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Highly localized impedance (LI) in combination with contact force (CF) during atrial fibrillation (AF) ablation may improve tissue characterization and lesion prediction during pulmonary vein isolation (PVI). This analysis explores the relationship between LI parameters, ablation spot locations and procedural success during isolation of PVs. Two-hundred twelve consecutive patients from 16 European centers undergoing de novo AF radiofrequency (RF) catheter ablation with an open-irrigated tip catheter enabled by CF and LI measurement (Stablepoint) were included. Ablation was guided by LI drop during RF delivery. The interlesion distance was set ≤ 6 mm. First pass isolation (FPI) was defined as successful PVI at or before completion of the first encircling. Procedural endpoint was PVI as assessed by entrance and exit block. Data are reported as mean ± SD. A total of 13891 ablation spots performed around PVs were analyzed (baseline LI = 161.2 ± 19 Ω; LI drop = 21.9 ± 9 Ω; LI drop rate = 3.1 ± 2 Ω/s; RF Delivery time = 9.2 ± 4 s; CF = 12.5 ± 7 g). LI drop was predicted by baseline LI (r = 0.56, 95%CI: 0.55 to 0.57, P < 0.0001). A total of 80 PV gaps were detected, mostly at the right pairs of the PV (63.7%, P = 0.013). The FPI rate per vein was 93.3% resulting from 180 patients (84.9%) with FPI (Figure 1). PV gaps were located at anterior (31.3%), posterior (31%), and carina (16%) sites after the FPI evaluation. At successful ablation spots, both baseline LI and LI drop were larger than at PV gap spots (161.4Ω vs. 153.0Ω, P < 0.0001 for baseline LI; 22.1Ω vs. 14.4Ω, P < 0.0001 for LI drop), whereas RF delivery time was shorter (9.1s at successful ablation spots vs. 10.1s at PV gap spots, P < 0.0001). CF values seem to be higher at successful ablation spot that at PV gap spots (12.5 g vs. 11.4 g, P = 0.0592). The best LI drop that predicts successful ablation spots was > 20Ω (sensitivity = 56.8%, specificity = 93.2%, PPV = 99.7%, area under the ROC curve = 0.7841, P < 0.0001). Optimal LI drops were identified by left atrial region and were > 21Ω at anterior sites and > 18Ω at posterior sites. No steam pops or complications were reported during the procedures. All PVs were successfully isolated in all study patients. Ablation strategy guided by LI and CF information results in a high first pass isolation rate. LI drop is predictive of PV segment isolation. A regional approach to RF ablation guided by LI information may be useful in patients with AF. [ABSTRACT FROM AUTHOR]

The aim of this work was to check the hypothesis that increased cardiac aldosterone level combined with arterial hypertension may be deleterious for the heart. Transgenic mice overexpressing Aldo Synthase (AS) in cardiomyocytes and wild type (WT) littermates were submitted to AngII treatment by osmotic pump (1mg/kg/day) during 3 and 8 weeks. Results: 1) Same levels of hypertension were observed in all treated groups whatever the genotype. Ventricular remodelling was equivalent in terms of LVH at 3wks and 8 wks in AngII-treated groups (ratio HW/BW +10 % for AS and WT after AngII, p<0.05) and fibrosis (×3 for AngII groups, p<0.05). Eplerenone treatment (50mg/kg/day) prevented these changes. In contrast, after 3 wks of AngII treatment atrial remodelling was worsened with increased dilatation (0.220±0.003cm vs 0.200±0.003cm for WT, p<0.05) and fibrosis (3.13±0.26 % vs 2.64±0.16 % for WT, p<0.05) in AS mice. This phenotype was aggravated in 8 weeks treated mice with an atrial diameter of 0.240±0.004cm in AS vs 0.220±0.004cm (p<0.05) in WT mice. Atrial fibrosis was 4.2±0.6 % in AS vs 3.6±0.2 % in WT (p<0.55). We also observed a longer P wave duration in AS mice after AngII than in WT (for 3 wks treatment, 18.78±0.45ms vs 17.15±0.38ms for WT, p<0.01 and at 8 wks 22.00±0.42ms vs 20.98±0.83ms for WT, p<0.05). 2) This electrical change led us to study the expression of atrial connexin (Cx) 40 and 43. AS mice showed a decrease of about 50 % of C×43 at basal state compared to WT but C×40 levels remained unchanged. AngII treatment decreased about 50 % C×43 and C×40 expression in WT mice. For AS mice, AngII induced an increase of about 50 % of C×40 expression but C×43 expression was not affected. In conclusion, these results suggest that cardiac aldosterone combined with AngII hypertension have deleterious effects on left atria: it increases dilatation and fibrosis and it increases conduction time by regulating expression of C×40 and 43. [Copyright &y& Elsevier]