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Regional distribution of low-voltage-substrate in persistent atrial fibrillation - implications for atrial conduction and risk stratification

Session Poster session 2

Speaker Bjoern Mueller-Edenborn

Event : EHRA 2018

  • Topic : arrhythmias and device therapy
  • Sub-topic : Atrial Fibrillation - Diagnostic Methods
  • Session type : Poster Session

Authors : B Mueller-Edenborn (Bad Krozingen,DE), J Chen (Bad Krozingen,DE), H Lehrmann (Bad Krozingen,DE), Z Moreno-Weidmann (Bad Krozingen,DE), T Arentz (Bad Krozingen,DE), A Jadidi (Bad Krozingen,DE)

B Mueller-Edenborn1 , J Chen1 , H Lehrmann1 , Z Moreno-Weidmann1 , T Arentz1 , A Jadidi1 , 1University Heart Center Freiburg-Bad Krozingen, electrophysiology - Bad Krozingen - Germany ,

European Heart Journal Supplements ( 2018 ) 20 ( Supplement 1 ), i162

Background: Fibro-fatty remodeling of the left atrium (LA) is a key contributor to persistency in atrial fibrillation (AF). Affected areas can be identified using invasive mapping as they display lower-than-normal voltages. While presence of extensive low-voltage-substrate (LVS) was clearly linked to arrhythmia recurrence following pulmonary vein isolation, it is unclear when during the course of AF and in what regions of the LA LVS develops. 

Purpose: To investigate the regional development of LVS and its influence on LA conduction.

Methods: 70 patients with persistent AF underwent high-density voltage mapping of the LA in sinus rhythm prior to pulmonary vein isolation. LVS was defined as regions displaying <0.5 mV, <1.0 mV or <1.5 mV bipolar voltage. A 10-segment model of the LA served to investigate the regional distribution of LVS. The impact of LVS on LA conduction was evaluated using LA activation time (LAT) at mapping and P-wave at digitized-amplified (40 mm/mV, 200 mm/s) 12-lead ECG. An algorithm using the derived ECG-parameters was developed and tested in a validation cohort of 90 patients with no history of AF. 

Results: A high variation of LVS was observed between patients at all three cutoff-values defining low-voltage (1.4 cm2 to >50 cm2). With increasing overall LVS, the antero-septal region was affected first, followed by the roof and finally the posterior parts of the LA. Significant LVS antero-septally was sufficient to induce marked prolongation of the p-wave (130 ms in control vs 186 ms with antero-septal LVA, p<0.0001). Advanced interatrial block (IAB) due to impaired conduction through the Bachmann-bundle which is located antero-septally was frequent once significant LVS in this region developped (2.9% in control vs 49% in antero-septal LVS, p<0.0001). While patients with IAB in general had longer p-wave duration and more overall LVS (144 ms/ 12.9 cm2 in control vs 193 ms/ 38.1 cm2 in IAB, p=<0.0001/<0.0001), we identified a subgroup in whom a late-terminal positive deflection in lead I was the only ECG-marker of severe LVS of the anteroseptal and posteroinferior LA. An algorithm based on these observations including p-wave duration and presence of IAB or late-terminal deflection in lead I identified three degrees of expected LVS with increasing risk to develop AF in the validation cohort (see figure, p<0.0001).

Conclusions: LVS in persistent AF begins in the antero-septal region of the LA, where it affects conduction through the Bachmann-bundle. Careful analysis of the amplified p-wave for duration, IAB and presence of late-terminal deflection in lead I can identify patients at risk for future AF.

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