key: cord-0692731-ioxir7y5 authors: Mitacchione, Gianfranco; Schiavone, Marco; Gasperetti, Alessio; Forleo, Giovanni B title: Ventricular tachycardia storm management in a COVID-19 patient: a case report date: 2020-07-04 journal: Eur Heart J Case Rep DOI: 10.1093/ehjcr/ytaa217 sha: 9943159b300f7da16bde9f99fd79ef9680b396d9 doc_id: 692731 cord_uid: ioxir7y5 BACKGROUND: Coronavirus disease 2019 (COVID-19) has been associated with myocardial involvement. Among cardiovascular manifestations, cardiac arrhythmias seem to be fairly common, although no specifics are reported in the literature. An increased risk of malignant ventricular arrhythmias and electrical storm (ES) has to be considered. CASE SUMMARY: We describe a 68-year-old patient with a previous history of coronary artery disease and severe left ventricular systolic disfunction, who presented to our emergency department describing cough, dizziness, fever, and shortness of breath. She was diagnosed with COVID-19 pneumonia, confirmed after three nasopharyngeal swabs. Ventricular tachycardia (VT) storm with multiple implantable cardioverter defibrillator (ICD) shocks was the presenting manifestation of cardiac involvement during the COVID-19 clinical course. A substrate-based VT catheter ablation procedure was successfully accomplished using a remote navigation system. The patient recovered from COVID-19 and did not experience further ICD interventions. DISCUSSION: To date, COVID-19 pneumonia associated with a VT storm as the main manifestation of cardiac involvement has never been reported. This case highlights the role of COVID-19 in precipitating ventricular arrhythmias in patients with ischaemic cardiomyopathy who were previously stable. In December 2019, an outbreak of an emerging disease, named coronavirus disease , occurred in Wuhan, China, due to a novel coronavirus (later named severe acute respiratory syndrome coronavirus 2, SARS-CoV-2), 1 and was declared a global pandemic in early March 2020. The clinical course of SARS-CoV-2 infection is mostly characterized by respiratory tract involvement, potentially leading to pneumonia and SARS, but it has also been associated with myocardial involvement and with arrhythmic events in a nonnegligible number of patients. [1] [2] [3] [4] Therefore, an increased risk of malignant ventricular arrhythmias (VAs) and electrical storm (ES) has to be considered. While it is established that ES is more likely to occur in patients with severe left ventricular (LV) dysfunction and coronary artery disease (CAD), evident triggers cannot always be identified. 5, 6 Electrolyte imbalance (such as hypokalaemia), worsening heart failure, myocardial infarction (MI), adrenergic hyperactivity, hyperthyroidism, and sepsis have to be considered in the initial evaluation of patients with ES. [6] [7] [8] [9] [10] [11] To date, evidence linking SARS-CoV-2 infection and ventricular tachycardia (VT) storm are lacking. A 68-year-old Caucasian woman presented to our emergency department at the end of February 2020 with cough and dizziness for the past 20 days and persistent fever unresponsive to antipyretic drugs for the past 6 days, associated with worsening shortness of breath. Her past medical history included a prior inferolateral STsegment elevation myocardial infarction (STEMI) in 2014. Due to the persistence of severe left ventricular (LV) dysfunction [LV ejection fraction (EF) 34%], she was implanted with a single-chamber implantable cardioverter defibrillator (ICD) for primary prevention of sudden cardiac death 3 months later. Follow-up was uneventful and she never experienced ICD interventions. Her medical therapy on admission was metoprolol 100 mg b.i.d., ramipril 5 mg/day, spironolactone 25 mg/day, rosuvastatin 10 mg/day, cardioaspirin 100 mg/day, and rabeprazole 20 mg/day. Her cardiovascular examination was unremarkable, while lung auscultation revealed left basal crackles. A 12lead electrocardiogram (ECG) showed sinus rhythm with signs of inferior MI ( Figure 1 ). Laboratory tests were within the normal range, except for C-reactive protein (CRP) (27.6 mg/L, reference range <1.0 mg/L). Arterial blood gas analysis revealed oxygen partial pressure of 67 mmHg and oxygen saturation of 94%. Two real-time reverse transcription-polymerase chain reaction (RT-PCR) assays on nasopharyngeal swabs resulted negative for SARS-CoV-2. A chest radiograph demonstrated a consolidation in the left inferior lobe, suggestive for pneumonia (Figure 2A and B). Non-invasive ventilation and antibiotic therapy were started. During her hospital stay, the patient had multiple episodes of sustained VT treated with ICD shocks ( Figure 2C ). Device interrogation detected frequent VA episodes over the past 20 days, selfterminating or successfully interrupted with antitachycardia pacing (ATP). ES (12 VT episodes within 24 h) persisted despite intravenous infusion of beta-blockers (metoprolol), amiodarone, and deep (Figure 4) . At the end of the ablation procedure, non-inducibility of clinical VT by programmed ventricular stimulation was confirmed. During the subsequent hospital stay, continuous ECG monitoring did not show further VT events. Repeated blood test showed progressive CRP reduction, while the high-sensitivity troponin T level remained negative (5 ng/L, normal values <15.0 ng/L). Despite clinical improvement, a third nasopharyngeal swab resulted positive for SARS-CoV-2 and the patient was finally diagnosed with COVID-19 pneumonia. Another chest radiograph showed a near-complete resolution of pneumonia findings and she was discharged home to self-isolate with the addition of amiodarone 200 mg/day and apixaban 5 mg b.i.d. During the first 2 months after discharge, the patient remained asymptomatic, without further ICD interventions. The spectrum of COVID-19 clinical manifestations is highly variable, ranging from asymptomatic cases to SARS and cardiac involvement. [1] [2] [3] [4] It is known that patients with pre-existing cardiovascular disease have worse outcomes, 13, 14 and some authors have suggested that SARS-CoV-2 infection might be associated with myocardial involvement and eventually with life-threatening ventricular arrhythmias. 15 Palpitations were reported in 7.3% of patients admitted for COVID-19, 16 while cardiac arrhythmias were noted in 44.4% of severely ill hospitalized COVID-19 patients, 2 although no specific data regarding the type of arrhythmia were reported. To date, this kind of presentation with atypical pneumonia, later proved to be COVID-19 related, associated with concurrent VT storm as the presenting manifestation of cardiac involvement has never been reported. We considered that the patient was suffering from SARS-CoV-2 infection from admission, since RT-PCR on nasopharyngeal swabs is prone to have false-negative results, 17, 18 and cases of patients with suspected COVID-19 who 'turn positive' have been described. 19 However as stated by Xiao et al., 20 some patients may experience false-negative RT-PCR results or prolonged viral clearance despite clinical improvement or radiological resolution of pneumonia, rather than simply 'turning positive '. Despite the history of pre-existing CAD, the patient had never experienced sustained VAs as documented by ICD interrogations, suggesting the role played by SARS-CoV-2 infection as a potential arrhythmogenic trigger. This finding can be corroborated by the detection of mildly symptomatic sustained/non-sustained VT episodes from symptom onset, 20 days before admission. The mechanisms of cardiac arrhythmias in COVID-19 patients may be multifactorial and may have not yet been completely understood. A cytokine storm triggered by an imbalanced type 1 and type 2 T-helper cell activity 4 , as well as hypoxia-induced intracellular calcium overload leading to early afterdepolarization, may represent a major trigger of reentrant VT in these patients, 21,22 more than myocardial injury per se. According to European guidelines, catheter ablation is recommended (class I A) in patients with CAD and recurrent ICD shocks due to sustained VT. Since the patient was not in stable VT after metoprolol and amiodarone administration, we decided to perform an extensive substrate-based ablation targeting LAVA 23 which has been proven to be feasible, safe, and associated with superior survival free from recurrent VT. 24, 25 We used a remote magnetic navigation system since it has been thought to be superior to manual navigation for VT ablation (due to better contact force and stability), 26, 27 and in order to minimize unnecessary exposure of the electrophysiology laboratory staff to a likely COVID-19 patient. Great attention is paid to respiratory failure in COVID-19 patients, but the real prevalence of cardiovascular involvement in such patients may be underestimated. To our knowledge, this is the first report describing a VT storm that may have been triggered by SARS-CoV-2 infection, underlining the complexity of the COVID-19 clinical profile. This case highlights the role of cardiac electrophysiologists during the COVID-19 outbreak and might be helpful for the management of similar cases. Supplementary Material is available at European Heart Journal -Case Reports online. Slide sets: A fully edited slide set detailing this case and suitable for local presentation is available online as Supplementary data. Consent: the authors confirm that written consent for submission and publication of this case report, including images and associated text, has been obtained from the patient in line with COPE guidance. Conflict of interest: none declared. 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