Assessment Of Cardiac Inflammation And Injury Following Prolonged Exercise Using Cardiovascular Magnetic Resonance (CMR) Imaging

Abstract

PURPOSE: Myocardial inflammation may be a potential mechanism for the release of troponin and NTproBNP following a Marathon. CMR has not been previously used to detect and quantify myocardial inflammation and fibrosis pre- and post-Marathon. METHODS: CMR was performed in 18 athletes 24hrs pre and 6 hours post a Marathon run. Each scan was performed on a 1.5T Siemens Avanto scanner using a 4 channel body array coil. Myocardial structure and function was assessed using breath hold SSFP cine imaging in long and short axis views. The presence of myocardial inflammation and oedema was assessed using STIR imaging and a 3-4 minute spin echo sequence immediately post 0.1mmol intravenous gadolinium-DTPA to assess relative gadolinium enhancement. Inversion recovery segmented-FLASH imaging with TI adjusted to null normal myocardium to highlight regions of fibrosis was used to image delayed enhancement. Each participant had bloods drawn for TnI, NT-proBNP, and CRP at baseline, immediately post and 6 hours after the run. Each CMR scan was analyzed for wall thickness per segment, volumes and function, myocardial oedema. Delayed enhancement images were analysed using Medis software. RESULTS: Biventricular volumes, stroke volume, ejection fraction, and mass were unchanged pre and 6 hrs post marathon. The majority of subjects were found to have a rise in BTproBNP levels immediately and 6 hours after the race as well as elevations in TnI above the level of cut off for myocardial infarction (P=0.001). There were no focal regions of visual signal increase on the STIR images in any of the 18 subjects. Global myocardial oedema was predefined using a cut off ratio of 1.9 comparing SI of myocardium to skeletal muscle on STIR imaging, and a relative 45% increase in the SI myocardium/skeletal muscle immediately post intravenous gadolinium on relative gadolinium enhancement imaging (rGE). No subject reached these cut off values. None had any visual myocardial fibrosis on late enhancement imaging or using automated software. CONCLUSIONS: Serum markers of myocardial cell damage post ultra endurance exercise are not associated with CMR detectable levels of myocardial oedema, inflammation or scarring, suggesting lower degrees of myocardial damage than in patients with acute myocardial infarction, inspite of similar levels of troponin elevation.