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  • br Material and methods br Results br


    Material and methods
    Financial support
    Conflicts of interest
    Introduction Metabolic syndrome comprises a cluster of conditions, including obesity, insulin resistance, hypertension, and abnormal cholesterol levels, which together increase cardiovascular risk. Metabolic syndrome and obesity have been reported to promote systemic nf-κb inhibitor and oxidative stress [1,2], and patients with metabolic syndrome have increased epicardial adipose tissue volumes [3]. The systemic and local conditions related to obesity and metabolic syndrome have been linked to the pathogenesis of atrial fibrillation (AF) [4–6]. In fact, numerous epidemiological studies have shown that obesity, one of the components of metabolic syndrome, is associated with both the new onset and progression of AF [7–9]. However, the mechanism explaining the link between obesity or metabolic syndrome and AF progression is unclear. To elucidate this mechanism, we investigated electrophysiological properties and vulnerability to AF in pigs fed on a high-fat diet (HFD).
    Material and methods
    Conflict of interest
    Funding sources This study was supported in part by a Grant-in-Aid for Scientific Research (KAKENHI) grant.
    Introduction Atrial fibrillation (AF) is the most common sustained arrhythmia, and as the average age of the population increases, the incidence of AF will continue to rise [1,2]. The past decade has seen the steady advance of catheter-based approaches to the management of AF. Fortunately, serious complications arising from AF ablation have declined as collective experience has increased and techniques have improved. Pulmonary vein stenosis, atrial-esophageal fistula, cerebral vascular accidents, and coronary artery injury are now uncommon complications [3]. Despite these advances, the prevalence of late-onset postprocedural left atrial (LA) flutter remains as high as 10% [4]. Presumably, in LA flutter, the conversion of AF to a more organized reentrant circuit results in the development of macroreentrant atrial tachycardias. These tachycardias possibly result from “proarrhythmic” lesion sets that create areas of slow conduction, predisposing the circuit to reentry [5]. Perimitral flutter (PMF) is responsible for a considerable percentage of cases of macroreentrant LA flutter, especially in the setting of AF ablation [6]. Despite recent technological advances and a better understanding of the anatomy, mitral isthmus ablation remains technically challenging, often requiring substantial ablation (>15min of radiofrequency [RF] energy), high ablation powers (≤50W), and epicardial ablation within the coronary sinus (CS) in approximately 70% of patients. Even so, success rates for mitral isthmus ablation in the acute setting are only moderately high [7].
    Material and methods
    Results Ablation at the anteroseptal line was performed in 27 PMF patients (aged 63±13 years; 9 female) with prior ablation for paroxysmal (n=3) or persistent (n=24) AF using electroanatomic activation mapping (70% CARTO, 30% NavX). All patients had previously been treated with ≥1 AF ablation procedure. After re-isolation of any recovered PV, a linear RF ablation was performed connecting the RSPV to the anteroseptal MA.
    Discussion Ablation at the classical mitral isthmus line, extending from the left inferior PV to the lateral mitral annulus, is far from the ideal approach to ablation in PMF. Several studies have made it clear that the anatomy of the mitral isthmus is not uniform and exhibits significant variation. In their series of 100 consecutive patients, Jais et al. required >30min of RF delivery in 20% of patients to achieve complete block [6]. In postmortem studies, the distance between the left inferior PV and the lateral mitral annulus averaged 35mm length and approximately 4mm depth: longer than the cavotricuspid isthmus with similar myocardial thickness. Certain anatomic features have been suggested as possible obstacles to successful mitral isthmus ablation [10–13]: myocardial depth >5mm; convective cooling by local blood vessels, such as the CS and circumflex artery, that act as a heat sink; a myocardial sleeve around the CS and continuities with the atrial myocardium that may bridge the lesion line; crevices in the isthmus area that may hinder safe and efficient RF energy delivery; continuation of atrial myocardium onto the atrial aspect of the mitral valve leaflet; and epicardial connections (e.g., the ligament of Marshall) across the mitral isthmus line.