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Letter to the Editor

Response to letter: ‘Bear tracks hypothesis: from atrial fibrillation to atrial fibrosis syndrome in stroke risk assessment’

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We would like to thank Ozeke et al. [Citation1] for their interest in our review article [Citation2]. We agree that stroke in atrial fibrillation (AF) appears to be a complex and poorly understood phenomenon. A number of recent studies have demonstrated an association between left atrial electrical remodeling and thrombogenesis [Citation3Citation6] suggesting that the underlying left atrial substrate may be an important determinant of stroke risk and that adverse atrial remodeling could convey an increased risk even in the absence of AF itself.

Building on these observations, we have employed more advanced techniques to evaluate electrical substrate in patients with AF. In a recently published study, we sought to evaluate the electrophysiological factors that may underpin variations in clinical presentations between patients uniformly classified with paroxysmal AF [Citation7]. Using detailed extra stimulus pacing we identified patterns of left atrial conduction delay associated with arrhythmia recurrence over 2 years of follow up. These techniques may have the potential to ‘unmask’ an underlying atrial myopathy that may be associated with disease severity or indeed stroke risk.

It is clear that traditional clinical risk scores for stroke and ablation outcome in AF do not fully reflect the complex process of atrial electrical and fibrotic remodeling. Further studies are needed to fully delineate electrophysiological parameters associated with AF severity and outcome in order to refine substrate targeted ablation strategies and stroke risk assessment.

Declaration of interest

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Additional information

Funding

This paper was not funded.

References

  • Ozeke O., et al. Bear tracks hypothesis: from atrial fibrillation to atrial fibrosis syndrome in stroke risk assessment. Expert Rev Cardiovasc Ther. 2017. DOI: 10.1080/14779072.2017.1355239. [ Epub ahead of print].
  • O’Neill L, Harrison J, O’Neill M, et al. Clinical, electrophysiological and imaging predictors of atrial fibrillation ablation outcome. Expert Rev Cardiovasc Ther. 2017;15(4):289–305.
  • Chao TF, Cheng -C-C, Lin W-S, et al. Associations among the CHADS(2) score, atrial substrate properties, and outcome of catheter ablation in patients with paroxysmal atrial fibrillation. Heart Rhythm. 2011;8(8):1155–1159.
  • Muller P, Maier J, Dietrich J-W, et al. Association between left atrial low-voltage area, serum apoptosis, and fibrosis biomarkers and incidence of silent cerebral events after catheter ablation of atrial fibrillation. J Interv Card Electrophysiol. 2015;44(1):55–62.
  • Park JH, Joung B, Son N-H, et al. The electroanatomical remodelling of the left atrium is related to CHADS2/CHA2DS2VASc score and events of stroke in patients with atrial fibrillation. Europace. 2011;13(11):1541–1549.
  • Wu JT, Wang S-L, Chu Y-J, et al. CHADS(2) and CHA(2)DS(2)-VASc scores predict the risk of ischemic stroke outcome in patients with interatrial block without atrial fibrillation. J Atheroscler Thromb. 2017;24(2):176–184.
  • Williams, S.E., et al. Intra-atrial conduction delay revealed by multisite incremental atrial pacing is an independent marker of remodeling in human atrial fibrillation. JACC: Clin Electrophysiology. 2017. DOI: 10.1016/j.jacep.2017.02.012.

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