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

Abstract

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 university hospital.

Patients: A patient, who developed severe heart failure secondary to 5-fluorouracil 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 enzymes, echocardiography, radial arterial catheterization, mechanical ventilatory support, continuous venovenous hemodialysis, vasopressors, and secondary intra-aortic balloon pump.

Measurement and main results: During shock, the patient's systolic blood pressure progressively decreased to 70 mm Hg, despite inotropic agents and vasopressors. Transesophageal echocardiography showed a calculated left ventricular ejection fraction within 20% with global hypokinesia. Electrocardiography showed sinus tachycardia with only nonspecific ST-T changes. Results of serial determination of levels of cardiac enzymes were not significant for myocardial infarction. Treatment with an intraaortic balloon pump was initiated 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 echocardiography was considered normal.

Conclusion: Intravenous 5-fluorouracil in combination with low doses of folinic acid can induce severe nonischemic heart failure. In such a case, an intra-aortic balloon pump could be useful by providing left ventricular function support when inotropic agents and vasopressors fail to restore normal hemodynamics.