IJCS | Volume 32, Nº1, January/ February 2019

DOI: 10.5935/2359-4802.20180078 87 CASE REPORT International Journal of Cardiovascular Sciences. 2019;32(1)87-90 Mailing Address: Juan Simon Rico University of Texas Health Science Center at San Antonio - UT Health San Antonio - 7703 Floyd Curl Dr, Postal Code: 78229, San Antonio, TX - USA. E-mail: mesa.juan@mayo.edu Acute Heart Failure Exacerbation in the Setting of Electrical Storm: Total Artificial Heart vs. Ventricle Assist Device Juan Simon Rico, 1 Daniela Arango-Isaza, 2 M egha Prasad, 1 Clara Saldarriaga 3 Mayo Clinic - Rochester, 1 Minnesota - EUA Universidad CES, 2 Antioquia - Colombia Universidad Pontificia Bolivariana, 3 Antioquia - Colombia Manuscript received September 12, 2017; revised manuscript February 18, 2018; accepted March 27, 2018. DilatedCardiomyopathy; Heart Failure; Defibrillators, Implantable; Cardiac Resynchronization Therapy; Arrhythmias Cardiac. Keywords Introduction Total artificial heart (TAH) is a novel device with over a thousand implantations worldwide, being a suitable option for patients as a bridge to transplantation (BTT). 1 The following case was the second implantation of a TAH at our institution. Case report We report the case of a 64-year-old Caucasian male with past medical history of idiopathic dilated cardiomyopathy, reduced left ventricular ejection fraction (LVEF of 16%) reported during his last acute decompensation in 2012, sinus bradycardia with biventricular implantable cardioverter defibrillator (ICD) placement for secondary prevention of sudden cardiac death, in 2015, and atrial fibrillation. The patient was brought to the emergency department complaining of severe dyspnea and palpitations, preceded by multiple electrical shocking episodes (46 episodes). At admission, his electrocardiogram (ECG) showed a ventricular tachycardia (VT). He was monitored on telemetry, which evidenced a monomorphic VT with a mean heart rate of 188 beats per minute (bpm). The electrophysiology team was consulted; the device was interrogated and confirmed the above-mentioned number of shocks. Initial treatment with Lidocaine 2 mcg/kg/hr and Amiodarone 150 mg IV bolus achieved rate control. Initial laboratory testing showed hemoglobin of 16.2, WBC 12.1, platelets 186, Na 139, K 4.8, Cl 104, Cr 1.8 (GFR 38), BUN 36, glucose 169, AST 39, ALT 42, ALP 140, Ca 9.4, albumin 4.4. INR 4.2, digoxin 2.2. The patient was transferred to the Coronary Care Unit (CCU), where physical examination revealed normal temperature, blood pressure of 94/65 mmHg, and heart rate of 91 bpm. His cardiovascular and lung exam was unremarkable. Chest X-ray showed small bilateral pleural effusions. Transthoracic Echocardiography showed markedly enlarged LVwith severely decreased function (EF of 10-15%), severely generalized left ventricular hypokinesis, severely decreased right ventricular systolic function, right ventricular systolic pressure (RVSP) of 41 mmHg, right-to-left shunt at atrial level. At that point, no inotropic support was necessary. The initial diagnosis was refractory VT (VT storm at presentation) in the setting of secondary acute systolic heart failure. Serial ECG strips were obtained, as shown in Figure 1. Unfortunately, his systolic blood pressure substantially decreased down to 60 mmHg, so he was placed on invasive monitoring, with a cardiac index of 1.81 L/min/m 2 , estimated right atrial pressure (RAP) of 16 mmHg and mean pulmonary arterial pressure of 36 mmHg. At that point, cardiogenic shock required hemodynamic support therapies. Electrophysiology staff attempted VT ablation, which showed possible endocardial and epicardial substrate. Consequently, EP performed epicardial VT ablation, with subsequent endocardial VT ablation, after an additional endocardial arrhythmic source was found during the procedure. Unfortunately, ablation was unsuccessful in controlling heart rhythm and his LVEF kept declining, this time to a LVEF of 5%.