# Lipoprotein(a) and plaque progression: insights from serial coronary computed tomography angiography and quantitative plaque assessment

## TL;DR

High levels of lipoprotein(a) are linked to increased coronary plaque buildup and faster plaque progression over time, even in people with otherwise low cardiovascular risk.

## Contribution

This study provides new evidence that elevated Lp(a) levels are associated with accelerated progression of specific plaque types in coronary arteries.

## Key findings

- Elevated Lp(a) levels were associated with higher baseline plaque burden and faster LAP volume progression.
- Patients with diabetes, female gender, or normal lipid profiles showed greater plaque progression.
- Statin users with elevated Lp(a) had more pronounced calcification progression.

## Abstract

Lipoprotein(a) [Lp(a)] is a well-established independent risk factor for cardiovascular disease. However, the long-term effects of Lp(a) on coronary plaque phenotype remain unclear.

To explore the potential association between Lp(a) levels and coronary plaque volume, composition, and progression using coronary computed tomography angiography (CCTA).

Patients with available data for Lp(a) and underwent baseline CCTA examinations between January 2009 to December 2015 and subsequently underwent a follow-up coronary CTA were retrospectively enrolled. Quantitative CCTA analyses measured plaque length, total plaque volume and composition volume. Patients were categorized into an elevated Lp(a) group (≥30 mg/dL) and a normal Lp(a) group (<30 mg/dL). The association between Lp(a) and baseline plaque characteristic and progression were investigated in linear mixed-effects models adjusted for clinical factors. Subgroup analyses were also conducted.

Among 453 patients (mean age 64.7 years, 77.7% male) with a median follow-up of 6.15 years. elevated Lp(a) was linked to higher baseline plaque burden (all p < 0.001) and accelerated LAP volume progression (β = 0.55 mm3/year, 95% CI: 0.04–1.06; p = 0.036) after adjusting for confounders. In addition, patients with diabetes, female gender, family history of CAD, or aged <60 years and with normal lipid profiles showed higher progression in total plaque volume and LAP, fibro-fatty, and fibrous components. Increased calcification volume progression was also seen in those with diabetes, female gender, smoking, drinking, or normal LDL-C levels. The association between Lp(a) and calcification progression was more pronounced in statin users.

Elevated Lp (a) level was associated with high coronary artery plaque burden at baseline and rapid progression of LAP at follow-up. Lp(a) may serve as a significant residual risk factor in seemingly “low-risk” populations.