B51-06 An R on T Nightmare: A Case of Difficult Ventricular Storm Management

Abstract Myocardial ischemia (MI) is a known etiology of polymorphic ventricular tachycardia (PVT) which can be triggered through the R on T phenomenon. We present a challenging case managing a 53-year-old male with persistent PVT post coronary intervention and refractory to multiple anti-arrhythmic medications.The patient presented to the hospital with worsening congestion and chest discomfort. Medical history included Jehovah’s Witness, diabetes, and hyperlipidemia. He was hemodynamically stable. Labs were significant for hs-Troponin 616 and proBNP 3720. Electrocardiogram showed Q waves in the inferior leads and poor R wave progression. A transthoracic echocardiogram showed severe left ventricular dysfunction with 20-25% ejection fraction and anterior, anteroseptal, and apical wall motion abnormalities. He was taken emergently for catheterization and had a severe proximal left anterior descending artery occlusion stented. Five days later nearing discharge, he had a cardiac arrest with initial rhythm showing PVT with resuscitation achieved after 2 defibrillations. He received intubation, magnesium, norepinephrine, and dopamine. Repeat emergent catheterization was unremarkable and amiodarone and lidocaine were initiated. Later that night, he had another PVT cardiac arrest requiring 9 shocks before resuscitation B, C, but telemetry and electrocardiogram showed no QT prolongation prior. Telemetry did exhibit frequent ectopic ventricular bigeminy with R on T likely the cause of the arrest A. He continued to have R on T induced PVT despite increasing anti-arrhythmic medications and decreasing pressors. However, ectopy burden and PVT events were significantly reduced with heart rates above 80 while on dopamine, making Torsades de Pointes (TdP) more likely. He had an Impella-CP placed to reduce tachyarrhythmia pressor effects, but later developed a left ventricular thrombus requiring anticoagulation. Patient was deemed high-risk for ablation given no administration of blood products. He was transferred to another hospital for second opinion, then to a hospital with a bloodless procedural program to be evaluated for heart transplant, but ultimately received an implantable defibrillator. TdP is a specific type of PVT with QT prolongation and is rarely seen post MI and intervention. This patient likely had TdP given overdrive pacing via dopamine. Amiodarone theoretically may have provoked the TdP events which emphasize the importance of identifying underlying tachyarrhythmias. QT shortening with magnesium is the main treatment for TdP. However, persistent TdP post MI necessitates ablation, if not overdrive pacing. If procedures are deemed high-risk (in this case - Jehovah’s Witness on anticoagulation), evaluation for heart transplantation is warranted. This abstract is funded by: None