp(a) with high-risk plaque formation and pericoronary adipose tissue inflammation.

Main Methods:

  • Prospective cohort study of 267 patients with suspected coronary artery disease (CAD).
  • Repeated coronary computed tomography angiography (CCTA) imaging over a median of 10.2 years.
  • Lp(a) levels measured using an isoform-insensitive assay; CCTA analyzed with AI-based algorithm.

Main Results:

  • Patients with Lp(a) ≥ 125 nmol/L had double the percent atheroma volume compared to those with lower levels.
  • Each doubling of Lp(a) correlated with increased plaque volume and odds of low-density plaque.
  • Higher Lp(a) levels were associated with increased pericoronary adipose tissue inflammation.

Conclusions:

  • Elevated Lp(a) levels are associated with accelerated coronary plaque progression and increased presence of high-risk plaque features.
  • Higher Lp(a) is linked to pericoronary adipose tissue inflammation, indicating an inflammatory role.
  • These findings suggest a significant long-term impact of Lp(a) on coronary atherogenesis, promoting inflammatory, rupture-prone plaques.