key: cord-0712895-5rre1kbn authors: Elsaid, Ossama; McCullough, Peter A.; Tecson, Kristen M.; Williams, Ryan S; Yoon, Anthony title: Ventricular Fibrillation Storm in Coronavirus 2019 date: 2020-08-29 journal: Am J Cardiol DOI: 10.1016/j.amjcard.2020.08.033 sha: bf7dfeaae2b2e505e829560d1a15c0a7ac7fa1e8 doc_id: 712895 cord_uid: 5rre1kbn Cardiac arrhythmia is a known manifestation of novel coronavirus 2019 (COVID-19) infection. Herein, we describe the clinical course of an otherwise healthy patient who experienced persistent ventricular tachycardia and fibrillation which is believed to be directly related to inflammation, as opposed to acute myocardial injury or medications that can prolong the QT interval. In addition to acute respiratory complications, coronavirus disease 2019 also causes significant consequences for the cardiovascular system, particularly arrhythmia. 1, 2 Due to the panoply of precipitating factors that can cause cardiac arrhythmia in COVID-19 patients, identifying the underlying culprit is crucial for proper management. Herein, we describe the course of a COVID-19 patient who experienced an electrical storm of ventricular fibrillation (VF). A 55-year-old woman with history significant for ischemic cerebral vascular infarction (6 years prior) presented with expressive aphasia and stroke-like symptoms. Computed tomography head scan ruled out acute cerebral stroke. Vital signs, laboratory data, and electrocardiogram are in Table 1 . Urine analysis was positive for bacteriuria. At screening, she tested positive for COVID-19. At that time she was not complaining of any constitutional or respiratory symptoms. She was admitted for cerebral vascular stroke workup and was started on intravenous ceftriaxone for urinary tract infection. Following admission, she became severely hypotensive and experienced worsening leukocytosis and renal function, causing concern for septic shock. Further laboratory workup revealed high interleuken 6 (16.4 pg/mL, upper limit normal = 1.8 pg/mL). She was transferred to the intensive care unit, where circulatory support and corticosteroids were initiated. She experienced sinus bradycardia with a heart rate of 40 beats per minute and was subsequently started on a dopamine infusion. Later that day, she went into cardiac arrest due to Torsades de Pointe (TdP) (Figure 1) . A 200 joules shock was delivered, the patient regained sinus rhythm, and was subsequently intubated; her QTc interval was 535ms. A lidocaine infusion and aggressive empiric magnesium supplementation were initiated. While receiving dopamine and lidocaine infusions, she remained bradycardic and experienced another VF and TdP cardiac arrest requiring defibrillation; transcutaneous pacing was started. Convalescent serum was administered as her inflammatory markers continued to rise along with worsening circulatory and respiratory failure. Despite dopamine, lidocaine, and transcutaneous pacing, she had multiple VF arrests requiring more than 60 defibrillator shocks. Her echocardiogram revealed normal left ventricular wall motion with normal function. Serial troponin levels were assessed, peaking at 0.064 ng/mL. At that point, the family signed comfort care only, the patient was extubated, and infusions stopped. Miraculously, she dramatically improved, with QTc improving from > 700 ms to 500 ms. The repeat echocardiogram did not reveal significant changes. The patient was never treated with hydroxychloroquine or azithromycin. She did not have any additional arrhythmias for the duration of her hospital stay. QTc interval returned to baseline. She had a full recovery and was discharged home on a life vest with plans for outpatient genetic tests for QTc prolongation. On a 4-week follow-up, her EKG showed normal QRS/QTC and she felt great without palpitations, syncope, or life vest shocks. One study reported ventricular tachycardia (VT)/VF in 5.9% (11/187) of COVID-19 patients (Table 2 3-9 ), with elevated troponin-T increasing risk, suggesting that myocardial injury precipitates arrhythmia 2 . However, VT/VF also occurs in patients with low troponin, suggesting alternative causes, such as QTc prolonging medication (e.g., hydroxychloroquine) 2 . Another possibility is the fulminant systemic inflammatory state in sick patients with cardiovascular morbidities and metabolic disarray. Inflammatory cardiac channelopathies, induced by inflammatory markers, can prolong the action potential and cause long QT syndrome and TdP 10, 11 . Moreover, systemic inflammation can increase risk for ventricular arrhythmia indirectly by inducing a hyper-sympathetic state or inhibiting cytochrome p450 11 . Other inflammatory responses, such as fever, can trigger undiagnosed conduction diseases or channelopathies, like Brugada syndrome 12 . Reducing this inflammatory state in COVID-19 patients can mitigate arrhythmic events, as well as other morbidity and mortality. Tocilizumab, an anti-interleuken 6 receptor monoclonal-antibody, yielded a survival benefit in COVID-19 patients [13] [14] [15] . Tocilizumab was shown to have a robust shortening of the QTc prolongation induced by abundant inflammatory cytokines in patients with acute rheumatoid arthritis 16 . Additionally, preliminary reports from ongoing trials indicate toclizumab may reduce adverse myocardial injury in acute inflammatory cardiac injury 2,13 . The initial hypothesis regarding our patient's VF storm etiology was acute myocarditis; however, with consistently normal troponins, the explanation is likely a constellation of factors, including hypokalemia, hypomagnesemia, bradycardia and long QTc, in the setting of hyperinflammation ( Figure 2 ). This hypothesis is supported by significantly elevated inflammatory markers. As such, this report suggests that the hyper-inflammatory state in COVID-19 patients can induce ventricular arrhythmias, which may cease abruptly following a reduction in inflammation, in our case from convalescent serum and/or hydrocortisone therapy. 17, 18 Hence, dampening this fulminant inflammatory condition may prevent or decrease cardiac arrhythmias. Table 2 . Articles describing arrhythmic events in patients with COVID-19 *The patient had prolonged QTc, heart failure with preserved ejection fraction, diabetes mellitus, and atrial fibrillation ** The patient was in Torsades de Pointe and on hydroxychloroquine + azithromycin *** The patient had heart failure with reduced ejection fraction and coronary artery disease Coronavirus Disease (COVID-19) Situation Reports Cardiovascular Considerations for Patients, Health Care Workers, and Health Systems During the Coronavirus Disease 2019 (COVID-19) Pandemic Cardiovascular Implications of Fatal Outcomes of Patients with Coronavirus Disease 2019 (COVID-19) Clinical Characteristics of Covid-19 in Cardiac Arrhythmias in COVID-19 Infection QT interval prolongation and torsade de pointes in patients with COVID-19 treated with hydroxychloroquine/azithromycin In-hospital cardiac arrest outcomes among patients with COVID-19 pneumonia in Wuhan COVID-19 and cardiac arrhythmias Ventricular tachycardia storm management in a COVID-19 patient: a case report Systemic inflammation and arrhythmic risk: lessons from rheumatoid arthritis Cardioimmunology of arrhythmias: the role of autoimmune and inflammatory cardiac channelopathies COVID-19 Infection Unmasking Brugada Syndrome A Recovered Case of COVID-19 Myocarditis and ARDS Treated with Corticosteroids, Tocilizumab, and Experimental AT-001 COVID-19, Arrhythmic Risk, and Inflammation: Mind the Gap! Effective treatment of severe COVID-19 patients with tocilizumab Antiarrhythmic potential of anticytokine therapy in rheumatoid arthritis: tocilizumab reduces corrected QT interval by controlling systemic inflammation Corticosteroids for critically ill COVID-19 patients with cytokine release syndrome: a limited case series Effects of corticosteroids on systemic inflammation in chronic obstructive pulmonary disease Foundation Disclosures: None