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Carotid atherosclerosis, changes in tissue remodeling and repair in patients with aortic coarctation
Joanna Hlebowicz1, Johan Holm1, Sandra Lindstedt2
1Department of Cardiology, Skåne University Hospital, Lund University, Lund, Sweden.
Insights
Aortic coarctation repair does not fully prevent cardiovascular complications. Patients show increased carotid atherosclerosis, indicating persistent vascular issues despite treatment.
Area of Science:
- Cardiovascular Medicine
- Vascular Biology
- Medical Imaging
Background:
- Aortic coarctation (CoA) repair is associated with ongoing cardiovascular complications.
- Understanding post-repair vascular changes is crucial for patient management.
Purpose of the Study:
- To assess cardiovascular markers, specifically intima-media thickness (IMT) and plaque presence, in patients after CoA repair compared to controls.
- To investigate potential differences in biomarkers related to inflammation, tissue remodeling, and repair between groups.
Main Methods:
- Ultrasound assessment of carotid arteries in 64 patients post-CoA repair and 64 controls.
- Analysis of circulating biomarkers using a multiplex platform to evaluate inflammation and tissue repair markers.
Main Results:
- Significantly increased carotid bulb and common carotid artery (CCA) IMT in both men and women with CoA compared to controls.
- Men with CoA had a higher likelihood of carotid artery plaque.
- Distinct alterations in specific biomarkers were observed: lower stem cell factor (SCF) in women with CoA, and lower matrix metalloproteinase-3 (MMP-3), tumor necrosis factor receptor 1 (TNF-R1), TRAIL-R2, and monocyte chemotactic protein 1 (MCP-1) in men with CoA.
Conclusions:
- Successful CoA repair does not eliminate carotid atherosclerosis.
- Patients exhibit increased atherosclerosis beyond what is explained by tissue remodeling and repair markers.
- This study highlights persistent vascular abnormalities post-CoA repair.
Background And Aims:
After aortic coarctation (CoA) repair, patients still suffer from cardiovascular complications. The aim of this study was to measure cardiovascular markers, intima-media thickness (IMT) and plaques in controls and patients with CoA.
Methods:
Sixty-four patients with CoA (66% male, mean age 48 ± 15 years) and controls (54% men, mean age 47 ± 16 years) underwent ultrasound of their arteries. A multiplex platform to analyze circulating blood levels biomarkers reflecting inflammation, tissue remodeling and repair was used.
Results:
In men following CoA repair, a significantly increased carotid bulb IMT was observed in comparison to the control group (1.05 [0.72-1.24] vs. 0.67 [0.59-0.95] mm; p = 0.003). Median common carotid artery (CCA) IMT was increased in men compared to controls (0.82 [0.61-0.97] mm vs. 0.58 [0.53-0.76] mm, p < 0.003) and in women compared to controls (0.83 [0.70-0.92] vs. 0.60 [0.55-0.69], p < 0.004). CoA demonstrated an independent association with IMT in both men and women. Men with CoA were also more likely to have a plaque in their carotid arteries (p = 0.010). In women with CoA, we observed significantly lower levels of stem cell factor (SCF, p = 0.004) while in men with CoA we observed significantly lower levels of matrix metalloproteinase-3 (MMP-3, p = 0.048), tumor necrosis factor receptor 1 (TNF-R1, p = 0.032), tumor necrosis factor receptor superfamily member 10B (TRAIL-R2, p = 0.019) and monocyte chemotactic protein 1 (MCP-1, p = 0.015).
Conclusions:
This is the first study to show that despite successful CoA repair, patients have more carotid atherosclerosis than can be explained by changes in tissue remodeling and repair.
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