Non-Culprit Lesion Plaque Vulnerability Progression and Regression Assessed by Serial Optical Coherence Tomography Imaging
Abstract
BACKGROUND: Acute coronary syndrome (ACS) patients remain at risk from non-culprit lesions. This study used serial optical coherence tomography (OCT) to explore metabolic profiles and morphological evolution (vulnerability progression or regression) of non-culprit lesions in ACS patients. METHODS AND RESULTS: This study included 406 ACS patients with 1,054 non-culprit lesions who underwent OCT at baseline and at the 1-year follow-up (median 368 days). Non-culprit plaques were classified as lipid rich (thin- [TCFA] or thick [ThCFA]-cap fibroatheroma [fibrous cap thickness <65 and ≥65 μm, respectively]), fibrous, or calcified. Patients were stratified into vulnerability progression (≥1 plaque progressing from non-TCFA to TCFA), regression (≥1 plaque regressing from TCFA to non-TCFA), or no-change groups. Vulnerability progression occurred in 10 patients (11 lesions), all from ThCFA to TCFA. Vulnerability regression occurred in 96 patients (118 lesions), mainly from TCFA to ThCFA (109 lesions). Patients with progression were older (mean age 64.4 vs. 53.1 years; P=0.005) and had higher rates of diabetes (80.0% vs. 34.4%; P<0.001) and hypertension (70.0% vs. 56.3%; P=0.046). Regression was accompanied by an increase in layered plaques (+17%) and calcium deposition (+9%), associated with greater reductions in low-density lipoprotein cholesterol, total cholesterol, and apolipoprotein B. Changes in lipid arc and fibrous cap thickness were positively correlated with on-treatment low-density lipoprotein cholesterol levels. CONCLUSIONS: Serial OCT identified divergent non-culprit lesion trajectories closely associated with lipid lowering. Intensive lipid-lowering therapy is critical for high-risk patients, and OCT enables objective evaluation of plaque stabilization.
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BibTeX
@article{zhang2026nonculprit,
title = {{Non-Culprit Lesion Plaque Vulnerability Progression and Regression Assessed by Serial Optical Coherence Tomography Imaging}},
author = {Dirui Zhang and Boling Yi and Luping He and Yishuo Xu and Chen Zhao and Ming Zeng and Yuhan Qin and Ziqian Weng and Ning Wang and Xue Feng and Lulu Li and Huai Yu and Yini Wang and Jingbo Hou and Gary S. Mintz and Sining Hu and Haibo Jia and Bo Yu},
journal = {Circulation Journal},
year = {2026},
month = jul,
doi = {10.1253/circj.cj-26-0255},
url = {https://www.jstage.jst.go.jp/article/circj/90/8/90_CJ-26-0255/_article},
note = {CC BY-NC-ND},
}
RIS
TY - JOUR
TI - Non-Culprit Lesion Plaque Vulnerability Progression and Regression Assessed by Serial Optical Coherence Tomography Imaging
AU - Dirui Zhang
AU - Boling Yi
AU - Luping He
AU - Yishuo Xu
AU - Chen Zhao
AU - Ming Zeng
AU - Yuhan Qin
AU - Ziqian Weng
AU - Ning Wang
AU - Xue Feng
AU - Lulu Li
AU - Huai Yu
AU - Yini Wang
AU - Jingbo Hou
AU - Gary S. Mintz
AU - Sining Hu
AU - Haibo Jia
AU - Bo Yu
PY - 2026
DA - 2026/07/24
JO - Circulation Journal
DO - 10.1253/circj.cj-26-0255
UR - https://www.jstage.jst.go.jp/article/circj/90/8/90_CJ-26-0255/_article
AB - BACKGROUND: Acute coronary syndrome (ACS) patients remain at risk from non-culprit lesions. This study used serial optical coherence tomography (OCT) to explore metabolic profiles and morphological evolution (vulnerability progression or regression) of non-culprit lesions in ACS patients. METHODS AND RESULTS: This study included 406 ACS patients with 1,054 non-culprit lesions who underwent OCT at baseline and at the 1-year follow-up (median 368 days). Non-culprit plaques were classified as lipid rich (thin- [TCFA] or thick [ThCFA]-cap fibroatheroma [fibrous cap thickness <65 and ≥65 μm, respectively]), fibrous, or calcified. Patients were stratified into vulnerability progression (≥1 plaque progressing from non-TCFA to TCFA), regression (≥1 plaque regressing from TCFA to non-TCFA), or no-change groups. Vulnerability progression occurred in 10 patients (11 lesions), all from ThCFA to TCFA. Vulnerability regression occurred in 96 patients (118 lesions), mainly from TCFA to ThCFA (109 lesions). Patients with progression were older (mean age 64.4 vs. 53.1 years; P=0.005) and had higher rates of diabetes (80.0% vs. 34.4%; P<0.001) and hypertension (70.0% vs. 56.3%; P=0.046). Regression was accompanied by an increase in layered plaques (+17%) and calcium deposition (+9%), associated with greater reductions in low-density lipoprotein cholesterol, total cholesterol, and apolipoprotein B. Changes in lipid arc and fibrous cap thickness were positively correlated with on-treatment low-density lipoprotein cholesterol levels. CONCLUSIONS: Serial OCT identified divergent non-culprit lesion trajectories closely associated with lipid lowering. Intensive lipid-lowering therapy is critical for high-risk patients, and OCT enables objective evaluation of plaque stabilization.
SN - 1347-4820
SN - 1346-9843
ER -