The proposed pathogenesis of PPCM includes viral vasculitis,[9] endothelial dysfunction,[10] selenium deficiency,[11] increased levels of prolactin,[12] oxidative stresses from the vascular hormone soluble fms-like tyrosine kinase receptor 1,[13] autoimmune response,[14,15] or genetic predisposition.[16,17] Previous studies have shown advanced age, black race, pre-eclampsia, hypertension, multiple gestations, anemia, and prolonged tocolysis to be risk factors for PPCM.[18] Long-term use of tocolytic agents may contribute to cardiovascular dysfunction. Here, PRL is linked to selenium deficiency.