Related Experiment Video
Updated: Jun 21, 2025
Optical Coherence Tomography Based Biomechanical Fluid-Structure Interaction Analysis of Coronary Atherosclerosis Progression
Published on: January 15, 2022
Mechanisms of Medial Wall Thinning in Chronic Total Occlusion
Takao Konishi1, Rika Kawakami2, Aimee E Vozenilek2
1Department of Cardiovascular Pathology, CVPath Institute, Gaithersburg, Maryland, USA; Department of Cardiovascular Medicine, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Insights
Coronary artery medial wall thinning is observed in chronic total occlusion (CTO) lesions, impacting percutaneous coronary intervention (PCI) success. This thinning may be linked to inflammation and apoptosis in CTO development.
Area of Science:
- Cardiovascular Research
- Interventional Cardiology
- Histopathology
Background:
- Percutaneous coronary intervention (PCI) for chronic total occlusion (CTO) presents lower success rates and higher complication risks compared to non-CTO PCI.
- While intimal plaque characteristics are a focus, the coronary medial layer's role in CTO PCI, particularly for dissection and re-entry techniques, remains poorly understood.
Purpose of the Study:
- To investigate coronary medial wall thinning in CTO lesions.
- To determine the potential impact of medial thinning on CTO PCI outcomes.
Main Methods:
- Analysis of 2,586 arterial sections from 54 subjects with CTO and 54 controls without CTO, matched for demographic and anthropometric factors.
- Comparison of medial thickness between CTO lesions and non-CTO lesions, as well as within CTO lesions based on luminal narrowing.
- Immunohistochemical analysis of CTO lesions to assess inflammation and apoptosis markers (caspase-3, CD3+, CD4+, CD8+, CD4+CD28null T cells).
Main Results:
- CTO lesions exhibited significantly thinner medial walls compared to non-CTO lesions (P < 0.001).
- Within CTO lesions, areas with thinner medial walls correlated with greater luminal narrowing (P < 0.001).
- Short-duration CTO showed increased cleaved caspase-3 and T cell infiltration (CD3+, CD4+, CD8+, CD4+CD28null) compared to long-duration CTO.
Conclusions:
- Coronary medial thinning is a characteristic feature of CTO lesions compared to non-CTO lesions.
- Inflammation and apoptosis may play a role in the development of coronary medial wall thinning in CTO.
- Further mechanistic studies are needed to elucidate the cause-and-effect relationship between inflammation, apoptosis, and medial thinning in CTO.
Background:
The success rate of percutaneous coronary intervention (PCI) for chronic total occlusion (CTO) is lower and the risk for complications higher compared with other non-CTO PCI. Although interventionalists focus on intimal plaque characteristics, the coronary media is an important (especially for techniques involving antegrade dissection and re-entry) but poorly understood structure in CTO PCI.
Objectives:
The aim of the present study was to investigate coronary medial wall thinning in CTO lesions and determine how this thinning might affect CTO PCI.
Methods:
A total of 2,586 sections were investigated, from arteries with evidence of CTO from 54 subjects (1,383 sections) and arteries without evidence of CTO from 54 subjects with non-coronary-related deaths (1,203 sections) after matching for age, gender, body weight, and body height.
Results:
The medial thickness in subjects with CTO was lower than that in those with non-coronary-related death (P < 0.001). In subjects with CTO, CTO lesions had thinner medial walls compared with those with lower luminal narrowing (P < 0.001). At the CTO distal segments, the 6- to 12-mm distal segment from the distal end of the CTO had significantly less luminal narrowing (P < 0.001), and similar medial thickness, compared with the distal end of the CTO. Immunohistochemical analysis revealed that short-duration CTO had more cleaved caspase-3-positive cells in media and had significantly more CD3+, CD4+, CD8+, and CD4+CD28null T cells compared with long-duration CTO.
Conclusions:
CTO lesions demonstrated coronary medial thinning compared with non-CTO lesions. Further investigation of the cause-and-effect relationship among inflammation, apoptosis, and coronary medial wall thinning is warranted in future mechanistic studies.
