title: Impact of cardiac magnetic resonance on endothelial function in type 2 diabetic patients.
abstract: OBJECTIVE
  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.
  
  
  BACKGROUND
  https://register.clinicaltrials.gov/, Unique Identifier: NCT02001753.
authors.affiliation: Department of Endocrinology, Wuhan General Hospital of Guangzhou Command, Wuluo Road 627, Wuhan 430070, Hubei, China. Electronic address: Guangda64@hotmail.com.
authors.forename: Guangda
authors.initials: G
authors.lastname: Xiang
authors.affiliation: Department of Endocrinology, Wuhan General Hospital of Guangzhou Command, Wuluo Road 627, Wuhan 430070, Hubei, China. Electronic address: Xianglin832010@hotmail.com.
authors.forename: Lin
authors.initials: L
authors.lastname: Xiang
authors.affiliation: Department of Radiology, Wuhan General Hospital of Guangzhou Command, Wuluo Road 627, Wuhan 430070, Hubei, China. Electronic address: Wdrf2004@163.com.
authors.forename: Honglin
authors.initials: H
authors.lastname: He
authors.affiliation: Department of Endocrinology, Wuhan General Hospital of Guangzhou Command, Wuluo Road 627, Wuhan 430070, Hubei, China. Electronic address: Zhangjx666@gmail.com.
authors.forename: Junxia
authors.initials: J
authors.lastname: Zhang
authors.affiliation: Department of Endocrinology, Wuhan General Hospital of Guangzhou Command, Wuluo Road 627, Wuhan 430070, Hubei, China. Electronic address: dongjing86115@hotmail.com.
authors.forename: Jing
authors.initials: J
authors.lastname: Dong
mesh_terms: D000328:Adult; D000368:Aged; D001916:Brachial Artery / Q000000981:diagnostic imaging; D002097:C-Reactive Protein / Q000378:metabolism; D002681:China; D004249:DNA Damage; D003924:Diabetes Mellitus, Type 2 / Q000473:pathology*; D004730:Endothelium, Vascular / Q000473:pathology*; D005260:Female; D005609:Free Radicals / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000473:pathology*; D018384:Oxidative Stress; D016037:Single-Blind Method; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014463:Ultrasonography
chemical_list: D005609:Free Radicals; C508600:IL6 protein, human; D015850:Interleukin-6; C439524:TNF protein, human; D017392:Thiobarbituric Acid Reactive Substances; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein
keywords: Cardiac magnetic resonance; Endothelial function; Oxidative stress; Type 2 diabetes