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Introduction: Epicardial adipose tissue (EAT) exacerbates both electrical and structural remodeling in obese atrial fibrillation (AF) patients, but the impacts of EAT on atrial arrhythmogenicity remain unclear in normal‐weight AF patients. Therefore, we sought to investigate this issue using electroanatomic mapping. Methods and Results: We enrolled drug‐refractory 105 paroxysmal AF patients in the normal body mass index range (18.5–24.9 kg/m2), who had undergone electroanatomic mapping after pulmonary vein isolation (PVI). One day before PVI, we assessed P‐wave duration in a 12‐lead electrocardiogram and left atrial (LA)‐EAT volumes using contrast‐enhanced computed tomography. The patients were divided into two groups based on the median LA‐EAT volume (16.0 ml); the high LA‐EAT group (≥16.0 ml, n = 53) and low LA‐EAT group (<16.0 ml, n = 52). We compared P‐wave duration, LA conduction velocity and bipolar voltage, the presence of low‐voltage zone (<0.5 mV), and LA volume index on echocardiography between the two groups. The LA bipolar voltage, low‐voltage zone, and LA volume index were not different between the high and low LA‐EAT groups. However, P‐wave duration was significantly longer in the high group than in the low group (p <.001). Additionally, the LA conduction velocity was significantly more depressed in the high group than in the low group (p <.001). Multivariate linear regression analysis revealed that LA‐EAT volume was correlated with P‐wave duration (β =.367, p <.001) and conduction velocity (β = −.566, p <.001), respectively. Conclusions: Increased LA‐EAT volumes were associated with electrical conduction disturbance after PVI in normal‐weight patients with AF. P‐wave duration may be a clinically useful predictor of LA‐EAT. [ABSTRACT FROM AUTHOR]

Background: The clinical implications of chronic kidney disease (CKD) and cardiac sympathetic nervous activity (CSNA) regarding lethal arrhythmic events have not yet been fully elucidated in patients with chronic heart failure (CHF). We hypothesized that the combination of CKD and abnormal CSNA, assessed by 123I‐metaiodobenzylguanidine (123I‐MIBG) scintigraphy, may provide useful prognostic information for lethal arrhythmic events. Methods: We studied 165 consecutive hospitalized CHF patients without dialysis. Cardiac 123I‐MIBG scintigraphy was performed in a clinically stable condition, and abnormal CSNA was defined as a late heart‐to‐mediastinum ratio of <1.6. CKD was defined as an estimated glomerular filtration rate of <60 ml/min/1.73 m2. We then investigated the incidence of lethal arrhythmic events (sustained ventricular tachyarrhythmia, appropriate implantable cardioverter‐defibrillator therapy, or sudden cardiac death). Results: During a median follow‐up of 5.3 years, lethal arrhythmic events were observed in 40 patients (24.2%). The patients were divided into four groups according to the presence of CKD and CSNA abnormality: non‐CKD/normal CSNA (n = 52), CKD/normal CSNA (n = 39), non‐CKD/abnormal CSNA (n = 33), and CKD/abnormal CSNA (n = 41). Kaplan–Meier analysis showed that CKD/abnormal CSNA had the highest event rate (log‐rank p =.004). Additionally, the Cox proportional hazard analysis revealed that CKD/abnormal CSNA was a predictor for lethal arrhythmic events compared with non‐CKD/normal CSNA (hazard ratio, 5.368, p =.001). However, the other two groups did not show significant differences compared with the non‐CKD/normal CSNA group. Conclusions: The combination of CKD and abnormal CSNA, assessed by 123I‐MIBG scintigraphy, had a high predictive value for lethal arrhythmic events in patients with CHF. [ABSTRACT FROM AUTHOR]