PO-04-103 WIDE COMPLEX TACHYCARDIA IN ACUTE ANTI-NMDA RECEPTOR ENCEPHALITIS

NA A 20-year-old male with no known past medical history presented two months of episodic right-sided weakness. An extensive workup was notable for a lumbar puncture that positive antibodies to the N-methyl-D-aspartate (NMDA) receptor, confirming anti-NMDA receptor (NMDAR) encephalitis. Baseline cardiac included transthoracic echocardiogram (TTE) showed left ventricular (LV) hypokinesis borderline ejection fraction (EF 52%), and an ECG showing sinus tachycardia (Figure-A). While admitted, patient developed shock, necessitating intubation vasopressors. Serial ECGs while in shock tachycardia, prolonged QTc, broad sail-like T wave V1 (similar type 1 Brugada pattern), ST elevations aVR diffuse depressions inferolaterally (Figure-B). troponins were minimally elevated (0.11 ug/L) TTE regional wall motion abnormalities, so invasive coronary angiography not pursued. During progressive wide complex (WCT, Figure-C), thought most likely be LV outflow tract tachycardia. The became hemodynamically unstable WCT, amiodarone, lidocaine, ultimately five cardioversions. Repeat severe biventricular dysfunction, needed veno-arterial extracorporeal membrane oxygenation (VA-ECMO). Ultimately, patient’s function recovered, he able decannulated from VA-ECMO. He managed intravenous immunoglobulin, steroids rituximab his anti-NMDAR Cardiac arrhythmias are complication encephalitis up one-third patients. To best our knowledge, this is first case anti-NDMAR associated suggestive ischemia. Models suggest NMDA receptor-mediated signaling nervous system can alter vagal heart, leading brady/tachycardia. Other explanations changes include focal myocarditis/vasospasm. This unusual marked elevation sustained VT Pathogenesis management related condition warrant further study.