CD 73, an ecto-enzyme catalysing the extracellular degradation from AMP to adenosine is present on immune cells, particularly T-cells and adenosine is well known for its potent anti-inflammatory action. We therefore explored whether CD73-derived adenosine plays a role in cardiac remodeling after ischemia/reperfusion (I/R). CD73^-/- and WT C57Bl/6 mice (n=4 each) underwent 50 min of coronary ligation with subsequent reperfusion. Functional and contrast enhanced MRI (DRX 9.4 T NMR) was done at baseline, 3, 7 and 14 days after I/R for functional analysis, measurement of infarct size (enhanced/non-enhanced myocardial signal intensity) and T2 times. Cardiac immune cell infiltration was measured by flow cytometry (BD FACS Canto II) at indicated time points in parallel experiments. One day after I/R infarct size was comparable between CD73^-/- (29.3 ± 5.3 %) and WT animals (32.9 ± 8.2 %). However, 14 days after I/R, CD73^-/- mice showed a significant (p<0.01) lower ejection fraction (CD 73^-/- 41.0 ± 3.7 %; WT 61.1 ± 2.9 %) and a significant (p<0.05) rise in myocardial area with increased T2 time (51.3 ± 3.8 % vs. 27.7 ± 9.1 %). FACS analysis at day 14 after I/R revealed that hearts from CD 73^-/- mice contained more T-cells and a higher percentage of ly6c^high monocytes as compared to WT controls. In summary, CD73-derived adenosine promotes cardiac healing and recovery of ventricular performance after I/R, most likely by acting on T-cells. Thus, adenosine appears to be an important modulator of cardiac healing.