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.

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R adiofrequency catheter ablation (RFCA) has an established therapeutic role in managing recurrent drug-refractory scar-related ventricular tachycardia (VT). 1 Owing to the complex substrate, concomitant heart failure, and associated comorbidities, patients undergoing catheter ablation of scarrelated VT experience significant morbidity and mortality rates. 2,3 In these patients, use of anesthesia, sustained hypotension as a result of spontaneous or induced VT, and fluid overload might contribute to periprocedural acute hemodynamic decompensation (AHD) requiring advanced hemodynamic support or procedure discontinuation. 4,5 Thus far, no data are available on the prevalence, predictors, and clinical significance of periprocedural AHD during catheter ablation of scarrelated VT. The proper identification of patients at high risk of periprocedural AHD would also have important implications for procedural planning because it would allow anticipation of the need for mechanical hemodynamic support. In this study, we evaluated the incidence and clinical predictors of periprocedural AHD during RFCA of scar-related VT and assessed its effect on mortality. MethodsThe study cohort consisted of consecutive patients who underwent RFCA of scar-related VT in the setting of ischemic or nonischemic cardiomyopathy at the Hospital of the University of Pennsylvania between January 2010 and December 2011. Patients with idiopathic VT and those with congenital heart disease were excluded. Whenever possible, antiarrhythmic drugs were discontinued for ≥4 half-lives before the procedure. Patients who were on chronic therapy with β-blockers or inhibitors of the renin-angiotensin-aldosterone system routinely held the medications the morning of the procedure (last dose administered the night before). Before the procedure, all patients © 2014 American Heart Association, Inc. P=0.004). At 21±7 months follow-up, the mortality rate was higher in the AHD group compared with the rest of the population (50% versus 11%, log-rank P<0.001). Conclusions-AHD occurs in 11% of patients undergoing radiofrequency catheter ablation of scar-related VT and is associated with increased risk of mortality over follow-up. AHD may be predicted by clinical factors, including advanced age, ischemic cardiomyopathy, more severe heart failure status (New York Heart Association class III/IV, lower ejection fraction), associated comorbidities (diabetes mellitus and chronic obstructive pulmonary disease), presentation with VT storm, and use of general anesthesia. (Circ Arrhythm Electrophysiol. 2015;8:68-75.

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Background-Radiofrequency ablation of multiple or unmappable ventricular tachycardias (VTs) remains a challenge with unclear end points. We present our experience with a new strategy isolating core elements of VT circuits. Methods and Results-Patients with structural heart disease presenting for VT radiofrequency ablation at 2 centers were included. Strategy involved entrainment/activation mapping if VT was hemodynamically stable, and voltage mapping with electrogram analysis and pacemapping. Core isolation (CI) was performed incorporating putative isthmus and early exit site(s) based on standard criteria. If VT was noninducible, the dense scar (<0.5 mV) region was isolated. Successful CI was defined by exit block (20 mA at 2 ms) within the isolated region. VT inducibility was also assessed. Forty-four patients were included (mean age, 63; 95% male; 73% ischemic cardiomyopathy; mean left ventricular ejection fraction, 31%; 68% with multiple unstable VTs [mean, 3+2]). CI area was 11+12 versus 55+40 cm 2 total scar area. Additional substrate modification was performed in 27 (61%), and epicardial radiofrequency ablation was performed in 4 (9%) patients. CI was achieved in 37 (84%) and led to better VT-free survival (log rank P=0.013). Conclusions-CI is a novel strategy with a discrete and measurable end point beyond VT inducibility to treat patients with multiple or unmappable VTs. The CI region can be selected based on standard characterization of suspected VT isthmus surrogates thus limiting ablation target size. Exit block within the isolated area is achievable in most and may further improve long-term success. (Circ Arrhythm Electrophysiol. 2015;8:353-361.