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. 2024 Dec 16:11:1427841.
doi: 10.3389/fcvm.2024.1427841. eCollection 2024.

The impact of atrial voltage and conduction velocity phenotypes on atrial fibrillation recurrence

Affiliations

The impact of atrial voltage and conduction velocity phenotypes on atrial fibrillation recurrence

Pedro Silva Cunha et al. Front Cardiovasc Med. .

Abstract

Introduction: Low atrial voltage and slow conduction velocity (CV) have been associated with atrial fibrillation (AF); however, their interaction and relative importance as early disease markers remain incompletely understood. We aimed to elucidate the relationship between atrial voltage and CV using high-density electroanatomic (HDE) maps of patients with AF.

Methods: HDE maps obtained during sinus rhythm in 52 patients with AF and five healthy controls were analysed. Atrial voltage and CV maps were generated, and their correlations were assessed. Subgroup analyses were performed based on clinically relevant factors such as AF type, CV, and voltage levels. Finally, cluster analysis was conducted to identify distinct phenotypes within the population, reflecting different patterns of conduction and voltage.

Results: A moderate positive correlation was found between the mean atrial voltage and CV (r = 0.570). Subgroup analysis revealed differences in voltage (p = 0.0044) but not in global CV (p = 0.42), with no significant differences between AF types. Three distinct phenotypes emerged: normal voltage/normal CV, normal voltage/low CV, and low voltage/low CV, with distinct recurrence rates, suggesting different disease progression paths. Slower atrial CV was identified as a significant predictor of arrhythmia recurrence at 12 and 24 months after AF ablation, surpassing the predictive potential of atrial voltage.

Conclusion: Atrial voltage and CV analyses revealed distinct phenotypes. Lower atrial CV emerged as a significant predictor of AF recurrence, exceeding the predictive significance of atrial voltage. These findings emphasise the importance of considering CV and voltage in managing AF and offer potential insights for personalised strategies.

Keywords: ablation & electrophysiology; atrial conduction velocity; atrial fibrillation; atrial myopathy; voltage.

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Conflict of interest statement

AR and MP are employees of Biosense Webster. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Electrogram display/annotation. OpenEP measurement of local electrical activity. Examples of electrogram annotation: Panel (A), normal conduction; Panel (B) slow conduction. Blue lines: bipolar electrograms; Green lines: unipolar electrograms.
Figure 2
Figure 2
Left atrial voltage and conduction velocity in control and AF groups. Panel (A) Examples of colour-coded maps for atrial voltage (left) and conduction velocity (right). Panel (B) Average voltage (left) and average conduction velocity (right) in control and AF patients.
Figure 3
Figure 3
Correlation between atrial voltage and conduction velocity in this cohort of atrial fibrillation patients. Each point on the plot corresponds to an individual patient, with the x-axis depicting conduction velocity (measured in meters per second) and the y-axis illustrating atrial voltage (measured in millivolts). The red regression line represents the moderate positive correlation between these two variables, with a correlation coefficient r = 0.570.
Figure 4
Figure 4
Comparison of the average left atrial voltage (A) and conduction velocity (B) in different conduction velocity groups.
Figure 5
Figure 5
Differences in average conduction velocity (A) and average voltage (B) between paroxysmal AF patients and persistent AF patients.
Figure 6
Figure 6
Visualisation of three unique phenotypes based on average conduction velocity and voltage in a cohort of 52 patients with atrial fibrillation. The normal conduction velocity and normal voltage define Cluster 0 (blue). Cluster 1 (red) is characterised by slow conduction velocity and normal voltage. Cluster 2 (green) encompasses slow conduction velocity and low voltage. The plot delineates the heterogeneity and multifaceted nature of AF, reflecting the different patterns of conduction and voltage.
Figure 7
Figure 7
Schematic depiction of the observed phenotypes of the relationship between atrial voltage and atrial conduction velocity. Cluster 0 is characterised by normal mean atrial voltage and normal conduction velocity, Cluster 1 by slow conduction velocity and normal voltage, whereas Cluster 2 encompasses slow conduction velocity and low voltage. In each cluster panel, the image on the left represents the voltage colour map and the image on the right represents the velocity colour map.
Figure 8
Figure 8
Arrhythmia recurrence according to cluster, kaplan-meier estimates recurrence-free survival. Log-rank test Cluster 0 vs. Cluster 1: p-value = 0.0468. Log-rank test Cluster 0 vs. Cluster 2: p-value = 0.3990. Log-rank test Cluster 1 vs. Cluster 2: p-value = 0.4027.
Figure 9
Figure 9
According to atrial voltage (panel A) and conduction velocity (panel B), kaplan-meier estimates recurrence-free survival at 24 months of follow-up. Panel (A): Average atrial voltage (cut-off ∼0.8 mV). Panel (B): Average conduction velocity (<0.6 m/s) (red line), average conduction velocity (>0.6 m/s) (green line).

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