Introduction The relationship between insulin resistance and atrial fibrillation (AF) recurrence after pulmonary vein isolation (PVI) remains unclear. Methods Drug‐refractory 114 paroxysmal AF patients (89 males, 62 ± 8 years) who underwent successful PVI were enrolled. Homeostasis model assessment of insulin resistance (HOMA‐IR) was calculated and a value of ≥2.5 was defined as insulin resistant. The left atrial volume index (LAVI) was measured using echocardiography before and 1 year after PVI. Tumor necrosis factor‐α (TNF‐α) and TGF‐β1 serum levels were measured before PVI, and the left atrium (LA) conduction velocity was calculated. The patients were divided into two groups (group 1: HOMA‐IR < 2.5, n = 81; group 2: HOMA‐IR ≥ 2.5, n = 33). Results The LAVI between the two groups before PVI did not significantly differ (P > 0.05), nor did TNF‐α (7.7 ± 2.0 vs 7.5 ± 1.0 pg/mL; P = 0.149) or TGF‐β1 (28.4 ± 12.0 vs 27.6 ± 10.3 ng/mL; P = 0.757). LAVI before and 1 year after PVI in each group did not change. The conduction velocity of group 2 was slower than that of group 1 (0.7 ± 0.1 vs 1.1 ± 0.3 m/s, P < 0.001). Kaplan‐Meier analysis showed significantly higher AF recurrence in group 2 than that in group 1 ( P = 0.019). Cox multivariable analysis revealed that insulin resistance was an independent predictor of recurrence (hazard ratio 1.287, P = 0.004). Conclusion Our results suggest that insulin resistance promotes LA electrical remodeling and might be related to AF recurrence after PVI.

Background Additional benefit of cryoballoon left atrial roof line ablation (CB‐RA) beyond cryoballoon pulmonary vein isolation (CB‐PVI) is suggested in patients with persistent atrial fibrillation (PsAF). We sought to investigate the feasibility of CB‐RA for PsAF and to determine the ablation area. Methods and Results Fifty‐three PsAF patients (67[58.5–75.5] years, 36 men, 11 longstanding PsAF) underwent CB‐PVI. Subsequently, 44(83.0%) out of 53 patients underwent additional CB‐RA. Voltage maps were created in all patients with a high‐resolution mapping system. The total number and duration of CB‐RAs were 3.9 ± 0.7 and 468 ± 84 s. LA roof areas were complete low voltage areas (LVAs) /scar in 37/44(84.1%) patients (“complete roof modification”). The normal LA posterior wall (LAPW) voltage area was 6.1(4.1–8.4) cm2, and the %LAPW isolation area was 61.0(47.2–71.7)%. The %LAPW isolation area was significantly greater in CB‐RA patients than those without (64.0[54.2–73.2] vs. 45.0[39.5–50.5]%, p = .041) despite significantly larger LAs in the former group. The %LAPW isolation area was significantly greater in patients with transverse LA diameters < 45 mm than those ≥ 45 mm (p < .0001). The single procedure 1‐year AF freedom was 87.4% (22.5% on antiarrhythmic drug) and tended to be higher in CB‐RA patients than those without. Among the 44 CB‐RA patients, it was significantly higher in patients with a complete roof modification than those without (94.4% vs. 75.0%, p = .0049). One CB‐RA patient experienced a delayed cardiac tamponade requiring drainage at 4‐months post‐procedure. Conclusions CB‐RA significantly expanded the LAPW isolation area, and a complete roof modification resulted in a high arrhythmia freedom in PsAF patients.

HTN induced heterogeneous LA hypertrophy regardless of whether HTN was controlled. Uncontrolled BP promoted atrial remodeling, and is therefore a strong predictor for recurrence of AF after PVI.

The anatomical proximities of the LA posterior wall, LIPV, and descending Ao surrounding the oesophagus are strongly associated with the prevalence of TTI.

Ventricular arrhythmias play a critical role in chronic heart failure (CHF) and are associated with adverse clinical outcomes. Sleep-disordered breathing (SDB) is associated with arrhythmias and/or a poor prognosis in CHF. Adaptive servo-ventilation (ASV) is a ventilatory support system designed to normalize ventilation in CHF patients with SDB. However, the effects of ASV on ventricular arrhythmias and sympathetic nervous activity are still unclear. Nineteen CHF patients with SDB were examined. We performed simultaneous overnight polysomnography and 24-h Holter ECG monitoring, and measured levels of daily urinary catecholamines for two consecutive days (baseline and on ASV). ASV significantly improved the apnea-hypopnea index (p < 0.01), arousal index (p < 0.01), and mean SpO(2) (p < 0.01), and decreased daily urinary catecholamines (0.466-0.353 mg/day, p = 0.016) compared to baseline. Furthermore, power in the low to high frequency range as a marker of sympathetic nervous activity decreased across a 24-h period (24-h period: 2.8-1.9, p = 0.017; during daytime: 3.7-2.3, p = 0.013; and during sleep time: 1.5-1.3, p = 0.026). Importantly, ASV significantly decreased ventricular premature complexes not only during sleep time but also across a 24-h period (40.5-21.9 beats/h, p = 0.013). The short-term use of ASV reduced ventricular arrhythmias with the attenuation of sympathetic nervous activity, as demonstrated by urinary catecholamines and heart rate variability. ASV may have anti-sympathetic nervous and anti-arrhythmic effects for CHF with SDB.