Electrophysiological efficacy of Epicor high-intensity focused ultrasound.

OBJECTIVES: Clinical success of atrial fibrillation (AF) ablation depends on persistent blocking of electrical conduction across the ablation lines. Epicor high-intensity focused ultrasound (HIFU) ablation has been credited with a variable clinical efficacy. The aim of this work is to ascertain the electrophysiological (EP) efficacy of such lesions, by assessing pulmonary vein isolation (PVI) after open chest HIFU ablation, in the clinical setting. METHODS: Ten consecutive mitral patients (mean age: 57±10 years) with paroxysmal AF undergoing concomitant ablation with the Epicor ablation system (St. Jude Inc.®, Minneapolis, MN, USA) were enrolled for EP assessment. During surgery, pairs of additional temporary wires were positioned on the right PVs (RPVs) and on the roof of the left atrium (RLA), before epicardial ablation. Exit block (no capture during PV pacing) of RPV and of RLA was assessed before, after ablating and immediately after closure of the chest, in order to check the correct positioning of the wires. EP assessment was repeated before discharge and at 3 weeks. RESULTS: Baseline RPV pacing threshold (PT) was 3.5±2 mA (range 1.5-8), of RLA 1.73±1.1 mA (range 0.7-4.3 mA). PVI was not reached any time after HIFU ablation. At the pre-discharge EP study, the absence of isolation was observed in all cases. At 3 weeks, the PTs were 6.8±5.8 mA on RPV (range 2-16) and 6.4±5.3 mA (range 1-19) on RLA. All patients were discharged in sinus rhythm. CONCLUSIONS: PVI was not achieved after Epicor HIFU ablations, up to 3 weeks after surgery.

Differential structural remodeling of the left-atrial posterior wall in patients affected by mitral regurgitation with or without persistent atrial fibrillation: a morphological and molecular study.

INTRODUCTION: Atrial fibrillation (AF) in mitral regurgitation (MR) is a complex disease where multiple factors may induce left-atrial structural remodeling (SR). We explored the differential SR of the left-atrial posterior wall (LAPW) of patients affected by MR with or without persistent AF, and the expression of key proteins involved in its pathogenesis. METHODS AND RESULTS: Light microscopy of LAPW samples from 27 patients with MR and persistent AF (group 1), 33 with MR in sinus rhythm (group 2), and 15 autopsy controls (group 3) was used to measure myocyte diameter, percentage of myocytolytic myocytes, interstitial fibrosis, and capillary density; RT-PCR and Western blotting were used to assess the mRNA and protein levels of SOD-1, SOD-2, HO-1, calpain, MMP-2, MMP-9, TIMP-1, TIMP-2, and VEGF; immunofluorescence was used to locate these proteins. Myocyte diameter was similar in groups 1 and 2, but larger than controls. Compared to group 2, group 1 had more myocytolytic myocytes (20.8 ± 5.6% vs 14.7 ± 4.5%; P < 0.0001), increased interstitial fibrosis (10.4 ± 5.1% vs 7.5 ± 4.2%; P < 0.05), and decreased capillary density (923 ± 107 No/mm(2) vs 1,040 ± 100 No/mm(2); P < 0.0001). All of the proteins were more expressed in groups 1 and 2 than in controls. The protein and mRNA levels of SOD-1, SOD-2, MMP-2, and MMP-9 were higher in group 1 than in group 2. CONCLUSIONS: The LAPW of MR patients with or without AF shows considerable SR. The former has more severe histopathological changes and higher levels of proteins involved in SR, thereby reaching a threshold beyond which the sinus impulse cannot normally activate atrial myocardium.