Human coronavirus-associated myocarditis is known, and a number of coronavirus disease 19 (COVID-19)-related myocarditis cases have been reported. The pathophysiology of COVID-19-related myocarditis is thought to be a combination of direct viral injury and cardiac damage due to the host's immune response. COVID-19 myocarditis diagnosis should be guided by insights from previous coronavirus and other myocarditis experience. The clinical findings include changes in electrocardiogram and cardiac biomarkers, and impaired cardiac function. When cardiac magnetic resonance imaging is not feasible, cardiac computed tomographic angiography with delayed myocardial imaging may serve to exclude significant coronary artery disease and identify myocardial inflammatory patterns. Because many COVID-19 patients have cardiovascular comorbidities, myocardial infarction should be considered. If the diagnosis remains uncertain, an endomyocardial biopsy may help identify active cardiac infection through viral genome amplification and possibly refine the treatment risks of systemic immunosuppression. Arrhythmias are not uncommon in COVID-19 patients, but the pathophysiology is still speculative. Nevertheless, clinicians should be vigilant to provide prompt monitoring and treatment. The longterm impact of COVID-19 myocarditis, including the majority of mild cases, remains unknown.

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.

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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.