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.

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.

Background— Catheter ablation (CA) of ventricular tachycardia (VT) in patients with nonischemic dilated cardiomyopathy can be challenging because of the complexity of underlying substrates. We sought to determine the long-term outcomes of endocardial and adjuvant epicardial CA in nonischemic dilated cardiomyopathy. Methods and Results— We examined 282 consecutive patients (aged 59±15 years, 80% males) with nonischemic dilated cardiomyopathy who underwent CA. Ablation was guided by activation/entrainment mapping for tolerated VT and pacemapping/targeting of abnormal electrograms for unmappable VT. Adjuvant epicardial ablation was performed for recurrent VT or persistent inducibility after endocardial–only ablation. Epicardial ablation was performed in 90 (32%) patients. Before ablation, patients failed a median of 2 antiarrhythmic drugs), including amiodarone, in 166 (59%) patients. The median follow-up after the last procedure was 48 (19–67) months. Overall, VT-free survival was 69% at 60-month follow-up. Transplant-free survival was 76% and 68% at 60- and 120-month follow-up, respectively. Among the 58 (21%) patients with VT recurrence, CA still resulted in a significant reduction of VT burden, with 31 (53%) patients having only isolated (1–3) VT episodes in 12 (4–35) months after the procedure. At the last follow-up, 128 (45%) patients were only on β-blockers or no treatment, 41 (15%) were on sotalol or class I antiarrhythmic drugs, and 62 (22%) were on amiodarone. Conclusions— In patients with nonischemic dilated cardiomyopathy and VT, endocardial and adjuvant epicardial CA is effective in achieving long-term VT freedom in 69% of cases, with a substantial improvement in VT burden in many of the remaining patients.

CRT is highly efficacious in reversing PICM, with 72% of severe PICM patients achieving LVEF >35% and most of the improvement occurring within 1 year. These data support initial upgrade to a CRT pacemaker with consideration of further upgrade to CRT defibrillator after 1 year if LVEF remains ≤35%.

Withholding ACEIs and ARBs 24 h before coronary angiography does not appear to influence the incidence of CIN in stable patients with CKD stages 3-4.

Background: Mitral valve prolapse (MVP) is a common valve condition and has been associated with sudden cardiac death. Premature ventricular contractions (PVCs) from the papillary muscles (PMs) may play a role as triggers for ventricular fibrillation (VF) in these patients.Objectives: To characterize the electrophysiological substrate and outcomes of catheter ablation in patients with MVP and PM PVCs.Methods: Of 597 patients undergoing ablation of ventricular arrhythmias during the period 2012-2015, we identified 25 patients with MVP and PVCs mapped to the PMs (64% female). PVC-triggered VF was the presentation in 4 patients and a fifth patient died suddenly during follow-up. The left ventricle ejection fraction (LVEF) was 50.5% ± 11.8% and PVC burden was 24.4% ± 13.1%. A cardiac magnetic resonance imaging was performed in nine cases and areas of late gadolinium enhancement were found in four of them. A detailed LV voltage map was performed in 11 patients, three of which exhibited bipolar voltage abnormalities. Complete PVC elimination was achieved in 19 (76%) patients and a significant reduction in PVC burden was observed in two (8%). In patients in which the ablation was successful, the PVC burden decreased from 20.4% ± 10.8% to 6.3% ± 9.5% (P = 0.001). In 5/6 patients with depressed LVEF and successful ablation, the LV function improved postablation. No significant differences were identified between patients with and without VF.Conclusions: PM PVCs are a source of VF in patients with MVP and can induce PVC-mediated cardiomyopathy that reverses after PVC suppression. Catheter ablation is highly successful with more than 80% PVC elimination or burden reduction.

Background-Catheter ablation (CA) of ventricular tachycardia (VT) in patients with cardiac sarcoidosis can be challenging because of the complex underlying substrate. We sought to determine the long-term outcome of CA of VT in patients with cardiac sarcoidosis. Methods and Results-We enrolled 31 patients (age, 55±10 years) with diagnosis of cardiac sarcoidosis based on Heart Rhythm Society criteria and VT who underwent CA. In 23 (74%) patients, preprocedure cardiac magnetic resonance imaging and positron emission tomographic (PET) evaluation were performed. Preprocedure magnetic resonance imaging was positive for late gadolinium enhancement in 21 of 23 (91%) patients, whereas abnormal 18-fluorodeoxyglucose uptake was found in 15 of 23 (65%) cases. In 14 of 15 patients with positive PET at baseline, PET was repeated after 6.1±3.7-month follow-up. After a median follow-up of 2.5 (range, 0-10.5) years, 1 (3%) patient died and 4 (13%) underwent heart transplant. Overall VT-free survival was 55% at 2-year follow-up. Among the 16 (52%) patients with VT recurrences, CA resulted in a significant reduction of VT burden, with 8 (50%) having only isolated (1-3) VT episodes and only 1 patient with recurrent VT storm. The presence of late gadolinium enhancement at magnetic resonance imaging, a positive PET at baseline, and lack of PET improvement over follow-up were associated with increased risk of recurrent VT. Conclusions-In patients with cardiac sarcoidosis and VT, CA is effective in achieving long-term freedom from VT or improvement in VT burden in the majority of patients. The presence of late gadolinium enhancement at magnetic resonance imaging, a positive PET scan at baseline, or lack of improvement at repeat PET over follow-up predict worse arrhythmia-free survival. (Circ Arrhythm Electrophysiol. 2016;9:e004333.

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