Preeclampsia (PE) is a disorder prevalent in 3-8% of pregnancies, characterised by maternal hypertension and end organ damage. Factors released by the placenta play a central role in the pathogenesis of PE, but whether they mediate cardiac injury in this cohort has not been studied. PE women have decreased cardiac global longitudinal strain (GLS), a sensitive measure of systolic function that indicates fibrosis and tissue injury. GLS is worse in PE compared to gestational hypertension, despite comparable blood pressures between these two cohorts, suggesting that placental factors may be involved. We recently showed that Activin A, a pro-fibrotic factor released by the placenta is increased during PE and is predictive of impaired GLS one year postpartum. Thus, we hypothesised that chronic excess levels of Activin A during pregnancy induces cardiac dysfunction. Rats were administered vehicle (n=6) or Activin A (n=6/group; A1, 1.9µg/day, A2, 3 µg/day, A3, 6µg/day) via osmotic pump on gestational day (GD) 14. All animals had an indwelling carotid catheter placed on GD 18 that was attached to a pressure transducer for blood pressure measurement on GD19. Animals then underwent comprehensive echocardiography assessment and blood samples were collected. Circulating Activin A, as measured by ELISA, was significantly increased in all treated groups (Vehicle, 585±47 pg/mL, A1, 2022±695 pg/mL, A2, 2511±409 pg/mL, A3, 2801±410 pg/mL, P<0.01). Activin A infusion was associated with significantly reduced GLS (Vehicle, -22.1±0.8 %, A2, -16.7±1.87 %, P<0.01, A3, -14.7±1.14 %, P<0.01). These data align with our clinical findings and suggest that Activin A may mediate cardiac dysfunction in PE. Importantly, blood pressure was not different between groups, indicating that Activin A alone is capable of injury to the heart. Future studies will utilise this model to understand the mechanisms of Activin A and whether blockade of this factor improves outcomes for these women.