Cardiovascular disease (CVD) is the leading cause of death in the United States. Ischemic heart failure is caused by adverse remodeling of the infarct scar after a myocardial infarction (MI). CD8+ T‐cells facilitate in the remodeling process and influence scar formation highlighting the importance of these cell types post‐MI. Single cell data from our laboratory identified a particular subset of CD8+ T‐cells in the infarct at post‐MI day 5 that expressed innate marker Nk1.1 (innate‐like T‐cells or ILTs). In cancer, ILTs were found to become activated in response to IL12 and IL18, independent of antigen‐presentation. We hypothesized that ILTs in the heart would lead to poor cardiac wound healing and eventual development of heart failure. Paraffin embedded left ventricular tissue from male mice (n=8; 3.75±0.63 months of age) 7 days post‐MI were stained with antibodies CD3 (1:100, #NBP2‐12159), CD8 (1:100, #CLANT280), and Nk1.1 (1:150, #BS‐4682R). Confocal images (10 images/tissue region) were taken at 40X and ImagePro was used to determine colocalization and percent area of CD3+ CD8+ Nk1.1+ cells in the infarct and remote tissue. Images were separated and correlated with echocardiography measurements and infarct size (calculated by triphenyltetrazolium chloride staining). Results indicated that while not significant, fractional shortening (R2=0.398; p=0.093) positively correlated with increased ILTs in the infarct whereas, infarct size (R2=0.528; p=0.064) negatively correlated with increased ILTs. None of the other measurements showed any trend in regard to the number of ILTs (p‐values were greater than 0.214). This data suggests that at post‐MI day 7, ILTs are associated with improved fractional shortening and decreased cardiac injury. Further analysis of additional time points will give us a better understanding of the role ILTs have on the post‐MI remodeling process.