Carotid atherosclerosis, changes in tissue remodeling and repair in patients with aortic coarctation.

Hlebowicz J, Holm J, Lindstedt S, Goncalves I, Nilsson J

Atherosclerosis 335 (-) 47-52 [2021-10-00; online 2021-09-21]

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. 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. 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). 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.

Affinity Proteomics Uppsala [Service]

PubMed 34564048

DOI 10.1016/j.atherosclerosis.2021.09.016

Crossref 10.1016/j.atherosclerosis.2021.09.016

pii: S0021-9150(21)01356-3 NCT03999073

Publications 8.1.1