Prevention & lipids

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

JAMA CardiolPublished Prospective cohort study

An erratum to this article was published (JAMA Cardiol, 1 Sep 2024 ↗)

Authors' conclusion

In this long-term prospective serial CCTA imaging study, higher Lp(a) levels were associated with increased progression of coronary plaque burden and increased presence of low-density noncalcified plaque and pericoronary adipose tissue inflammation.

Study context

Population
Patients with suspected coronary artery disease (CAD) undergoing repeated coronary computed tomography angiography (CCTA) 10 years apart (excluding CABG)299 enrolled
Participants
267 patients
Exposure
Lp ≥125 nmol/L vs <125 nmol/L
Outcome
Change in percent plaque volumes (linear mixed-effects models adjusted for clinical risk factors)
Follow-up
Median scan interval 10.2 years
Methodological detailssingle-centre, serial CCTA, interscan interval 10 years
  • Single-centre
  • Serial CCTA, interscan interval 10 years

Main finding

As reported in the abstract

Percent atheroma volume

P = 0.01

Per doubling of Lp(a), additional increment in percent atheroma volume over 10 years (adjusted)
0.32% (95% CI, 0.04-0.60)

Observational data: associations, not effects.

Secondary outcomes

OutcomeOR (95% CI)
Presence of low-density plaque, per doubling of Lp(a) · baseline and follow-upLp(a) per doubling · baseline1.23 (1.00–1.51)
Presence of low-density plaque, per doubling of Lp(a) · baseline and follow-upLp(a) per doubling · follow-up1.21 (1.01–1.45)

Pericoronary adipose tissue attenuation (RCA and LAD) · baseline and follow-up

Increased with higher Lp(a) levels around both RCA and LAD

Original publication

Lipoprotein(a) and Long-Term Plaque Progression, Low-Density Plaque, and Pericoronary Inflammation. JAMA Cardiol. Published 1 September 2024. doi:10.1001/jamacardio.2024.1874

Summarised from the published abstract; every number is checked against it

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