Author + information
- Amir S. Jadidi, MD∗ (, )
- Zoraida Moreno-Weidmann, MD and
- Thomas Arentz, MD
- Arrhythmia Division, Cardiology Department II, University Heart Center Freiburg-Bad Krozingen, Bad Krozingen, Germany
- ↵∗Address for correspondence:
Dr. Amir S. Jadidi, Department of Cardiology II, University Heart Center Freiburg-Bad Krozingen, Südring 15, 79189 Bad Krozingen, Germany.
In this issue of JACC: Clinical Electrophysiology, Williams et al. (1) assess the arrhythmogenic electrophysiological substrate in 15 patients with paroxysmal atrial fibrillation (AF) prior to their first pulmonary vein isolation (PVI) procedure. The authors identify “rate-dependent conduction delay” as a novel marker of arrhythmogenesis that identifies patients at risk for AF recurrences after successful PVI. Electrogram-based electrophysiological parameters (voltage amplitude, duration, and fractionation) were rate- and direction-dependent and did not predict arrhythmia recurrences after PVI.
The novel atrial arrhythmogenic marker “rate-dependent atrial conduction delay” was assessed during incremental pacing from the high right atrium and coronary sinus. Incremental S1S2 pacing led to increasing intra-atrial conduction delay. Importantly, 2 patient groups could be differentiated within the paroxysmal AF group: patients developing atrial conduction delay at long (326 ms) versus short (275 ms) coupling intervals. Development of conduction delay at long S1S2 coupling intervals was associated with susceptibility for arrhythmia recurrences 2 years following PVI.
Furthermore, AF induction was only achieved in patients with increased atrial activation dispersion (corresponding to atrial conduction slowing revealed at short coupling intervals between 2 sites >60 mm distant from each other).
Currently, electrophysiological substrate mapping in patients with atrial fibrillation is mainly based on bipolar voltage mapping. The authors report in their current paper that bipolar voltage mapping of the atria during sinus rhythm did not reveal important low voltage areas <0.3 mV.
However, a recent study established normal atrial bipolar voltage cut-off in patients without history of AF >2.5 mV during sinus rhythm (2). Further studies in patients with persistent AF revealed that arrhythmogenic atrial substrate with local evidence of conduction slowing (local abnormal/delayed potentials [LAP]) develops within a bipolar voltage threshold of 1.3 mV during sinus rhythm (3,4). Moreover, selective ablation of atrial low voltage areas <0.5 mV in persistent AF is associated with acute AF termination and amelioration of arrhythmia freedom rates at 1-year follow-up (5,6). Therefore, a comparison of the novel arrhythmogenic marker “rate-dependent atrial conduction delay” to the extent of low voltage areas <1.3 mV during sinus rhythm and low-voltage areas <0.5 mV during AF would be interesting to study.
Noninvasive diagnostic tools (such as amplified p-wave at electrocardiogram, signal-averaged electrocardiogram, echocardiographic parameters, and delayed enhancement at cardiac magnetic resonance imaging) that may identify patients with “intra-atrial conduction disturbances” need to be established to predict outcome after PVI prior to the invasive procedure.
The work by Williams et al. (1) may explain why atrial voltage mapping at high activation rates and variable activation directions during AF may show discrepancies when compared with voltage mapping during regular slow rhythms (such as sinus rhythm). In fact, substrate mapping during AF (analyzing electrogram voltage, cycle length, and regional slow conduction) might represent a valuable alternative to voltage mapping during slow regular sinus rhythm, especially in patients who do not maintain stable sinus rhythm during the AF ablation procedure.
The current work reveals the potential importance of atrial activation rate on the ability to identify the arrhythmogenic substrate with conduction disturbance that is associated with arrhythmia recurrences after PVI. The underlying causes (genetic disorders/channelopathies, minor structural cardiomyopathies, and aging) associated with pathological atrial rate-dependent conduction delay need to be determined in future studies.
↵∗ Editorials published in JACC: Clinical Electrophysiology reflect the views of the authors and do not necessarily represent the views of JACC: Clinical Electrophysiology or the American College of Cardiology.
The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
All authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the JACC: Clinical Electrophysiology author instructions page.
- 2017 American College of Cardiology Foundation
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