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Updated: Jul 3, 2026
Optical Coherence Tomography Based Biomechanical Fluid-Structure Interaction Analysis of Coronary Atherosclerosis Progression
Published on: January 15, 2022
Non-Culprit Lesion Plaque Vulnerability Progression and Regression Assessed by Serial Optical Coherence Tomography
Dirui Zhang1, Boling Yi1, Luping He1,2
1State Key Laboratory of Frigid Zone Cardiovascular Diseases (SKLFZCD), Key Laboratory of Myocardial Ischemia, Chinese Ministry of Education, Department of Cardiology of the Second Affiliated Hospital, Harbin Medical University.
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.
