Background: Temporary transvenous pacing (TTP) is a common procedure, predominantly performed in the catheterization laboratory (cath lab) because of presumed lower complication rate. This study aims to evaluate the efficacy and safety of TTP placement in the ICU compared to TTP placement in the cath lab. Methods and results: This retrospective, real-life study included all patients requiring TTP in a tertiary care ICU between 2019 and 2022. Patients’ characteristics, TTP-related data, outcomes, and complications were compared between groups (ICU vs. cath lab). Data from 193 patients receiving TTP were analyzed; 68.4% received TTP in the ICU and 31.6% in the cath lab. The main indication was atrioventricular block in 154 patients (79.8%). The operator was less frequently an interventional cardiologist in the ICU (12.1%) compared to the cath lab (100%, p<0.001). TTP in the ICU was more frequently performed using a jugular access (72.0 vs. 1.6%), a right-sided laterality (88.7 vs. 43.6%), and a balloon-tipped catheter (100% vs. 0%, p<0.001 for all comparisons). Success was 100% in both groups. The overall complication rate was 16.6%, with no significant difference between both groups (14.4% ICU vs. 21.3% cath lab, p=0.13), but a tendency toward higher complications in the cath lab group (especially tamponade, lead displacement, and CIED infection). Conclusion: In a daily clinical scenario, TTP placement appears as safe in the ICU than in the cath lab, regardless of the operator’s level of expertise when performed in accordance with best practices. Nevertheless, TTP complications remain high and alternatives should be used whenever possible.

BACKGROUND: Nav1.5, which is encoded by the SCN5A gene, is the predominant voltage-gated Na+ channel in the heart. Several mutations of this gene have been identified and have been reported to be involved in several cardiac rhythm disorders, including type 3 long QT syndrome (LQT3), that can cause sudden cardiac death. We analyzed the biophysical properties of two novel variants of the Nav1.5 channel (Q1491H and G1481V) detected in 5- and 12-week-old infants diagnosed with a prolonged QT interval. METHODS: The Nav1.5 wild-type (WT) and the Q1491H and G1481V mutant channels were reproduced in vivo. WT or the mutant channels were co-transfected in HEK 293 cells with the beta 1 regulatory subunit. Na+ currents were recorded using the whole-cell configuration of the patch-clamp technique. RESULTS: The Q1491H mutant channel exhibited a lower current density, a persistent Na+ current, an enhanced window current due to a +20-mV shift of steady-state inactivation, a +10-mV shift of steady-state activation, a faster onset of slow inactivation, and a recovery from fast inactivation with fast and a slow time constants of recovery. The G1481V mutant channel exhibited an increase in current density and a +7-mV shift of steady-state inactivation. The observed defects are characteristic of gain-of-function mutations typical of LQT3. DISCUSSION AND CONCLUSION: The 5- and 12-week-old infants displayed prolonged QT intervals. Our analyses of the Q1491H and G1481V mutations correlated with the clinical diagnosis. The observed biophysical dysfunctions associated with both mutations were most likely responsible for the sudden deaths of the two infants.