BACKGROUND Early studies suggest that coronavirus disease 2019 (COVID-19) is associated with a high incidence of cardiac arrhythmias. Severe acute respiratory syndrome coronavirus 2 infection may cause injury to cardiac myocytes and increase arrhythmia risk.OBJECTIVES The purpose of this study was to evaluate the risk of cardiac arrest and arrhythmias including incident atrial fibrillation (AF), bradyarrhythmias, and nonsustained ventricular tachycardia (NSVT) in a large urban population hospitalized for COVID-19. We also evaluated correlations between the presence of these arrhythmias and mortality.METHODS We reviewed the characteristics of all patients with COVID-19 admitted to our center over a 9-week period. Throughout hospitalization, we evaluated the incidence of cardiac arrests, arrhythmias, and inpatient mortality. We also used logistic regression to evaluate age, sex, race, body mass index, prevalent cardiovascular disease, diabetes, hypertension, chronic kidney disease, and intensive care unit (ICU) status as potential risk factors for each arrhythmia.RESULTS Among 700 patients (mean age 50 6 18 years; 45% men; 71% African American; 11% received ICU care), there were 9 cardiac arrests, 25 incident AF events, 9 clinically significant bradyarrhythmias, and 10 NSVTs. All cardiac arrests occurred in patients admitted to the ICU. In addition, admission to the ICU was associated with incident AF (odds ratio [OR] 4.68; 95% confidence interval [CI] 1.66-13.18) and NSVT (OR 8.92; 95% CI 1.73-46.06) after multivariable adjustment. Also, age and incident AF (OR 1.05; 95% CI 1.02-1.09) and prevalent heart failure and bradyarrhythmias (OR 9.75; 95% CI 1.95-48.65) were independently associated. Only cardiac arrests were associated with acute in-hospital mortality.CONCLUSION Cardiac arrests and arrhythmias are likely the consequence of systemic illness and not solely the direct effects of COVID-19 infection.

Background-Efficacy of endocardial ventricular tachycardia (VT) ablation in arrhythmogenic right ventricular cardiomyopathy/dysplasia may be limited by epicardial VT, right ventricular thickening, or both. We sought to characterize the endocardial versus epicardial substrate, measure right ventricular free wall thickness, and determine epicardial ablation efficacy in patients with right ventricular cardiomyopathy/dysplasia. Methods and Results-Thirteen consecutive patients (3 female; aged 43Ϯ15 years; range, 17 to 70 years) undergoing endocardial and epicardial sinus rhythm voltage mapping and epicardial VT ablation after failed endocardial VT ablation were included. In each patient, the low bipolar voltage area (Ͻ1.0 mV for epicardium and Ͻ1.5 mV for endocardium) was more extensive on the epicardium (95Ϯ47 versus 38Ϯ32 cm 2 ; PϽ0.001) and was uniformly marked by multicomponent and late electrograms. The basal right ventricular thickness assessed by electroanatomic map was Ͼ10 mm in 6 of 13 patients compared with 5 to 10 mm in 4 reference patients without structural disease. Twenty-seven VTs were targeted on the epicardium with the use of activation, entrainment, or pace mapping with focal/linear ablation and targeting of late potentials. Epicardial VTs were targeted opposite normal endocardium in 10 patients (77%) and/or opposite ineffective endocardial ablation sites in 11 patients (85%). During 18Ϯ13 months, 10 of the 13 patients (77%) had no VT, with 2 patients having only a single VT at 2 and 38 months, respectively. Conclusions-Patients

Background-Patients with nonischemic left ventricular cardiomyopathy (LVCM) and ventricular tachycardia (VT) havecomplex 3-dimensional substrate with variable involvement of the endocardium (ENDO) and epicardium (EPI). The purpose of this study was to determine whether ENDO unipolar (UNI) mapping with a larger electric field of view could identify EPI low bipolar (BIP) voltage regions in patients with LVCM undergoing VT ablation. Methods and Results-The reference value for normal ENDO unipolar voltage was determined from 6 patients without structural heart disease. Consecutive patients undergoing VT ablation over an 8-year period with detailed (Ͼ100 points) LV ENDO and EPI mapping and normal LV ENDO BIP voltage were identified. From this cohort, we compared patients with structurally normal hearts and normal EPI BIP voltage (EPIϪ, group 1) with patients with LVCM and low LV EPI BIP voltage regions present (EPIϩ, group 2). Confluent regions of ENDO UNI and EPI BIP low voltage (Ͼ2 cm 2 ) were measured. The normal signal amplitude was Ͼ8.27 mV for LV ENDO UNI electrograms. Detailed LV ENDO-EPI maps in 5 EPIϪ patients were compared with 11 EPIϩ patients. Confluent ENDO UNI low-voltage regions were seen in 9 of 11 (82%) of the EPIϩ (group 2) patients compared with none of 5 EPIϪ (group 1) patients (PϽ0.001). In all 9 patients with ENDO UNI low voltage, the ENDO UNI low-voltage regions were directly opposite to an area of EPI BIP low voltage (61% ENDO UNI-EPI BIP low-voltage area overlap). Conclusions-EPI arrhythmia substrate can be reliably identified in most patients with LVCM using ENDO UNI voltage mapping in the absence of ENDO BIP abnormalities. (Circ Arrhythm Electrophysiol. 2011;4:49-55.)

In patients with NICM and VT of epicardial origin, the substrate is characterized by areas of basal LV epicardial > endocardial bipolar low voltage. The electrograms in these areas are not only small (<1.0 mV) but wide (>80 ms), split, and/or late, and help identify the substrate targeted for successful ablation.