TOPLINE:

In adults without prior coronary artery disease at the time of imaging, elevated lipoprotein(a) (Lp[a]) levels (≥ 150 nmol/L) were independently associated with increased non-calcified plaque volume and higher odds of high-risk plaque features at the plaque level but not associated with calcified plaque volume.

METHODOLOGY:

• Researchers conducted a post hoc analysis using data from three prospective cohorts in Netherlands to determine whether plasma Lp(a) levels were associated with coronary plaque type at the individual plaque level.
• They included 710 adults (mean age, 56 years; 53% men) without prior coronary artery disease who underwent coronary CT angiography and had Lp(a) levels measured between 2008 and 2024.
• A total of 3642 individual plaques were identified and analysed using a US Food and Drug Administration-cleared AI-based algorithm. Elevated Lp(a) levels were defined as ≥ 150 nmol/L.
• Co-primary plaque‑level outcomes were non-calcified plaque volume (30-350 Hounsfield units [HU]), calcified plaque volume (> 350 HU), and the presence of high‑risk plaques — defined as low-density plaques with positive remodelling.

TAKEAWAY:

• Adults with elevated Lp(a) levels had a 14.6% increase in non-calcified plaque volume per plaque after adjustment (P = .009). Each 100 nmol/L increase in Lp(a) levels was associated with a 6.0% increase in non-calcified plaque volume (P = .006).
• Elevated Lp(a) levels were associated with 78% increased odds of high-risk plaques at the plaque level (P = .001). Each 100 nmol/L increase in Lp(a) levels was linked to 21% increased odds (P = .004).
• Elevated Lp(a) levels were not associated with calcified plaque volume.
• Low-density lipoprotein cholesterol and high-sensitivity C-reactive protein had no significant association with the odds of high-risk plaques.

IN PRACTICE:

"[The study] findings elucidate the impact of Lp(a) on unstable plaque phenotypes in an intermediate- to high-risk primary prevention population, and, although prospective outcome studies are warranted, may support early Lp(a) measurement to guide more intensive preventive therapy in patients with elevated Lp(a)," the researchers of the study wrote.

SOURCE:

This study was led by Victor A. Verpalen, MD, University of Amsterdam, Amsterdam, Netherlands. It was published online on April 29, 2026, in the European Journal of Preventive Cardiology.

LIMITATIONS:

The post hoc sample from three selected cohorts may have limited generalisability and introduced selection bias. The cross‑sectional design could only show associations and could not prove causation. Variable scanners, protocols, and enrolment periods may have influenced the findings.

DISCLOSURES:

Several authors reported receiving research grants, consultancy or advisory fees, speaker honoraria, and other personal payments from pharmaceutical, device, and diagnostic companies, and a few reported receiving non‑industry research support. One author reported being a co‑founder of a commercial lipid‑related company.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.