Catheter ablation of atrial fibrillation in cardiac amyloidosis.


Journal

Pacing and clinical electrophysiology : PACE
ISSN: 1540-8159
Titre abrégé: Pacing Clin Electrophysiol
Pays: United States
ID NLM: 7803944

Informations de publication

Date de publication:
09 2020
Historique:
received: 15 03 2020
revised: 20 05 2020
accepted: 21 06 2020
pubmed: 24 6 2020
medline: 13 10 2021
entrez: 24 6 2020
Statut: ppublish

Résumé

Cardiac amyloidosis is a progressive infiltrative disease involving deposition of amyloid fibrils in the myocardium and cardiac conduction system that frequently manifests with heart failure (HF) and arrhythmias, most frequently atrial fibrillation (AF), atrial flutter (AFL), and atrial tachycardia (AT). We performed an observational retrospective study of patients with a diagnosis of cardiac amyloid who underwent catheter ablation at our institution between January 1, 2011 and December 1, 2018. Patient demographics, procedural characteristics, and outcomes were determined by manual chart review. A total of 13 catheter ablations were performed over the study period in patients with cardiac amyloidosis, including 10 AT/AF/AFL ablations and three atrioventricular nodal ablations. Left ventricular ejection fraction was lower at the time of AV node ablation than catheter ablation of AT/AF/AFL (23% vs 40%, P = .003). Cardiac amyloid was diagnosed based on the results of preablation cardiac MRI results in the majority of patients (n = 7, 70%). The HV interval was prolonged at 60 ± 15 ms and did not differ significantly between AV nodal ablation patients and AT/AF/AFL ablation patients (69 ± 18 ms vs 57 ± 14 ms, P = .36). The majority of patients undergoing AT/AF/AFL ablation had persistent AF (n = 7, 70%) and NYHA class II (n = 5, 50%) or III (n = 5, 50%) HF symptoms, whereas patients undergoing AV node ablation were more likely to have class IV HF (n = 2, 66%, P = .014). Arrhythmia-free survival in CA patients after catheter ablation of AT/AF/AFL was 40% at 1 year and 20% at 2 years. Catheter ablation of AT/AF/AFL may be a feasible strategy for appropriately selected patients with early to mid-stage CA, whereas AV node ablation may be more appropriate in patients with advanced-stage CA.

Sections du résumé

BACKGROUND
Cardiac amyloidosis is a progressive infiltrative disease involving deposition of amyloid fibrils in the myocardium and cardiac conduction system that frequently manifests with heart failure (HF) and arrhythmias, most frequently atrial fibrillation (AF), atrial flutter (AFL), and atrial tachycardia (AT).
METHODS
We performed an observational retrospective study of patients with a diagnosis of cardiac amyloid who underwent catheter ablation at our institution between January 1, 2011 and December 1, 2018. Patient demographics, procedural characteristics, and outcomes were determined by manual chart review.
RESULTS
A total of 13 catheter ablations were performed over the study period in patients with cardiac amyloidosis, including 10 AT/AF/AFL ablations and three atrioventricular nodal ablations. Left ventricular ejection fraction was lower at the time of AV node ablation than catheter ablation of AT/AF/AFL (23% vs 40%, P = .003). Cardiac amyloid was diagnosed based on the results of preablation cardiac MRI results in the majority of patients (n = 7, 70%). The HV interval was prolonged at 60 ± 15 ms and did not differ significantly between AV nodal ablation patients and AT/AF/AFL ablation patients (69 ± 18 ms vs 57 ± 14 ms, P = .36). The majority of patients undergoing AT/AF/AFL ablation had persistent AF (n = 7, 70%) and NYHA class II (n = 5, 50%) or III (n = 5, 50%) HF symptoms, whereas patients undergoing AV node ablation were more likely to have class IV HF (n = 2, 66%, P = .014). Arrhythmia-free survival in CA patients after catheter ablation of AT/AF/AFL was 40% at 1 year and 20% at 2 years.
CONCLUSIONS
Catheter ablation of AT/AF/AFL may be a feasible strategy for appropriately selected patients with early to mid-stage CA, whereas AV node ablation may be more appropriate in patients with advanced-stage CA.

Identifiants

pubmed: 32573789
doi: 10.1111/pace.13992
doi:

Types de publication

Journal Article Observational Study

Langues

eng

Sous-ensembles de citation

IM

Pagination

913-921

Informations de copyright

© 2020 Wiley Periodicals LLC.

Références

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Auteurs

Eric Black-Maier (E)

Division of Electrophysiology, Duke University Medical Center, Durham, North Carolina.

Michael Rehorn (M)

Division of Electrophysiology, Duke University Medical Center, Durham, North Carolina.

Rahul Loungani (R)

Division of Cardiology, Duke University Medical Center, Durham, North Carolina.

Daniel J Friedman (DJ)

Section of Cardiac Electrophysiology, Yale School of Medicine, New Haven, Connecticut.

Fawaz Alenezi (F)

Division of Cardiology, Duke University Medical Center, Durham, North Carolina.

Kyle Geurink (K)

Department of Medicine, Duke University Medical Center, Durham, North Carolina.

Sean D Pokorney (SD)

Division of Electrophysiology, Duke University Medical Center, Durham, North Carolina.

James P Daubert (JP)

Division of Electrophysiology, Duke University Medical Center, Durham, North Carolina.

Albert Y Sun (AY)

Division of Electrophysiology, Duke University Medical Center, Durham, North Carolina.

Brett D Atwater (BD)

Division of Electrophysiology, Duke University Medical Center, Durham, North Carolina.

Kevin P Jackson (KP)

Division of Electrophysiology, Duke University Medical Center, Durham, North Carolina.

Donald D Hegland (DD)

Division of Electrophysiology, Duke University Medical Center, Durham, North Carolina.

Kevin L Thomas (KL)

Division of Electrophysiology, Duke University Medical Center, Durham, North Carolina.

Tristram D Bahnson (TD)

Division of Electrophysiology, Duke University Medical Center, Durham, North Carolina.

Michel G Khouri (MG)

Division of Cardiology, Duke University Medical Center, Durham, North Carolina.

Jonathan P Piccini (JP)

Division of Electrophysiology, Duke University Medical Center, Durham, North Carolina.

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