Our finding that markers of collagen turnover were elevated in patients who experienced AF recurrence after ablation indicate that these markers might be a useful guide to identify a subgroup of AF patients who require extensive ablation strategies. A 2-month postablation elevation in collagen turnover markers suggests that the wound healing process persists for that long after ablation.

Background— Although increased epicardial adipose tissue (EAT) volume is known to be associated with increased prevalence of atrial fibrillation (AF), the exact mechanisms are unclear. Therefore, we investigated whether EAT locations were associated with high dominant frequency (DF) sites or complicated fractionated atrial electrogram sites during AF. Methods and Results— Three-dimensional reconstruction computed tomography images depicting EAT volumes (obtained by 320-detector-row multislice computed tomography) were merged with NavX-based DF and complicated fractionated atrial electrogram maps obtained during AF for 16 patients with paroxysmal AF and for 18 patients with persistent AF. Agreement between locations of the EAT, especially EAT surrounding the left atrium, and of high DF or complicated fractionated atrial electrogram sites was quantified. In addition, serum biomarker levels were determined. EAT surrounding the left atrium volumes was significantly greater in patients with persistent AF than in patients with paroxysmal AF (52.9 cm 3 [95% CI, 44.2–61.5] versus 34.8 cm 3 [95% CI, 26.6–43.0]; P =0.007). Serum high-sensitivity C-reactive protein and interleukin-6 levels were significantly higher in persistent AF patients than in paroxysmal AF patients (median high-sensitivity C-reactive protein, 969 ng/mL [interquartile range, 307–1678] versus 320 ng/mL [interquartile range, 120–660]; P =0.008; median interleukin-6, 2.4 pg/mL [interquartile range, 1.7–3.2] versus 1.3 [interquartile range, 0.8–2.4] pg/mL; P =0.017). EAT locations were in excellent agreement with high DF sites (κ=0.77 [95% CI, 0.71–0.82]) but in poor agreement with complicated fractionated atrial electrogram sites (κ=0.22 [95% CI, 0.13–0.31]). Conclusions— Increased EAT volume and elevation of inflammatory biomarkers are noted in persistent AF rather than paroxysmal AF patients. High DF sites are located adjacent to EAT sites. Thus, EAT may be involved in the maintenance of AF.

Background: Whether epicardial adipose tissue (EAT) is independently associated with atrial fibrillation (AF) and outcome after catheter ablation (CA) for AF remains unclear. Conclusions: EAT volume increases in AF patients independent of conventional risk factors and is greater in patients with lone AF than in non-AF patients. EAT volume might be useful for predicting AF recurrence after CA. (Circ J 2011; 75: 2559 - 2565 Methods and

The pre-FPD may strongly reflect atrial dysfunction, and thus may be useful for predicting a successful PVI. Shortening of the FPD after the PVI and similar FPD and BAT values suggest that the last component of the FPD represents the activation of the left PVs.

A higher LA-DF value, smaller PV-to-LA DF gradient, and wider LA-CFAE distribution were noted more often in the nonresponders to CPVI than in the responders. This suggested the presence of an arrhythmogenic substrate in the LA beyond the PVs in patients whose AF persisted after CPVI, which was further associated with post-ablation AF recurrence.

Background: Ablation of ventricular tachycardia originating from the interventricular septum (IVS) is often limited by the presence of re-entrant pathways deep in the IVS. We compared the efficacy of bipolar ablation vs. sequential unipolar ablation in creating a transmural lesion across the porcine IVS. Methods and Results:Seventeen excised swine hearts were superfused by pulsatile saline flow. Bipolar ablation (at 30 W, 50 W or 70 W for 120 s) was performed between 2 saline-irrigated (20 ml/min) 4-mm tip electrodes, 1 on the left and 1 on the right side of the IVS. Sequential unipolar ablation (at 30 W, 50 W or 70 W for 120 s) was performed on the left and right sides of the IVS with an irrigated-tip catheter. Bipolar ablation produced a narrower, deeper lesion than did unipolar ablation. A transmural lesion was created by sequential unipolar ablation in 7.7%, 8.3% and 0% of tissue preparations and by bipolar ablation in 50.0%, 46.7% and 71.4% of tissue preparations at 30 W, 50 W and 70 W.Conclusions: Bipolar ablation of the IVS was highly effective for creating a transmural IVS lesion. (Circ J 2011; 75: 565 - 570)

SummaryBrugada syndrome is an inherited disorder that predisposes some patients to sudden cardiac death. It is not well established which Brugada syndrome patients are at risk of life-threatening arrhythmias. We investigated whether standard 12-lead electrocardiograms (ECG) can identify such patients. The subjects were 35 men with Brugada syndrome (mean age, 50.1 ± 12.4 years). Documented ventricular fibrillation or aborted sudden cardiac arrests were judged to be related to the Brugada syndrome. Ten patients (mean age, 49.6 ± 14.9 years) were symptomatic, and 25 (mean age, 50.3 ± 11.5 years) were asymptomatic. We determined the PR interval, QRS duration, and QT interval from baseline 12-lead ECG leads II and V2 as well as the J point elevation amplitude of lead V2. The QRS interval was measured from QRS onset to the J point in leads II and V2. The only significant difference between the symptomatic and asymptomatic patients was the QRS duration measured from lead V2. The mean QRS interval was 129.0 ± 23.9 ms in symptomatic patients versus 108.3 ± 15.9 ms in asymptomatic patients (P = 0.012). A QRS interval in lead V2 ≥ 120 ms was found to be a possible predictor of a life-threatening ventricular arrhythmia and/or syncope (P = 0.012). Prolonged QRS duration as measured on a standard 12-lead ECG is associated with ventricular arrhythmia and could serve as a simple noninvasive marker of vulnerability to life-threatening cardiac events in patients with Brugada syndrome. (Int Heart J 2011; 52: 98-102) Key words: Brugada syndrome, Sudden death, Ventricular fibrillation, QRS width B rugada syndrome, which was introduced as a clinical entity in 1992, is a genetic disorder that increases the risk of sudden death secondary to ventricular tachycardia/fibrillation (VT/VF) in patients with structurally normal hearts.1,2) The syndrome is estimated to be responsible for 4% of all sudden deaths and at least 20% of sudden deaths in patients with structurally normal hearts.3) Inheritance of Brugada syndrome occurs via an autosomal dominant mode of transmission with variable penetrance involving several genes. SC-N5A, which codes subunit I Na of sodium channel α, is mutated in 20%-30% of Brugada syndrome patients. 4,5) Mutations in the GPD1L gene 6) and the CACNA1 and CACNB2 genes 7) have also been identified, but these gene variations are infrequent. The typical ST segment elevation in the precordial leads that characterizes Brugada syndrome electrocardiographically can be transitory, vary over time, or be modified by various factors such as vagal tonus, body temperature, and medications. 8,9) This elevation can have a saddleback appearance with a J wave amplitude of ≥ 2 mm and an elevation in the terminal portion of the ST segment of ≥ 1 mm, and then either a positive or biphasic T wave (type 2 electrocardiogram [ECG]) or can be characterized by either a saddleback or coved appearance with an ST segment elevation of < 1 mm (type 3 ECG).10)The vulnerability of individuals with the "Brugada sign" to sudden cardiac death or a life...

SummaryThe reported pathogenesis of Brugada syndrome is phase 2 reentry resulting from shortening of the epicardial action potential duration at the right ventricular outflow tract (RVOT). However, several studies have revealed a high incidence of ventricular late potentials and high rate of ventricular fibrillation (VF) induced by programmed ventricular stimulation (PVS). The aim of the present study was to evaluate the role of slow conduction at the RVOT for the initiation of VF by PVS and any underlying pathological conditions in Brugada syndrome. Endocardial mapping of the RVOT and endomyocardial biopsy of the right ventricle were performed in 25 patients with Brugada syndrome with inducible VF. Late potentials were positive in 11 of the 25 (44%) patients. Low-amplitude fragmented and delayed electrograms were recorded at the RVOT in 13 of 18 (72.2%) patients. Histologic examination of the biopsy samples revealed fatty tissue infiltration, interstitial fibrosis, lymphocyte infiltration, and/or myocyte disorganization in 13 patients. Slow conduction at the RVOT may contribute to the induction of VF by PVS in Brugada syndrome. Various pathomorphologic changes may contribute to slow conduction at the RVOT. (Int Heart J 2010; 51: 17-23)