Currently, approximately 40% of heart transplant recipients experience at least one acute rejection episode during the first year after heart transplantation (HTx), which is a life-threatening complication. Acute cardiac allograft rejection is associated with tissue edema and inflammatory cell infiltration. Still, invasive endomyocardial biopsy is the gold standard for diagnosis and grading of cardiac allograft rejection (1). Periodic rejection surveillance by endomyocardial biopsy is mandatory in all patients after HTx, as patients with cardiac allograft rejection are often primarily asymptomatic and early detection of cardiac allograft rejection is important to timely adjust immunosuppressive therapy and to prevent progression and irreversible damage of the allograft. The aim of our experimental study was to examine whether T2 mapping can detect tissue edema and inflammation associated with acute cardiac allograft rejection.Heterotopic allogenic HTx was performed in n=6 mice to induce acute cardiac allograft rejection (donor C57Bl/6; recipient Balb/c) (2). C57Bl/6 mice after isogenic HTx were used as reference group (n=6). Healthy donor mice and mice on day 1 and day 6 post HTx were investigated on a 7 Tesla MR system (Pharmascan, Bruker) using a 72-mm-diameter volume transmit coil in combination with a four-element mouse cardiac phased-array surface receive coil (Bruker). For T2 mapping of the heart a respiratory and ECG gated multi slice multi echo sequence with the following parameters was acquired: effective TR approximately 2000 ms; TE 11, 22, 33, 44, 55, 66, 77 ms; matrix 256 x 256; FOV 35 x 35 mm; slice thickness 1 mm. Parameter maps of myocardial T2 relaxation time reflecting tissue edema were calculated by a pixel wise mono-exponential fit (cvi42, Circle Cardiovascular Imaging Inc., Calgary, Canada). T2 maps were compared to histology. Student’s t-tests were used to compare MRI parameters between groups and time points. Values are given as mean±standard deviation.Myocardial T2 in healthy donors was not different (isogenic HTx 22.8±0.5 ms; allogenic HTx 23.1±0.6 ms). On day 1 post HTx myocardial T2 was significantly prolonged in both groups without significant difference potentially due to acute ischemia reperfusion injury (isogenic HTx 33.0±3.6 ms; allogenic HTx 33.2±3.1 ms). Until day 6 post HTx myocardial T2 further increased in allogenic, but not in isogenic cardiac grafts and was significantly increased in the allogenic group (42.9±5.5 ms vs. 31.9±2.5 ms; p<0.001). Correspondingly, the extent of myocardial T cell infiltration on day 6 post HTx was significantly higher in allogenic compared to isogenic HTx mice. T2 mapping allows the detection and quantification of myocardial edema due to acute cardiac allograft rejection and corresponds to the extent of T cell infiltration. Thus, T2 mapping might be suitable for non-invasive assessment and grading of acute cardiac allograft rejection.