Impact of cardiac magnetic resonance on endothelial function in type 2 diabetic patients

- CMR scanning can reversibly impair endothelial function.
- The intervention with CMR significantly increase the levels of oxidative stress and inflammation markers reversibly.
- The changes of endothelial function during CMR strongly depended on the magnitude of oxidative stress and inflammation.

Objectives Recent studies have shown that cardiac magnetic resonance (CMR) scanning is associated with cellular DNA damage. The aim of the present study was to assess the impact of CMR scanning on endothelial function in Chinese men with type 2 diabetes. Methods A randomized, single-blind, parallel-group study was conducted in 60 Chinese men with type 2 diabetes treated with or without CMR (CMR and sham CMR group), and the changes of endothelial function before and after CMR were compared. High-resolution ultrasound was used to measure flow-mediated endothelium-dilation (FMD) of the brachial artery. Results The FMD in CMR group at Day 1 after CMR was 3.60%, which was significantly lower than that (3.85%) in sham CMR group (p < 0.001). The levels of C-reactive protein (CRP), thiobarbituric acid-reactive substances (TBARS), tumor necrosis factor alpha (TNF-α) and interleukin-6(IL-6) in CMR group were significantly higher than those in sham CMR group at Day 1 (p < 0.001). But these characteristics did not differ between two groups at baseline, Day 2 and Day 3 (p > 0.05). Linear correlation and multiple regression analyses showed that CRP, TBARS, TNF-α and IL-6 were associated with FMD in the CMR group (p < 0.01). Conclusions The present data showed that CMR scanning can reversibly suppress endothelial function, probably through the increased production of oxygen-derived free radicals and inflammatory reactions in Chinese men with type 2 diabetes, indicating that CMR should be used with caution in order to avoid unnecessary damage to the endothelium. Clinical Trial Registration URL: https://register.clinicaltrials.gov/, Unique Identifier: NCT02001753.