Arrhythmogenic propensity of the fibrotic substrate after atrial fibrillation ablation

a longitudinal study using magnetic resonance imaging-based atrial models

Rheeda L. Ali, Joe B. Hakim, Patrick M. Boyle, Sohail Zahid, Bhradeev Sivasambu, Joseph Marine, Hugh Calkins, Natalia A. Trayanova, David D Spragg

Research output: Contribution to journalArticle

Abstract

AIMS: Inadequate modification of the atrial fibrotic substrate necessary to sustain re-entrant drivers (RDs) may explain atrial fibrillation (AF) recurrence following failed pulmonary vein isolation (PVI). Personalized computational models of the fibrotic atrial substrate derived from late gadolinium enhanced (LGE)-magnetic resonance imaging (MRI) can be used to non-invasively determine the presence of RDs. The objective of this study is to assess the changes of the arrhythmogenic propensity of the fibrotic substrate after PVI. METHODS AND RESULTS: Pre- and post-ablation individualized left atrial models were constructed from 12 AF patients who underwent pre- and post-PVI LGE-MRI, in six of whom PVI failed. Pre-ablation AF sustained by RDs was induced in 10 models. RDs in the post-ablation models were classified as either preserved or emergent. Pre-ablation models derived from patients for whom the procedure failed exhibited a higher number of RDs and larger areas defined as promoting RD formation when compared with atrial models from patients who had successful ablation, 2.6 ± 0.9 vs. 1.8 ± 0.2 and 18.9 ± 1.6% vs. 13.8 ± 1.5%, respectively. In cases of successful ablation, PVI eliminated completely the RDs sustaining AF. Preserved RDs unaffected by ablation were documented only in post-ablation models of patients who experienced recurrent AF (2/5 models); all of these models had also one or more emergent RDs at locations distinct from those of pre-ablation RDs. Emergent RDs occurred in regions that had the same characteristics of the fibrosis spatial distribution (entropy and density) as regions that harboured RDs in pre-ablation models. CONCLUSION: Recurrent AF after PVI in the fibrotic atria may be attributable to both preserved RDs that sustain AF pre- and post-ablation, and the emergence of new RDs following ablation. The same levels of fibrosis entropy and density underlie the pro-RD propensity in both pre- and post-ablation substrates.

Original languageEnglish (US)
Pages (from-to)1757-1765
Number of pages9
JournalCardiovascular research
Volume115
Issue number12
DOIs
StatePublished - Oct 1 2019

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Pulmonary Veins
Atrial Fibrillation
Longitudinal Studies
Magnetic Resonance Imaging
Gadolinium
Entropy
Fibrosis
Recurrence

Keywords

  • Atrial fibrillation
  • Cardiac MRI
  • Drivers
  • Fibrosis
  • Modelling

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Arrhythmogenic propensity of the fibrotic substrate after atrial fibrillation ablation : a longitudinal study using magnetic resonance imaging-based atrial models. / Ali, Rheeda L.; Hakim, Joe B.; Boyle, Patrick M.; Zahid, Sohail; Sivasambu, Bhradeev; Marine, Joseph; Calkins, Hugh; Trayanova, Natalia A.; Spragg, David D.

In: Cardiovascular research, Vol. 115, No. 12, 01.10.2019, p. 1757-1765.

Research output: Contribution to journalArticle

Ali, Rheeda L. ; Hakim, Joe B. ; Boyle, Patrick M. ; Zahid, Sohail ; Sivasambu, Bhradeev ; Marine, Joseph ; Calkins, Hugh ; Trayanova, Natalia A. ; Spragg, David D. / Arrhythmogenic propensity of the fibrotic substrate after atrial fibrillation ablation : a longitudinal study using magnetic resonance imaging-based atrial models. In: Cardiovascular research. 2019 ; Vol. 115, No. 12. pp. 1757-1765.
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abstract = "AIMS: Inadequate modification of the atrial fibrotic substrate necessary to sustain re-entrant drivers (RDs) may explain atrial fibrillation (AF) recurrence following failed pulmonary vein isolation (PVI). Personalized computational models of the fibrotic atrial substrate derived from late gadolinium enhanced (LGE)-magnetic resonance imaging (MRI) can be used to non-invasively determine the presence of RDs. The objective of this study is to assess the changes of the arrhythmogenic propensity of the fibrotic substrate after PVI. METHODS AND RESULTS: Pre- and post-ablation individualized left atrial models were constructed from 12 AF patients who underwent pre- and post-PVI LGE-MRI, in six of whom PVI failed. Pre-ablation AF sustained by RDs was induced in 10 models. RDs in the post-ablation models were classified as either preserved or emergent. Pre-ablation models derived from patients for whom the procedure failed exhibited a higher number of RDs and larger areas defined as promoting RD formation when compared with atrial models from patients who had successful ablation, 2.6 ± 0.9 vs. 1.8 ± 0.2 and 18.9 ± 1.6{\%} vs. 13.8 ± 1.5{\%}, respectively. In cases of successful ablation, PVI eliminated completely the RDs sustaining AF. Preserved RDs unaffected by ablation were documented only in post-ablation models of patients who experienced recurrent AF (2/5 models); all of these models had also one or more emergent RDs at locations distinct from those of pre-ablation RDs. Emergent RDs occurred in regions that had the same characteristics of the fibrosis spatial distribution (entropy and density) as regions that harboured RDs in pre-ablation models. CONCLUSION: Recurrent AF after PVI in the fibrotic atria may be attributable to both preserved RDs that sustain AF pre- and post-ablation, and the emergence of new RDs following ablation. The same levels of fibrosis entropy and density underlie the pro-RD propensity in both pre- and post-ablation substrates.",
keywords = "Atrial fibrillation, Cardiac MRI, Drivers, Fibrosis, Modelling",
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T1 - Arrhythmogenic propensity of the fibrotic substrate after atrial fibrillation ablation

T2 - a longitudinal study using magnetic resonance imaging-based atrial models

AU - Ali, Rheeda L.

AU - Hakim, Joe B.

AU - Boyle, Patrick M.

AU - Zahid, Sohail

AU - Sivasambu, Bhradeev

AU - Marine, Joseph

AU - Calkins, Hugh

AU - Trayanova, Natalia A.

AU - Spragg, David D

PY - 2019/10/1

Y1 - 2019/10/1

N2 - AIMS: Inadequate modification of the atrial fibrotic substrate necessary to sustain re-entrant drivers (RDs) may explain atrial fibrillation (AF) recurrence following failed pulmonary vein isolation (PVI). Personalized computational models of the fibrotic atrial substrate derived from late gadolinium enhanced (LGE)-magnetic resonance imaging (MRI) can be used to non-invasively determine the presence of RDs. The objective of this study is to assess the changes of the arrhythmogenic propensity of the fibrotic substrate after PVI. METHODS AND RESULTS: Pre- and post-ablation individualized left atrial models were constructed from 12 AF patients who underwent pre- and post-PVI LGE-MRI, in six of whom PVI failed. Pre-ablation AF sustained by RDs was induced in 10 models. RDs in the post-ablation models were classified as either preserved or emergent. Pre-ablation models derived from patients for whom the procedure failed exhibited a higher number of RDs and larger areas defined as promoting RD formation when compared with atrial models from patients who had successful ablation, 2.6 ± 0.9 vs. 1.8 ± 0.2 and 18.9 ± 1.6% vs. 13.8 ± 1.5%, respectively. In cases of successful ablation, PVI eliminated completely the RDs sustaining AF. Preserved RDs unaffected by ablation were documented only in post-ablation models of patients who experienced recurrent AF (2/5 models); all of these models had also one or more emergent RDs at locations distinct from those of pre-ablation RDs. Emergent RDs occurred in regions that had the same characteristics of the fibrosis spatial distribution (entropy and density) as regions that harboured RDs in pre-ablation models. CONCLUSION: Recurrent AF after PVI in the fibrotic atria may be attributable to both preserved RDs that sustain AF pre- and post-ablation, and the emergence of new RDs following ablation. The same levels of fibrosis entropy and density underlie the pro-RD propensity in both pre- and post-ablation substrates.

AB - AIMS: Inadequate modification of the atrial fibrotic substrate necessary to sustain re-entrant drivers (RDs) may explain atrial fibrillation (AF) recurrence following failed pulmonary vein isolation (PVI). Personalized computational models of the fibrotic atrial substrate derived from late gadolinium enhanced (LGE)-magnetic resonance imaging (MRI) can be used to non-invasively determine the presence of RDs. The objective of this study is to assess the changes of the arrhythmogenic propensity of the fibrotic substrate after PVI. METHODS AND RESULTS: Pre- and post-ablation individualized left atrial models were constructed from 12 AF patients who underwent pre- and post-PVI LGE-MRI, in six of whom PVI failed. Pre-ablation AF sustained by RDs was induced in 10 models. RDs in the post-ablation models were classified as either preserved or emergent. Pre-ablation models derived from patients for whom the procedure failed exhibited a higher number of RDs and larger areas defined as promoting RD formation when compared with atrial models from patients who had successful ablation, 2.6 ± 0.9 vs. 1.8 ± 0.2 and 18.9 ± 1.6% vs. 13.8 ± 1.5%, respectively. In cases of successful ablation, PVI eliminated completely the RDs sustaining AF. Preserved RDs unaffected by ablation were documented only in post-ablation models of patients who experienced recurrent AF (2/5 models); all of these models had also one or more emergent RDs at locations distinct from those of pre-ablation RDs. Emergent RDs occurred in regions that had the same characteristics of the fibrosis spatial distribution (entropy and density) as regions that harboured RDs in pre-ablation models. CONCLUSION: Recurrent AF after PVI in the fibrotic atria may be attributable to both preserved RDs that sustain AF pre- and post-ablation, and the emergence of new RDs following ablation. The same levels of fibrosis entropy and density underlie the pro-RD propensity in both pre- and post-ablation substrates.

KW - Atrial fibrillation

KW - Cardiac MRI

KW - Drivers

KW - Fibrosis

KW - Modelling

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DO - 10.1093/cvr/cvz083

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EP - 1765

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JF - Cardiovascular Research

SN - 0008-6363

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