A 26-year-old woman developed severe postpartum cardiomyopathy in early puerperium. Ligation of the inferior vena cava prevented recurrent pulmonary embolism but did not affect her hemodynamic condition, which deteriorated constantly. During continuous hemodynamic monitoring only vigorous volume replacement with an increase of the left ventricular filling pressure to 32 mm Hg improved cardiac output significantly. The presence of a high titer of antiactin antibodies 9 months after the delivery supports the theory that the Peripartum cardiomyopathy was of autoimmune etiology.
