Diagnostic tests in hospital failed to disclose the cause of her bleeding tendency. Yet another skin biopsy specimen showed only subepidermal hemosiderin, with extravasated RBCs, lymphocytes, and some fibrosis, but no signs of vasculitis. Indicative of iron deficiency and/or subacute blood loss, serum iron level was 5.4 μM (reference range, 9-34 μM), transferrin saturation 10% (reference range, 17%-52%), and transferrin receptor concentration, 7.0 mg/L (reference range, 1.9-4.4 mg/L). A bone marrow aspirate showed reduced but not totally absent stainable iron. The patient was given 5 units of packed RBCs altogether and treatment with oral iron was started later. Because of a vague clinical suspicion of vasculitis, treatment with oral prednisone was initiated. Within a few days, the patient became increasingly dyspneic and the oxygen saturation dropped from 99% to 77% to 80% on ambient air. Echocardiography (Fig 1, Table 1, Videos 1-3) showed a dilated and poorly contracting right ventricle, tricuspid regurgitation with a peak jet velocity of 3.5 m/s, an eccentrically deformed left ventricle, pericardial effusion, and flow from right to left atrium through open foramen ovale. Pulmonary CT scan angiography revealed dilatation of the pulmonary artery but no signs of pulmonary embolism. A confirmatory ventilation-perfusion lung scan was also normal. Right-sided heart catheterization, with the patient breathing room air, revealed severe precapillary pulmonary hypertension, right ventricular failure, and a large right-to-left shunt (Table 1). A nonformal vasodilatory test was done by infusing epoprostenol at doses of 1 and 5 ng/kg/min. At baseline, with the patient now breathing oxygen, pulmonary artery pressure measured 84/39 mm Hg (mean, 52 mm Hg), and finger oxygen saturation was 82%. At 5 ng/kg/min of epoprostenol, pulmonary artery pressure dropped to 53/36 mm Hg (mean, 42 mm Hg), and oxygen saturation rose to 95%. The response was interpreted as suggestive of pulmonary vasodilation unloading the right side of the heart and leading to less shunt flow through the foramen ovale.