A FEBRILE CRISIS: MONOMORPHIC VENTRICULAR TACHYCARDIA IN A STRUCTURALLY INTACT HEART

ABSTRACT

SESSION TITLE Cardiovascular Complications in Patients with COVID-19 SESSION TYPE Rapid Fire Case Reports PRESENTED ON 10/19/2022 1245 pm - 145 pm INTRODUCTION: COVID-19 infection has been shown to exhibit an array of deleterious cardiac effects specifically arrhythmias. While arrhythmias of ventricular origin are less common, direct insult to the myocardium is cited as the most common etiology [1]. Here we present a unique case of hyperthermia induced monomorphic ventricular tachycardia (VT) in the setting of COVID-19 infection. CASE PRESENTATION A 65-year-old male with medical history of dyslipidemia and hypertension presented with cough, dyspnea and subsequently diagnosed with COVID-19 pneumonia and was noted to be persistently febrile with a peak temperature of 40.1° C, which coincided with the onset of sustained monomorphic VT for approximately 40 minutes. He was treated with amiodarone. He did not have chest pain and troponin levels were normal. Cooling measures were initiated in the ICU. While normothermic, he did not have episodes of VT until the following day when his temperature again peaked at 40.6° C. A lidocaine drip was started to maintain sinus rhythm. However, due to multi-system organ failure, the family decided to proceed with comfort care. DISCUSSION: COVID-19 infection associated with fatal VT has been documented in the literature mainly attributed to ischemia and myocarditis. [1,2]. COVID-19 virus has the potential to trigger a massive inflammatory response causing systemic illness. Classically, the prototypical patient has a scar from previous ischemic heart disease that allows reentry to occur. Our patient had no prior history of structural heart disease, evidence of acute coronary syndrome or myocarditis. Other known causes of VT were ruled out. It became clear that the patient’s induction of VT had a temporal association with hyperthermia. Once the patient’s temperature was above 40° C, VT would ensue and only terminate with resolution of the fever. Temperature has been shown to affect the transmembrane gradient and the flow velocity of ions through myocardial ion gated channels [3]. These physiological changes could lead to increased automaticity or triggered events that induce VT. Therefore, hyperthermia should not be neglected as a potential trigger for VT in an otherwise intact myocardium. CONCLUSIONS: A systemic illness like COVID-19 associated with cytokine storm can drastically influence the thermal regulation of the body. This can cause a shift in the transmembrane gradient and resting membrane potential, which could in turn alter automaticity. Therefore, hyperthermia could be a possible trigger for monomorphic VT in an otherwise intact myocardium. Early recognition and rapid external cooling are crucial to minimize the risk of ventricular dysrhythmias. Reference #1 Manolis, Antonis S et al. "COVID-19 infection and cardiac arrhythmias.” Trends in cardiovascular medicine vol. 30,8 (2020) 451-460. doi10.1016/j.tcm.2020.08.002 Reference #2 Bhatla, A., Mayer, M., Adusumalli, S., Hyman, M., Oh, E., Tierney, A., Moss, J., Chahal, A., Anesi, G., Denduluri, S., Domenico, C., Arkles, J., Abella, B., Bullinga, J., Callans, D., Dixit, S., Epstein, A., Frankel, D., Garcia, F., Kumareswaram, R., Nazarian, S., Riley, M., Santangeli, P., Schaller, R., Supple, G., Lin, D., Marchlinski, F. and Deo, R., 2020. COVID-19 and cardiac arrhythmias. Heart Rhythm, 17(9), pp.1439-1444. Reference #3 Huckell, V F et al. "Cardiac Manifestations Of Malignant Hyperthermia Susceptibility.". Circulation, vol 58, no. 5, 1978, pp. 916-925. Ovid Technologies (Wolters Kluwer Health), doi10.1161/01.cir.58.5.916. Accessed 1 June 2021. DISCLOSURES No relevant relationships by Robert Cacdac No relevant relationships by Nami Moradi