A51-19 A Rare Case of Ventricular Fibrillation Cardiac Arrest From Abiraterone Induced Hypokalemia

Introduction Abiraterone is an antineoplastic commonly used to treat metastatic prostate cancer. As an irreversible 17 alpha hydroxylase inhibitor, it prevents the formation of testosterone precursors which is commonly found in prostatic tumor tissues, as well as the adrenals. Very rarely, abiraterone has been shown to prolong the qt interval as a result of hypokalemia, putting patients at risk for a potentially reversible cause of ventricular tachyarrhythmias and even sudden cardiac death. We present the case of a patient who developed Ventricular Fibrillation (V-fib) cardiac arrest secondary to severe hypokalemia with the use of abiraterone. Case Description An 83 year old male with a history of metastatic prostate adenocarcinoma and chronic anemia presented to the emergency department (ED) with progressive shortness of breath. He subsequently became unresponsive in the ED waiting room, where he was found to be in V-Fib. Resuscitation was initiated with the patient requiring defibrillation twice and administration of amiodarone, before receiving return of spontaneous circulation (ROSC). Initial workup was significant for diffuse ST depressions as well as hypokalemia of 3.2mmol/L and a mild troponin elevation. Patient was started on an amiodarone drip, loaded with aspirin and aggressively supplemented with potassium. His home abiraterone was also stopped. The next morning, patient was found to be in pulseless ventricular tachycardia (VTach) requiring a one-time dose of epinephrine, lidocaine and 5 minutes of CPR before achieving ROSC. Workup was still significant for a profound hypokalemia of 3.4mmol/L, and anemia requiring 1 unit of blood. A heparin drip was started, and patient was transferred to a tertiary center for further evaluation. After evaluation by the ICU team and electrophysiology, patient developed hypokalemia related qt prolongation, likely due to the use of abiraterone which likely triggered non-sustained polymorphic VTach. After adequate electrolyte supplementation, patient was weaned off amiodarone with no further episodes of ventricular arrhythmias and did not require further cardiology intervention. Discussion Severe anemia, even chronically, is a known trigger to compromise myocardial oxygen supply and increase arrhythmogenic potential, while hypokalemia can increase myocardial excitability and trigger ventricular arrhythmias. 17 alpha hydroxylase inhibitors will reduce androgen levels in the body, and in the process increase mineralocorticoid excess hypokalemia. Abiraterone should be used cautiously in patients at risk of anemia and electrolyte abnormalities as it can lower the threshold for malignant arrhythmia’s.