Easily available ECG and echocardiographic parameters for prediction of left atrial remodeling and atrial fibrillation recurrence after pulmonary vein isolation: A multicenter study.


Journal

Journal of cardiovascular electrophysiology
ISSN: 1540-8167
Titre abrégé: J Cardiovasc Electrophysiol
Pays: United States
ID NLM: 9010756

Informations de publication

Date de publication:
06 2021
Historique:
revised: 07 02 2021
received: 15 10 2020
accepted: 14 02 2021
pubmed: 28 3 2021
medline: 11 8 2021
entrez: 27 3 2021
Statut: ppublish

Résumé

The assessment of noninvasive markers of left atrial (LA) low-voltage substrate (LVS) enables the identification of atrial fibrillation (AF) patients at risk for arrhythmia recurrence after pulmonary vein isolation (PVI). In this prospective multicenter study, 292 consecutive AF patients (72% male, 62 ± 11 years, 65% persistent AF) underwent high-density LA voltage mapping in sinus rhythm. LA-LVS (<0.5 mV) was considered as significant at 2 cm Significant LA-LVS was identified in 123 (42%) patients. The amplified sinus P-wave duration (APWD) best predicted LA-LVS, with a 148-ms value providing the best-balanced sensitivity (0.81) and specificity (0.88). An APWD over 160 ms was associated with LA-LVS in 96% of patients, whereas an APWD under 145 ms in 15%. Remaining gray zones improved their accuracy by introduction of systolic pulmonary artery pressure (sPAP) of 35 mmHg or above, age, and sex. According to COX regression, the risk of arrhythmia recurrence 12 months following PVI was twofold and threefold higher in patients with APWD 145-160 and over 160 ms, compared to APWD under 145 ms. Integration of pulmonary hypertension further improved the outcome prediction in the intermediate APWD group: Patients with APWD 145-160 ms and normal sPAP had similar outcome than patients with APWD under 145 ms (hazard ratio [HR] 1.62, p = .14), whereas high sPAP implied worse outcome (HR 2.56, p < .001). The APWD identifies LA-LVS and risk for arrhythmia recurrence after PVI. Our prediction model becomes optimized by means of integration of the pulmonary artery pressure.

Sections du résumé

BACKGROUND
The assessment of noninvasive markers of left atrial (LA) low-voltage substrate (LVS) enables the identification of atrial fibrillation (AF) patients at risk for arrhythmia recurrence after pulmonary vein isolation (PVI).
METHODS
In this prospective multicenter study, 292 consecutive AF patients (72% male, 62 ± 11 years, 65% persistent AF) underwent high-density LA voltage mapping in sinus rhythm. LA-LVS (<0.5 mV) was considered as significant at 2 cm
RESULTS
Significant LA-LVS was identified in 123 (42%) patients. The amplified sinus P-wave duration (APWD) best predicted LA-LVS, with a 148-ms value providing the best-balanced sensitivity (0.81) and specificity (0.88). An APWD over 160 ms was associated with LA-LVS in 96% of patients, whereas an APWD under 145 ms in 15%. Remaining gray zones improved their accuracy by introduction of systolic pulmonary artery pressure (sPAP) of 35 mmHg or above, age, and sex. According to COX regression, the risk of arrhythmia recurrence 12 months following PVI was twofold and threefold higher in patients with APWD 145-160 and over 160 ms, compared to APWD under 145 ms. Integration of pulmonary hypertension further improved the outcome prediction in the intermediate APWD group: Patients with APWD 145-160 ms and normal sPAP had similar outcome than patients with APWD under 145 ms (hazard ratio [HR] 1.62, p = .14), whereas high sPAP implied worse outcome (HR 2.56, p < .001).
CONCLUSIONS
The APWD identifies LA-LVS and risk for arrhythmia recurrence after PVI. Our prediction model becomes optimized by means of integration of the pulmonary artery pressure.

Identifiants

pubmed: 33772926
doi: 10.1111/jce.15013
doi:

Types de publication

Journal Article Multicenter Study Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1584-1593

Informations de copyright

© 2021 Wiley Periodicals LLC.

Références

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Auteurs

Zoraida Moreno-Weidmann (Z)

Arrhythmia Unit, Department of Cardiology, Hospital Universitario Sant Pau, Barcelona, Spain.
Arrhythmia Unit, Department of Cardiology, Universitäts Herzzentrum Freiburg-Bad Krozingen, Bad Krozingen, Germany.

Björn Müller-Edenborn (B)

Arrhythmia Unit, Department of Cardiology, Universitäts Herzzentrum Freiburg-Bad Krozingen, Bad Krozingen, Germany.

Amir S Jadidi (AS)

Arrhythmia Unit, Department of Cardiology, Universitäts Herzzentrum Freiburg-Bad Krozingen, Bad Krozingen, Germany.

Victor Bazan-Gelizo (V)

Arrhythmia Unit, Department of Cardiology, Hospital Universitario Sant Pau, Barcelona, Spain.

Juan Chen (J)

Arrhythmia Unit, Department of Cardiology, Universitäts Herzzentrum Freiburg-Bad Krozingen, Bad Krozingen, Germany.

Chan-Il Park (CI)

Arrhythmia Unit, Department of Cardiology, Hôpital de la Tour, Geneva, Switzerland.

Hari Vivekanantham (H)

Arrhythmia Unit, Department of Cardiology, Hôpital de la Tour, Geneva, Switzerland.

Enrique Rodriguez-Font (E)

Arrhythmia Unit, Department of Cardiology, Hospital Universitario Sant Pau, Barcelona, Spain.

Concepción Alonso-Martín (C)

Arrhythmia Unit, Department of Cardiology, Hospital Universitario Sant Pau, Barcelona, Spain.

José M Guerra (JM)

Arrhythmia Unit, Department of Cardiology, Hospital Universitario Sant Pau, Barcelona, Spain.

Bieito Campos-García (B)

Arrhythmia Unit, Department of Cardiology, Hospital Universitario Sant Pau, Barcelona, Spain.

Hildemari Espinosa-Viamonte (H)

Arrhythmia Unit, Department of Cardiology, Hospital Universitario Sant Pau, Barcelona, Spain.

Stéphane Combes (S)

Arrhythmia Unit, Department of Cardiology, Clinique Pasteur, Toulouse, France.

Jean-Paul Albenque (JP)

Arrhythmia Unit, Department of Cardiology, Clinique Pasteur, Toulouse, France.

Martin Eichenlaub (M)

Arrhythmia Unit, Department of Cardiology, Universitäts Herzzentrum Freiburg-Bad Krozingen, Bad Krozingen, Germany.

Benoit Guy-Moyat (B)

Arrhythmia Unit, Department of Cardiology, CHU, Limoges, France.

Luc de Roy (L)

Arrhythmia Unit, Department of Cardiology, CHU, Namur, Belgium.

Pascal Defaye (P)

Arrhythmia Unit, Department of Cardiology, CHU, Grenoble-Alpes, France.

Serge Boveda (S)

Arrhythmia Unit, Department of Cardiology, Clinique Pasteur, Toulouse, France.

Thomas Arentz (T)

Arrhythmia Unit, Department of Cardiology, Universitäts Herzzentrum Freiburg-Bad Krozingen, Bad Krozingen, Germany.

Xavier Viñolas (X)

Arrhythmia Unit, Department of Cardiology, Hospital Universitario Sant Pau, Barcelona, Spain.

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