Use of Extracorporeal Membrane Oxygenation for Mechanical Circulatory Support in a Patient With 5-Fluorouracil Induced Acute Heart Failure

Abstract

Extracorporeal life support has evolved to become a viable support option in patients with acute cardiac failure. Tailored mechanical circulatory support (MCS) can now be provided to patients using existing extracorporeal life support devices. 1 We report the successful use of peripheral venoarterial extracorporeal membrane oxygenation (ECMO) to provide MCS to a patient with acute 5-flurouracil (5-FU)-induced cardiomyopathy. 5-FU is a key component of adjuvant chemotherapy for colorectal cancer. It is also frequently used in the treatment of gastric, esophageal, pancreatic, breast, bladder, and prostate cancer. There is a wide range of cardiotoxicity with this 5-FU, including ischemia, vasospasm, arrhythmia, hypertension, Q-T interval prolongation, and acute cardiomyopathy and 5-FU-induced cardiac complications are not rare.2 This case illustrates the crucial place of ECMO as a bridge to recovery in chemotherapy, cardiomyopathy, or decision making. Case ReportA 32-year-old man began adjuvant treatment for colorectal adenocarcinoma with 5-FU continuous infusion after presumed curative bowel resection. He experienced stuttering chest pain from day 1 of therapy with progressive shortness of breath. His risk factors for cardiovascular disease included a positive family history of ischemic heart disease and previous methamphetamine use. He presented to the emergency department in a peripheral hospital on completion of his first cycle, where he was noted to be in paroxysmal atrial fibrillation with rapid ventricular response alternating with sinus tachycardia with inferolateral ST elevation. Cardiac troponin was mildly elevated and a presumptive diagnosis of 5-FU-induced cardiotoxicity was made. Sublingual glyceryl trinitrate, oral atenolol, and amlodipine were administered. After this, the patient became hypotensive, with cool and clammy peripheries. He was commenced on dobutamine and noradrenaline infusions and transferred to our center.Urgent cardiac catheterization confirmed angiographically normal coronary arteries (Figure 1). His left ventricular enddiastolic pressure was elevated at 30 mm Hg. An intra-aortic balloon pump was inserted through the left femoral artery. Transthoracic echocardiogram revealed severe global dysfunction with an ejection fraction of 10% to 15% with normal valves and no pericardial effusion. There was no evidence of significant dilation or thinning of ventricular chambers, thus inferring an acute and potentially reversible process (Figure 2).The patient was transferred to the intensive care unit with severe cardiogenic shock despite intra-aortic balloon counterpulsation and high doses of dobutamine (10 μg/kg per minute), noradrenaline (0.25 μg/kg per minute), and adrenaline (0.25 μg/kg per minute). There was evidence of end-organ malperfusion with increasing lactate, altered mentation, and early hepatic and renal dysfunction. In the face of impending circulatory collapse, peripheral venoarterial ECMO was instituted as a bridge to recovery. He was deemed unsuitable for cardiac transplanta...

Cardiotoxicity of Fluoropyrimidines: Epidemiology, Mechanisms, Diagnosis, and Management

“…Further investigation is required, and other substances are also being investigated [143]. Rateesh et al (2015) reported the successful use of peripheral venoarterial extracorporeal membrane oxygenation (ECMO) in a patient with acute 5-fluorouracil-induced cardiomyopathy. Together with medical therapy for heart failure, almost complete recovery of cardiac function was possible.…”

“…The authors emphasized that early use of ECMO for hemodynamic stabilization enables myocardial recovery after improving initial stunning. An aggressive strategy, including mechanical support, has been associated with improved survival compared with conservative treatment [144]. In 2017, Sundaravel et al reported the first case of FOLFOX-induced Takotsubo cardiomyopathy treated with an Impella device.…”

Cardiac Toxicity of Cancer Chemotherapy

“…32 CHF, myocarditis, and ventricular arrhythmias have also been reported, suggesting a direct myocardial toxicity. [33][34][35] Although cardiotoxicity is typically reversible on withdrawal of the offending agent, sudden death has been reported in the setting of fluoropyrimidine use. 36 Proposed mechanisms of coronary vasospasm include protein kinase C-mediated vasoconstriction, 37 impaired handling of reactive oxygen species, 38 and direct endothelial toxicity.…”

Rechallenge capecitabine after fluoropyrimidine-induced cardiotoxicity in rectal cancer

“…Severe heart failure due to 5-FU-induced cardiotoxicity has also been reported. [6] The likely mechanisms of fluoropyrimidine-induced cardiotoxicity include coronary vasospasm and direct cytotoxicity. When 5-FU-induced cardiotoxicity occurs, discontinuation of 5-FU usually relieves symptoms within hours.…”