Backgrounds
Ablation index (AI) is useful to complete circumferential pulmonary vein isolation (CPVI) for atrial fibrillation (AF), but the role of radiofrequency power in AI‐guided CPVI remains to be elucidated.
Methods
We investigated 60 patients with AF undergoing AI‐guided CPVI (mean age, 66 ± 9 years; nonparoxysmal AF in 16). The first 40 patients were randomly assigned to low‐power (LP; n = 20) and medium‐power (MP; n = 20) groups and the following 20 patients to high‐power (HP). In LP, radiofrequency (RF) application was done at 30 W at the anterior and 20 W at the posterior left atrial (LA) wall, while in MP, it was at 40 W at the anterior and 30 W at the posterior LA wall. In HP, 50 W was applied at the anterior, 40 W at posterior LA wall and 30 W on the esophagus. At each ablation point, target AI was 400 at the anterior, 360 at the posterior LA wall, and 260 on the esophagus.
Results
The time to complete both‐side CPVI was shortest in HP (median, 40 minutes, interquartile range [IQR], 28‐63) followed by MP (58 [49‐83] minutes, P = .008 vs HP) and LP (84 [72‐93] minutes, P = .002 vs MP). Higher RF power application significantly increased first‐pass isolation rate (55% in LP, 80% in MP and 85% in HP, P = .002) and decreased LA‐PV reconnection rate (10% in LP, 8% in MP, and 0% in HP, P = .03).
Conclusion
In AI‐guided PVI, the HP RF application can shorten the time to complete PVI with a high rate of first‐pass isolation and a low rate of LA‐PV reconnection.
Background and purpose: Many drugs associated with acquired long QT syndrome (LQTS) directly block human ether-a-gogo-related gene (hERG) K þ channels. Recently, disrupted trafficking of the hERG channel protein was proposed as a new mechanism underlying LQTS, but whether this defect coexists with the hERG current block remains unclear. This study investigated how ketoconazole, a direct hERG current inhibitor, affects the trafficking of hERG channel protein.Experimental approach: Wild-type hERG and SCN5A/hNa v 1.5 Na þ channels or the Y652A and F656C mutated forms of the hERG were stably expressed in HEK293 cells. The K þ and Na þ currents were recorded in these cells by using the whole-cell patch-clamp technique (231C). Protein trafficking of the hERG was evaluated by Western blot analysis and flow cytometry. Key results: Ketoconazole directly blocked the hERG channel current and reduced the amount of hERG channel protein trafficked to the cell surface in a concentration-dependent manner. Current density of the hERG channels but not of the hNa v 1.5 channels was reduced after 48 h of incubation with ketoconazole, with preservation of the acute direct effect on hERG current. Mutations in drug-binding sites (F656C or Y652A) of the hERG channel significantly attenuated the hERG current blockade by ketoconazole, but did not affect the disruption of trafficking. Conclusions and implications: Our findings indicate that ketoconazole might cause acquired LQTS via a direct inhibition of current through the hERG channel and by disrupting hERG protein trafficking within therapeutic concentrations. These findings should be considered when evaluating new drugs.
It is still difficult to predict the occurrence of an electrical short circuit in current ICD systems. To reduce the probability of an electrical short circuit, we suggest the following: (i) avoid lead stress at ICD implantation, (ii) select a single-coil lead instead of a dual-coil lead, or (iii) use a unique algorithm which automatically disconnect can or SVC lead from shock deliver circuit when excessive current was detected.
Purpose Localization of the esophagus and the left atrium (LA) posterior wall thickness (LAPWT) should be taken into account when delivering radiofrequency energy. To validate the visualization of the esophagus and analyze LAPWT by ICE advanced into the LA in patients with atrial fibrillation (AF) undergoing ablation index (AI)-guided pulmonary vein (PV) isolation. Methods In 73 patients (mean age, 68 ± 12; paroxysmal AF in 45), a 3-dimensional (3D) esophagus image was created with CARTO Soundstar Ⓡ and its location was compared with contrast esophagography saved in Carto UNIVU™. LAPWT adjacent to the esophagus was measured at 4 levels: left superior PV (LSPV), intervenous carina (IC), left inferior PV (LIPV), and LIPV bottom. A target AI value was 260 (25 W power) on the esophagus demonstrated by ICE. Results All patients had the esophagus posterior to the left PV antrum. Creating a 3D esophagus and measurement of LAPWT with ICE was done without any complications. ICE esophagus image was completely overlapped with contrast esophagography. LAPWT (mm) was 2.8 (interquartile range, 2.5-3.2), 2.2 (1.9-2.5), 1.9 (1.8-2.1), and 2.1 (1.9-2.4) for LSPV, IC, LIPV, and LIPV bottom, respectively, while LA roof thickness was 3.2 (2.9-3.6) (P < 0.0001 by ANOVA). No residual conduction gap on the esophagus after the first circumferential PV isolation was found in 64 of 73 (88%) patients. Conclusions ICE inserted into the LA can reliably locate and display the esophagus and its relationship to the LA. LAPWT was the thinnest at the LIPV level. AI-guided ablation targeting at AI value 260 on the esophagus seemed to be effective.
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