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Updated: Feb 24, 2026

Optical Coherence Tomography Based Biomechanical Fluid-Structure Interaction Analysis of Coronary Atherosclerosis Progression
Published on: January 15, 2022
Lipoprotein(a) and plaque progression: insights from serial coronary computed tomography angiography and quantitative
Xiaofang Chen1, Yonghong Zheng1, Shaowei Lin2
1Department of Radiology, Shengli Clinical Medical College of Fujian Medical University, Fujian Provincial Hospital, Fuzhou University Affiliated Provincial Hospital, Fuzhou, Fujian, China.
Background:
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.
Objective:
To explore the potential association between Lp(a) levels and coronary plaque volume, composition, and progression using coronary computed tomography angiography (CCTA).
Methods:
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.
Results:
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.
Conclusions:
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.
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