Performance and safety of temperature- and flow-controlled radiofrequency ablation for ventricular arrhythmia

AIMS High-power ablation is effective for ventricular arrhythmia ablation; however, it increases the risk of steam pops. The aim of this study was to define the safety and efficacy of QMODE ablation in the ventricle and the risk of steam pop. METHODS AND RESULTS Consecutive patients undergoing ventricular ablation using QDOT were included in a prospective single-centre registry. Procedural data, complications, and follow-up were systematically analysed and compared with a historical ventricular tachycardia (VT) and premature ventricular complexes (PVC) cohort ablated using STSF. QMODE (≤50 W) ablation was performed in 107 patients [age 62 ± 13 years; 76% male; VT (n = 41); PVC (n = 66)]. A total of 2456 applications were analysed [power: 45.9 ± 5.0 W with minimal power titration (90% > 95% max power); duration 26 ± 8 s; impedance drop 9.4 ± 4.7 Ω; ablation index: 569 ± 163; mean-max temperature 44.3 ± 2.6°C]. Ventricular tachycardia ablation was associated with shorter radiofrequency (RF) time and a trend towards shorter procedure times using QDOT (QDOT vs. STSF: 20.1 ± 14.7 vs. 31 ± 17 min; P = 0.002, 151 ± 59 vs. 172 ± 48 min; P = 0.06). Complications, VT recurrence, and mortality rates were comparable (QDOT vs. STSF: 2% vs. 2%; P = 0.9, 24% vs. 27%; P = 0.82, and 2% vs. 4%; P = 0.67). Five audible steam pops (0.02%) occurred. Premature ventricular complex ablation was associated with comparable RF and procedure times (QDOT vs. STSF: 4.8 ± 4.6 vs. 3.9 ± 3.1 min; P = 0.25 and 96.1 ± 31.9 vs. 94.6 ± 24.7 min; P = 0.75). Complication and PVC recurrence were also comparable (QDOT vs. STSF: 0% vs. 3%; P = 0.17 and 19% vs. 22%; P = 0.71). CONCLUSION Ventricular ablation using QMODE ≤ 50 W is safe and effective for both VT and PVC ablation and is associated with a low risk for steam pop

Integrated hybrid Raman/fiber Bragg grating interrogation scheme for distributed temperature and point dynamic strain measurements

We propose and experimentally demonstrate the feasibility of an integrated hybrid optical fiber sensing interrogation technique that efficiently combines distributed Raman-based temperature sensing with fiber Bragg grating (FBG)-based dynamic strain measurements. The proposed sensing system is highly integrated, making use of a common optical source/receiver block and exploiting the advantages of both (distributed and point) sensing technologies simultaneously. A multimode fiber is used for distributed temperature sensing, and a pair of FBGs in each discrete sensing point, partially overlapped in the spectral domain, allows for temperature-independent discrete strain measurements. Experimental results report a dynamic strain resolution of 7.8  nε/√Hz within a full range of 1700 με and a distributed temperature resolution of 1°C at 20 km distance with 2.7 m spatial resolution

Resuming Training in High-Level Athletes After Mild COVID-19 Infection: A Multicenter Prospective Study (ASCCOVID-19)

BACKGROUND: There is a paucity of data on cardiovascular sequelae of asymptomatic/mildly symptomatic SARS-Cov-2 infections (COVID). OBJECTIVES: The aim of this prospective study was to characterize the cardiovascular sequelae of asymptomatic/mildly symptomatic COVID-19 among high/elite-level athletes. METHODS: 950 athletes (779 professional French National Rugby League (F-NRL) players; 171 student athletes) were included. SARS-Cov-2 testing was performed at inclusion, and F-NRL athletes were intensely followed-up for incident COVID-19. Athletes underwent ECG and biomarker profiling (D-Dimer, troponin, C-reactive protein). COVID(+) athletes underwent additional exercise testing, echocardiography and cardiac magnetic resonance imaging (CMR). RESULTS: 285/950 athletes (30.0%) had mild/asymptomatic COVID-19 [79 (8.3%) at inclusion (COVID(+)(prevalent)); 206 (28.3%) during follow-up (COVID(+)(incident))]. 2.6% COVID(+) athletes had abnormal ECGs, while 0.4% had an abnormal echocardiogram. During stress testing (following 7-day rest), COVID(+) athletes had a functional capacity of 12.8 ± 2.7 METS with only stress-induced premature ventricular ectopy in 10 (4.3%). Prevalence of CMR scar was comparable between COVID(+) athletes and controls [COVID(+) vs. COVID(-); 1/102 (1.0%) vs 1/28 (3.6%)]. During 289 ± 56 days follow-up, one athlete had ventricular tachycardia, with no obvious link with a SARS-CoV-2 infection. The proportion with troponin I and CRP values above the upper-limit threshold was comparable between pre- and post-infection (5.9% vs 5.9%, and 5.6% vs 8.7%, respectively). The proportion with D-Dimer values above the upper-limit threshold increased when comparing pre- and post-infection (7.9% vs 17.3%, P = 0.01). CONCLUSION: The absence of cardiac sequelae in pauci/asymptomatic COVID(+) athletes is reassuring and argues against the need for systematic cardiac assessment prior to resumption of training (clinicaltrials.gov; NCT04936503).L'Institut de Rythmologie et modélisation Cardiaqu

Understanding the genetic basis of atrial fibrillation : next steps after genome-wide association studies

Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia in clinical practice. Over the past two decades, we have come to appreciate that AF has a significant heritable component. The recent advent of next-generation sequencing technology has spawned a new era of research into the genetic basis of AF. Genome-wide association studies (GWAS) have identified multiple common variants underlying AF. Further, exome sequencing has emerged as a potentially powerful technique for the identification of mutations underlying familial forms of AF. In this thesis, we sought to further elucidate the genetic basis of AF though two specific aims. Firstly, we investigated the mechanistic link between KCNN3, a potassium channel gene which was identified in a GWAS for lone AF, and arrhythmia pathogenesis. Secondly, we performed exome sequencing and classical linkage analysis in two AF pedigrees to identify novel mutations for the arrhythmia. We demonstrate that overexpression of Kcnn3 in a murine model results in an increased susceptibility to AF. Interestingly, these mice also display a high incidence of sudden death due to heart block. Exome sequencing in an AF pedigree identified a potentially causative mutation in the transcription factor gene GATA6. In a second AF pedigree, we identified a novel locus for the arrhythmia on chromosome 1. However the causative mutation at this locus remains elusive. Ultimately, the identification of the genetic substrate underlying AF is likely to uncover novel therapeutic targets as well as enhancing risk stratification for this common and morbid arrhythmia

Monogenic atrial fibrillation as pathophysiological paradigms

Atrial fibrillation (AF) is the most common cardiac rhythm abnormality and represents a major burden, both to patients and to health-care systems. In recent years, increasing evidence from population-based studies has demonstrated that AF is a heritable condition. Although familial forms of AF have been recognized for many years, they represent a rare subtype of the arrhythmia. However, despite their limited prevalence, the identification of mutations in monogenic AF kindreds has provided valuable insights into the molecular pathways underlying the arrhythmia and a framework for investigating AF encountered in the general population. In contrast to these rare families, the typical forms of AF occurring in the community are likely to be multigenic and have significant environmental influences. Recently, genome-wide association studies have uncovered common sequence variants that confer increased susceptibility to the arrhythmia. In the future, the elucidation of the genetic substrate underlying both familial and more typical forms of AF will hopefully lead to the development of novel diagnostic tools as well as more targeted rhythm control strategies. In this article, we will focus on monogenic forms of AF and also provide an overview of case-control association studies for AF