Author + information
- Published online January 15, 2018.
- Thomas Arentz, MD∗ (, )
- Björn Müller-Edenborn, MD and
- Amir Jadidi, MD
- Department of Cardiology II, Arrhythmia Division, University Heart Center Freiburg-Bad Krozingen, Bad Krozingen, Germany
- ↵∗Address for correspondence:
Dr. Thomas Arentz, Herz-Zentrum, Rhythmologie, University Heart Center Freiburg-Bad Krozingen, Sudring 15, Bad Krozingen 79188, Germany 49-7633-4020.
In their current work in this issue of JACC: Clinical Electrophysiology, Prabhu et al. (1) assessed the impact of heart failure (HF) on the development of biatrial low-voltage substrate (LVS) in patients with persistent and long-persistent atrial fibrillation (AF). Because the success rate of pulmonary vein isolation crucially depends on the presence and extent of atrial arrhythmogenic slow conduction areas that are associated with low-voltage areas (2–5), it is important to characterize the underlying disease processes leading to development of arrhythmogenic atrial LVS.
The authors quantitatively assessed AF cycle length (AFCL) within the pulmonary veins and left atrial (LA) appendage. Following electrical cardioversion to sinus rhythm, the authors measured the extent and distribution of biatrial LVS, atrial conduction velocity, and occurrence of complex fractionated electrograms during atrial pacing from coronary sinus. Atrial voltage mapping was performed by using a contact force-sensing catheter with a 3.5-mm tip electrode. Mapping density was 221 ± 79 points per map, with evenly distributed mapping sites and a contact force of >10 g during mapping.
The total study group consisted of 40 patients with (long-) persistent AF. Twenty patients had HF with reduced left ventricle ejection fraction (LVEF) (rEF: 33 ± 8%), whereas the remaining 20 patients had normal LVEF (nEF: 61 ± 4%). Patients with HF due to ischemic heart disease or valvopathy were not included. Notably, 11 of 20 patients (55%) with initially reduced LVEF experienced a marked improvement after AF ablation and restoration of sinus rhythm (tachycardiomyopathy-related HF [TCMP-HF]), whereas the remaining 9 patients demonstrated sustained impairment of LVEF (non-TCMP-HF).
The authors report an important reduction of uni- or bipolar voltage amplitudes within both atria in patients with reduced LVEF (2.4 mV/1.5 mV in rEF vs. 3.6 mV/2.3 mV in nEF) and in turn, a higher percentage of LA mapping points displaying bipolar voltages of <0.5 mV (23% in rEF vs. 6% in nEF).
Patients with reduced LVEF displayed the lowest regional voltage values in the pulmonary vein antra, the posterior LA wall up to the anterior LA roof area, and the septal LA wall. In all regions, voltages were significantly lower and presented more fractionated potentials (31% vs. 9%, respectively) than in patients with normal LVEF. Also, pulmonary veins were surrounded by low-voltage antral areas and displayed slower local cycle lengths than the pulmonary vein cycle lengths in patients with normal EF.
A very interesting finding in this context is that the response to restoration of sinus rhythm in patients with initially reduced LVEF was indeed reflected in the extent of LVS of <0.5 mV and atrial voltage amplitudes: patients with normalization of LVEF in sinus rhythm (TCMP-HF) demonstrated a smaller area of low voltage (17% vs. 31%, respectively) and higher unipolar or bipolar voltages (2.7 mV/1.7 mV vs. 1.9 mV/1.2 mV, respectively) than those with sustained impairment of LVEF (non-TCMP-HF).
This is an important aspect of atrial LVS development and treatment strategy in patients with persistent AF. In fact, several recent studies have suggested the arrhythmogenic role of atrial LVS for maintenance of persistent AF (2–4,6). We recently showed that rotational and rapid focal activities preferentially develop at atrial slow conduction sites within LVS, displaying prolonged low-voltage electrograms during AF (4). Focal radiofrequency ablation, in addition to pulmonary vein isolation, leads to acute AF termination by limited RF delivery that is only applied to low-voltage areas (4).
However, the question to what extent atrial tissue can heal, reverse remodeling, and possibly restore “normal voltage displaying atrial myocardium” has not been addressed to date. A recent histological study revealed myocardial macrophage infiltration with lower extent of fibrosis in ventricular biopsy of TCMP-HF patients, compared to those with dilated or ischemic HF (7). The current voltage mapping study reveals that TCMP-HF is associated with development of LVS to a lesser extent than non-TCMP-HF does. It would be highly important to remap patients with TCMP-induced LVS several weeks after restoration and maintenance of sinus rhythm to assess the extent to which the LVS has reversed or reduced. The lower extent of atrial LVS in TCMP-HF potentially reveals a distinct mechanism for LVS development in these patients and raises the question of reversibility of LVS, if sinus rhythm was maintained for longer period.
The current study is the first to report development of a biatrial LVS in persistent AF patients due to different causes of cardiac HF (TCMP-HF vs. non-TCMP-HF). Further studies should address the underlying molecular and cellular mechanisms involved in development of atrial LVS and how reverse remodeling could be achieved.
↵∗ 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.
All authors have reported that they have no relationships relevant to the contents of this paper to disclose. Katia Zeppenfeld, MD, served as Guest Editor for this paper.
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.
- 2018 American College of Cardiology Foundation
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