Sep 2026· Journal of Clinical Lipidology· 0 citations· 35 references
Medicine
TL;DR
Increasing Lp(a) levels were associated with OCT-defined coronary plaque phenotypes related to vulnerability and instability, including high-risk and layered plaques, and given the limited patient-level sample size, these findings should be considered exploratory and hypothesis-generating.
Abstract
Background
Lipoprotein(a) [Lp(a)] is a causal risk factor for coronary artery disease, but its relationship with coronary plaque morphology assessed by optical coherence tomography (OCT) remains incompletely characterized.
Objective
To investigate the association between circulating Lp(a) levels and OCT-defined coronary plaque phenotypes using a comprehensive segment-level approach.
Methods
In this prospective single-center study (RELACS registry; NCT05496790), consecutive patients undergoing intracoronary OCT with available Lp(a) measurements were included. Coronary vessels were divided into 3 mm segments and analyzed for plaque characteristics. Lp(a) was primarily modeled as a continuous variable to assess its association with OCT-defined plaque phenotypes, including high-risk, layered, and fibrous plaques. High-risk plaque was defined as the presence of ≥2 criteria between lipid-rich plaque, thin-cap fibroatheroma (TCFA), and macrophages. Mixed-effects logistic regression models were used to account for within-patient clustering.
Results
A total of 952 coronary segments from 50 patients were analyzed. Increasing Lp(a) levels were significantly associated with multiple features of plaque vulnerability, including TCFA, lipid-rich plaques, macrophages, and microchannels. In the multivariate mixed-effects analysis, higher Lp(a) levels were independently associated with a greater likelihood of high-risk plaque (odds ratios [OR] 1.31, 95% CI 1.16-1.48; P < .001) and layered plaques (OR 1.15, 95% CI 1.02-1.29; P = .024), whereas an inverse association was observed with fibrous plaques (OR 0.84, 95% CI 0.70-1.00; P = .047).
Conclusion
Increasing Lp(a) levels were associated with OCT-defined coronary plaque phenotypes related to vulnerability and instability, including high-risk and layered plaques. Given the limited patient-level sample size, these findings should be considered exploratory and hypothesis-generating.
This meta-analysis suggests that high Lp(a) levels are associated with several imaging-defined high-risk coronary plaque features, with the most robust evidence observed for OCT-derived TCFA and plaque rupture.
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Background and aims Elevated lipoprotein(a) [Lp(a)] levels are recognized as a genetic risk factor for atherosclerotic cardiovascular disease. Previous coronary imaging studies have linked elevated Lp(a) levels to vulnerable coronary plaque characteristics. However, the relationship between elevated Lp(a) levels and vu...
K. Kojima, Yudai Tanaka, Katsunori Fukumoto et al.· Atherosclerosis Plus· 0 citations
BACKGROUND
Lipoprotein(a) [Lp(a)] is a genetically determined, causal risk factor for atherosclerotic cardiovascular disease. Whether elevated Lp(a) is associated with premature coronary artery disease (pCAD) in young and middle-aged adults with low levels of low-density lipoprotein cholesterol (LDL-C) remains poorly c...
Yahya Bawahab, V. C. Vasile· Journal of Clinical Lipidolo...· 0 citations
BACKGROUND
Patients with polyvascular disease (PolyVD) or atherosclerosis in the coronaries and at least 1 additional arterial bed are at increased risk of subsequent clinical cardiovascular events. While lowering low-density lipoprotein cholesterol (LDL-C) is recommended in the secondary prevention settings, whether P...
Aya Katasako-Yabumoto, Yu Kataoka, S. Nicholls et al.· Journal of the American Hear...· 0 citations
Lp(a) is associated with subclinical atherosclerosis, and imaging for subclinical atherosclerosis is useful for risk-stratifying individuals with elevated Lp(a), and CAC scoring has demonstrated utility for risk stratification among individuals with elevated Lp(a).
Apurva Khedagi, Yu-Si Gong, G. Dharmavaram et al.· Journal of Clinical Lipidolo...· 0 citations
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