Cardiovascular dysfunctions complicate 10-20% of pregnancies, increasing the risk for postpartum mortality. Various gestational insults, including preeclampsia are reported to be associated with adverse maternal cardiovascular outcomes. One such insult, gestational hyperandrogenism increases the risk for preeclampsia and other gestational morbidities but its impact on postpartum maternal health is not well known. We hypothesize that gestational hyperandrogenism such as testosterone (T) excess will adversely impact the maternal heart in the postpartum period. Pregnant ewes were injected with T propionate from day 30 to 90 of gestation (term 147 days). Three months postpartum, echocardiograms, plasma cytokine profiles, cardiac morphometric and molecular analysis were conducted (control (C) n=6, T-treated (T) n=7). Data were analyzed by two-tailed Student's t-test and Cohen's effect size (d) analysis. There was a non-significant large magnitude decrease in cardiac output (7.64±1.27 L/min vs. 10.19±1.40, p=0.22, d=0.81) and fractional shortening in the T ewes compared to C (35.83±2.33% vs. 41.50±2.84, p=0.15, d=0.89). T treatment significantly increased: 1) left ventricle (LV) weight to body weight ratio (2.82±0.14 g/kg vs. 2.46±0.08) and LV thickness (14.56±0.52 mm vs. 12.50±0.75), 2) pro-inflammatory marker (tumor necrosis factor-alpha (TNF-α) in LV (1.66±0.35 vs. 1.06±0.18), 3) LV collagen (Masson's Trichrome Stain: 3.38±0.35 vs. 1.49±0.15, and Picrosirius Red stain: 5.50±0.32 vs. 3.01±0.23) 4) markers of LV apoptosis, including TUNEL (8.3±1.1 vs. 0.9±0.18), Bax+/Bcl2+ ratio (0.68±0.30 vs. 0.13±0.02), and cleaved caspase 3 (15.4±1.7 vs. 4.4±0.38). These findings suggest that gestational testosterone excess adversely programs the maternal LV, leading to adverse structural and functional consequences in the postpartum period.