Abstract 14751: A Rare Presentation of 5-Fluorouracil-Induced Cardiotoxicity

Abstract

Background: 5-fluorouracil (5-FU) is associated with numerous cardiotoxic effects, most commonly chest pain and acute coronary syndrome. Less common effects include arrhythmias, myocarditis, pericarditis, and heart failure. We present a rare case of 5-FU causing cardiogenic shock. Case: A 54-year-old man with metastatic esophageal adenocarcinoma presented at 3:50 with chest pain that began the day before at 16:00, shortly after starting a 5-FU pump. Electrocardiogram (EKG) showed normal sinus rhythm with no ST or T wave changes. High sensitivity troponin T was 18 ng/L, followed by 24 ng/L at 1 hour and 81 ng/L at 6 hours. Computed tomography angiography (CTA) ruled out pulmonary embolism. Transthoracic echocardiogram (TTE) showed a globally reduced left ventricular ejection fraction (LVEF) of 35-40%. The patient received metoprolol and was scheduled for coronary CTA to investigate for coronary disease. Over the next few hours, he continued to report chest pain. Repeat troponin at 18:12 was 235 ng/L. Repeat EKG showed new anterior ST depressions. Posterior EKG did not show ST elevations. Repeat TTE revealed LVEF of 15%. The patient underwent left and right heart catheterization at 21:14, which showed normal coronary arteries, pulmonary artery pressure 50/31 mmHg (mean 38 mmHg), pulmonary capillary wedge pressure 36 mmHg, and cardiac index 1.1 L/min/m 2 . An Impella device was placed for circulatory support. He was treated with vasopressors and milrinone. Given concern for 5-FU toxicity, he received the antidote uridine triacetate 10 g IV every 6 hours for 5 days. LVEF improved to 70%. He was treated with nifedipine for possible coronary vasospasm. He was discharged 8 days later with heart failure medications. Conclusion: The incidence of cardiotoxicity from 5-FU ranges from 1.2-18%. Mechanistic theories include coronary vasospasm and direct cellular injury. Symptoms usually present within 12 hours of initiation but may present up to 2 days later. Management includes stopping the offending agent and starting anti-anginal drugs and uridine triacetate. Uridine triacetate is deacetylated to uridine, which prevents cell damage and death via competitive inhibition of 5-FU.