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Atherosclerosis II: Clinical Manifestations and Diagnostic Tests01:27

Atherosclerosis II: Clinical Manifestations and Diagnostic Tests

Atherosclerosis is a progressive disorder that leads to the thickening and narrowing of arterial walls due to plaque buildup. This condition can cause various symptoms depending on the arteries affected:Coronary Artery Disease (CAD): This condition affects the coronary arteries and may lead to chest pain (angina), shortness of breath (dyspnea), heart attacks, and other heart disease symptoms.Cerebrovascular Disease: This affects blood flow to the brain, causing transient ischemic attacks (TIAs)...

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Optical Coherence Tomography Based Biomechanical Fluid-Structure Interaction Analysis of Coronary Atherosclerosis Progression
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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.

Circulation Journal : Official Journal of the Japanese Circulation Society
|July 1, 2026
PubMed
Summary

Serial optical coherence tomography (OCT) reveals non-culprit lesions in acute coronary syndrome (ACS) patients can regress with lipid-lowering therapy. Plaque stabilization is crucial for high-risk individuals.

Keywords:
Acute coronary syndromeAtherosclerosisOptical coherence tomographyPlaque compositionPlaque evolution

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Area of Science:

  • Cardiology
  • Medical Imaging
  • Atherosclerosis Research

Background:

  • Acute coronary syndrome (ACS) patients face ongoing risks from non-culprit lesions.
  • Serial optical coherence tomography (OCT) is utilized to assess these lesions.

Purpose of the Study:

  • To explore metabolic profiles and morphological evolution of non-culprit lesions in ACS patients.
  • To investigate plaque vulnerability progression or regression using serial OCT.

Main Methods:

  • 406 ACS patients with 1,054 non-culprit lesions underwent OCT at baseline and 1-year follow-up.
  • Non-culprit plaques were classified as lipid-rich (thin/thick-cap fibroatheroma), fibrous, or calcified.
  • Patients were stratified into vulnerability progression, regression, or no-change groups.

Main Results:

  • Vulnerability progression occurred in 10 patients (11 lesions), primarily from thick-cap to thin-cap fibroatheroma (TCFA).
  • Vulnerability regression occurred in 96 patients (118 lesions), mainly from TCFA to thick-cap fibroatheroma.
  • Regression correlated with increased layered plaques, calcium deposition, and reduced lipids; progression associated with older age, diabetes, and hypertension.

Conclusions:

  • Serial OCT identified distinct non-culprit lesion changes linked to lipid-lowering therapy.
  • Intensive lipid-lowering is vital for high-risk ACS patients.
  • OCT provides objective plaque stabilization assessment.