Severe heart failure secondary to 5-fluorouracil and low-doses of folinic acid: Usefulness of an infra-aortic balloon pump

Objectives: To report 5-fluorouracil in combination with folinic acid as a cause of severe nonischemic heart failure and to demonstrate the potential usefulness of an intra-aortic balloon pump. Design: Case report. Setting: An adult, 19-bed medical/surgical intensive care unit of a univers ity hospital. Patients: A patient, who developed severe heart failure secondary to 5-fluo rouracil infusion with low-dose folinic acid, which was introduced to treat a rectal cancer, was transferred from a cancer institute to our intensive care unit 4 days after the treatment was initiated. Interventions: Electrocardiography, determination of level of cardiac enzym es, echocardiography, radial arterial catheterization, mechanical ventilato ry support, continuous venovenous hemodialysis, vasopressors, and secondary intra-aortic balloon pump. Measurement and Main Results: During shack, the patient's systolic blood pr essure progressively decreased to 70 mm Hg, despite inotropic agents and va sopressors. Transesophageal echocardiography showed a calculated left ventr icular ejection fraction within 20% with global hypokinesia, Electrocardiog raphy showed sinus tachycardia with only nonspecific ST-T changes. Results of serial determination of levels of cardiac enzymes were not significant f or myocardial infarction. Treatment with an intraaortic balloon pump was in itiated and resulted in a dramatical improvement within 48 hrs. The patient was gradually weaned from vasopressors and the intra-aortic balloon pump. By the tenth day, echocardiography showed a septoapical hypokinesia with a 50% left ventricular ejection fraction. On the 30th day, the echocardiograp hy was considered normal. Conclusion: Intravenous 5-fluorouracil in combination with low doses of fol inic acid can induce severe nonischemic heart failure. In such a case, an i ntra-aortic balloon pump could be useful by providing left ventricular func tion support when inotropic agents and vasopressors fail to restore normal hemodynamics.