Lesion Delivery and Scar Formation in Catheter Ablation for Atrial Fibrillation The DECAAF II Trial.

Atrial fibrillation atrial fibrosis cardiac magnetic resonance imaging catheter ablation lesion delivery

Journal

Heart rhythm
ISSN: 1556-3871
Titre abrégé: Heart Rhythm
Pays: United States
ID NLM: 101200317

Informations de publication

Date de publication:
06 Sep 2024
Historique:
received: 18 04 2024
revised: 27 08 2024
accepted: 29 08 2024
medline: 9 9 2024
pubmed: 9 9 2024
entrez: 8 9 2024
Statut: aheadofprint

Résumé

The DECAAF-II randomized trial showed no difference in AF recurrence with additional delayed enhancement MRI (DE-MRI) fibrosis-targeted ablation to pulmonary vein isolation (PVI) in persistent AF. We evaluated the impact of lesion delivery on ablation-induced scarring and AF recurrence. Lesions delivered, targeting fibrotic and non-fibrotic areas identified from pre-ablation DE-MRI, were studied in relation to ablation-induced scarring on 3-months DE-MRI, including their association with arrhythmia recurrence. 593 patients, treated with radiofrequency were analyzed: 293 underwent PVI and 300 underwent additional fibrosis-guided ablation. Lesion analysis showed that 80.9% in the MRI fibrosis-guided group vs 16.5% in the PVI group (p<0.001), had ≥ 40% of baseline fibrosis targeted. MRI assessment of ablation-induced scar showed that 44.8% of fibrosis-guided ablation and 15.5% of PVI had ≥ 40% of their fibrosis covered by scar (P<0.001), demonstrating a significant attenuation from lesions delivered to scar formed. In the overall population, fibrosis coverage with scar was not associated with recurrence (HR 0.90, 95% confidence interval [CI] 0.80-1.01, p = 0.08 per 20% increase). In patients with baseline fibrosis <20%, fibrosis coverage with scar was associated with lower recurrence than PVI (HR 0.85; 95% CI [0.73-0.97]; p=0.03), whereas the association was not significant when baseline fibrosis ≥20% (HR 0.97; [0.80-1.17], p=0.77). Significant center variation was observed in fibrosis targeting and coverage with scarring. Radiofrequency ablation lesions do not uniformly result in scar formation. Post hoc analysis suggests reduced arrhythmia recurrence when ablation-induced scarring covers fibrotic regions in patients with low baseline fibrosis.

Sections du résumé

BACKGROUND BACKGROUND
The DECAAF-II randomized trial showed no difference in AF recurrence with additional delayed enhancement MRI (DE-MRI) fibrosis-targeted ablation to pulmonary vein isolation (PVI) in persistent AF.
OBJECTIVES OBJECTIVE
We evaluated the impact of lesion delivery on ablation-induced scarring and AF recurrence.
METHODS METHODS
Lesions delivered, targeting fibrotic and non-fibrotic areas identified from pre-ablation DE-MRI, were studied in relation to ablation-induced scarring on 3-months DE-MRI, including their association with arrhythmia recurrence.
RESULTS RESULTS
593 patients, treated with radiofrequency were analyzed: 293 underwent PVI and 300 underwent additional fibrosis-guided ablation. Lesion analysis showed that 80.9% in the MRI fibrosis-guided group vs 16.5% in the PVI group (p<0.001), had ≥ 40% of baseline fibrosis targeted. MRI assessment of ablation-induced scar showed that 44.8% of fibrosis-guided ablation and 15.5% of PVI had ≥ 40% of their fibrosis covered by scar (P<0.001), demonstrating a significant attenuation from lesions delivered to scar formed. In the overall population, fibrosis coverage with scar was not associated with recurrence (HR 0.90, 95% confidence interval [CI] 0.80-1.01, p = 0.08 per 20% increase). In patients with baseline fibrosis <20%, fibrosis coverage with scar was associated with lower recurrence than PVI (HR 0.85; 95% CI [0.73-0.97]; p=0.03), whereas the association was not significant when baseline fibrosis ≥20% (HR 0.97; [0.80-1.17], p=0.77). Significant center variation was observed in fibrosis targeting and coverage with scarring.
CONCLUSIONS CONCLUSIONS
Radiofrequency ablation lesions do not uniformly result in scar formation. Post hoc analysis suggests reduced arrhythmia recurrence when ablation-induced scarring covers fibrotic regions in patients with low baseline fibrosis.

Identifiants

pubmed: 39245248
pii: S1547-5271(24)03288-0
doi: 10.1016/j.hrthm.2024.08.062
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2024. Published by Elsevier Inc.

Auteurs

Nazem Akoum (N)

Cardiology Department, University of Washington Medical Center, Seattle, WA, United States.

Mario Mekhael (M)

Cardiology Department, Tulane University School of Medicine, New Orleans, LA, United States.

Felipe Bisbal (F)

Heart Institute, University Hospital Germans Trias i Pujol, Barcelona, Spain.

Oussama Wazni (O)

Cleveland Clinic, Cleveland, OH, United States.

Christopher McGann (C)

Swedish Heart Center, Seattle, Washington, United States.

Hyejung Lee (H)

University of Utah, Salt Lake City, UT, United States.

Tyler Bardsley (T)

University of Utah, Salt Lake City, UT, United States.

Tom Greene (T)

University of Utah, Salt Lake City, UT, United States.

J Michael Dean (JM)

University of Utah, Salt Lake City, UT, United States.

Lilas Dagher (L)

Cardiology Department, Tulane University School of Medicine, New Orleans, LA, United States.

Eugene Kholmovski (E)

Cardiology Department, Johns Hopkins Medicine, Baltimore, MD, United States.

Moussa Mansour (M)

Cardiology Department, Massachusetts General Hospital, Boston, MA, United States.

Francis Marchlinski (F)

Cardiology Department, University of Pennsylvania, Philadelphia, Pennsylvania, United States.

David Wilber (D)

Cardiology Department, Loyola University Chicago, Chicago, IL, United States.

Gerhard Hindricks (G)

Cardiology Department, Leipzig University, Leipzig, Germany.

Christian Mahnkopf (C)

Klinikum Coburg, Coburg, Germany.

Darryl Wells (D)

Swedish Heart Center, Seattle, Washington, United States.

Pierre Jaïs (P)

Cardiology Department, Segalen University, Bordeaux, France.

Prashanthan Sanders (P)

Cardiology Department, Adelaide Medical School, Adelaide, Australia.

Johannes Brachmann (J)

Klinikum Coburg, Coburg, Germany.

Jeroen J Bax (JJ)

Cardiology Department, Leiden University Medical Center, Leiden, Netherlands and Cardiology Department, Turku Heart Center, Turku, Finland.

Leonie Morrison- de Boer (LM)

University of Utah, Salt Lake City, UT, United States.

Thomas Deneke (T)

Heart Center Bad Neustadt, Bad Neustadt, Germany.

Hugh Calkins (H)

Swedish Heart Center, Seattle, Washington, United States.

Christian Sohns (C)

Heart and Diabetes Center NRW, Bad Oeynhausen, Germany.

Nassir Marrouche (N)

Cardiology Department, Tulane University School of Medicine, New Orleans, LA, United States. Electronic address: nmarrouche@tulane.edu.

Classifications MeSH