Dams lacking NKG2A show insufficient spiral artery remodelling, abnormal utero-placental blood flow, fetal growth restriction with impaired brain development (Immunity. 54(6):1231-1244, 2021).  Here, we tested the hypothesis that an NKG2A-deficient uterine microenvironment may programme an increased cardiovascular risk in the adult offspring. We compared offspring generated from B6 mothers x NKG2A KO fathers (Control, C) and from NKG2A mothers x B6 KO fathers (NKG2A KO, KO).  This experimental design permitted direct comparison between genetically matched offspring developing in either NKG2A-sufficient or NKG2A-deficient wombs. In addition, this strategy isolated the effects of the maternal from the offspring genotype because the progeny were heterozygous in both groups. At 4 months of adulthood, offspring’s hearts (C, n=10 and KO, n=13) were isolated to determine cardiac function via a Langendorff preparation. Data (mean±SEM) were compared with the Student’s t test for unpaired data. Significance was accepted when P<0.05. Relative to C, offspring from KO which display growth restriction at birth showed increased body weight at adulthood (29.3+0.6 vs. 31.5+0.7 g, P<0.05), indicating catch up postnatal growth. Relative to C, hearts of KO offspring were heavier (0.14±0.01 vs. 0.16±0.01 g), they showed similar left ventricular (LV) developed pressure but elevated LV end diastolic pressure (10.8±2.5 vs. 13.9±2.2 mmHg, P<0.05) and lower values for peak rate of relaxation dP/dt_min (-915.1±106.9 vs. -1072.0±137.1, P<0.05), indicating significant diastolic dysfunction. The data support the hypothesis that NKG2A regulates the uterine microenvironment, and its absence leads to cardiac dysfunction in mice adult offspring.  Therefore, NK cells not only influence successful pregnancy, but they also have a role in modulating lifelong cardiovascular health in the offspring.