Heart failure with preserved ejection fraction or non-cardiac dyspnea in paroxysmal atrial fibrillation: The role of left atrial strain.


Journal

International journal of cardiology
ISSN: 1874-1754
Titre abrégé: Int J Cardiol
Pays: Netherlands
ID NLM: 8200291

Informations de publication

Date de publication:
15 01 2021
Historique:
received: 30 03 2020
revised: 25 06 2020
accepted: 26 08 2020
pubmed: 4 9 2020
medline: 28 5 2021
entrez: 4 9 2020
Statut: ppublish

Résumé

Diagnosis of heart failure with preserved ejection fraction (HFpEF) in patients with dyspnea and paroxysmal atrial fibrillation (AF) is challenging. Speckle tracking-derived left atrial strain (LAS) provides an accurate estimate of left ventricular (LV) filling pressures and left atrial (LA) phasic function. However, data on clinical utility of LAS in patients with dyspnea and AF are scarce. To assess relationship between the LAS and the probability of HFpEF in patients with dyspnea and paroxysmal AF. The study included 205 consecutive patients (62 ± 10 years, 58% males) with dyspnea (NYHA≥II), paroxysmal AF and preserved LV ejection fraction (≥50%), who underwent speckle tracking echocardiography during sinus rhythm. Probability of HFpEF was estimated using H Patients with high probability of HFpEF were significantly older, had higher body mass index, NT-proBNP, E/e', pulmonary artery pressure and larger LA volume index than patients in low-to-intermediate probability groups (all p < 0.05). All components of LAS and LA strain rate showed proportional impairment with increasing probability of HFpEF (all p < 0.05). Out of the speckle tracking-derived parameters, reservoir LAS showed the largest area under the curve (AUC = 0.78, p < 0.001) and the strongest independent predictive value (OR: 1.22, 95% CI 1.08-1.38) to identify patients with high probability of HFpEF. Reservoir LAS shows a high diagnostic performance to distinguish HFpEF from non-cardiac causes of dyspnea in symptomatic patients with paroxysmal AF.

Sections du résumé

BACKGROUND
Diagnosis of heart failure with preserved ejection fraction (HFpEF) in patients with dyspnea and paroxysmal atrial fibrillation (AF) is challenging. Speckle tracking-derived left atrial strain (LAS) provides an accurate estimate of left ventricular (LV) filling pressures and left atrial (LA) phasic function. However, data on clinical utility of LAS in patients with dyspnea and AF are scarce.
OBJECTIVE
To assess relationship between the LAS and the probability of HFpEF in patients with dyspnea and paroxysmal AF.
METHODS
The study included 205 consecutive patients (62 ± 10 years, 58% males) with dyspnea (NYHA≥II), paroxysmal AF and preserved LV ejection fraction (≥50%), who underwent speckle tracking echocardiography during sinus rhythm. Probability of HFpEF was estimated using H
RESULTS
Patients with high probability of HFpEF were significantly older, had higher body mass index, NT-proBNP, E/e', pulmonary artery pressure and larger LA volume index than patients in low-to-intermediate probability groups (all p < 0.05). All components of LAS and LA strain rate showed proportional impairment with increasing probability of HFpEF (all p < 0.05). Out of the speckle tracking-derived parameters, reservoir LAS showed the largest area under the curve (AUC = 0.78, p < 0.001) and the strongest independent predictive value (OR: 1.22, 95% CI 1.08-1.38) to identify patients with high probability of HFpEF.
CONCLUSIONS
Reservoir LAS shows a high diagnostic performance to distinguish HFpEF from non-cardiac causes of dyspnea in symptomatic patients with paroxysmal AF.

Identifiants

pubmed: 32882295
pii: S0167-5273(20)33720-7
doi: 10.1016/j.ijcard.2020.08.093
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

161-167

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2020 Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest None declared.

Auteurs

A Katbeh (A)

Cardiovascular Center Aalst, OLV Clinic Aalst, Aalst, Belgium; Department of Advanced Biomedical Sciences, University of Naples Federico II, Naples, Italy.

T De Potter (T)

Cardiovascular Center Aalst, OLV Clinic Aalst, Aalst, Belgium.

P Geelen (P)

Cardiovascular Center Aalst, OLV Clinic Aalst, Aalst, Belgium.

G Di Gioia (G)

Cardiovascular Center Aalst, OLV Clinic Aalst, Aalst, Belgium; Department of Advanced Biomedical Sciences, University of Naples Federico II, Naples, Italy.

M Kodeboina (M)

Cardiovascular Center Aalst, OLV Clinic Aalst, Aalst, Belgium; Department of Advanced Biomedical Sciences, University of Naples Federico II, Naples, Italy.

Z Balogh (Z)

Cardiovascular Center Aalst, OLV Clinic Aalst, Aalst, Belgium.

M Albano (M)

Cardiovascular Center Aalst, OLV Clinic Aalst, Aalst, Belgium.

M Vanderheyden (M)

Cardiovascular Center Aalst, OLV Clinic Aalst, Aalst, Belgium.

J Bartunek (J)

Cardiovascular Center Aalst, OLV Clinic Aalst, Aalst, Belgium.

E Barbato (E)

Cardiovascular Center Aalst, OLV Clinic Aalst, Aalst, Belgium; Department of Advanced Biomedical Sciences, University of Naples Federico II, Naples, Italy.

G Van Camp (G)

Cardiovascular Center Aalst, OLV Clinic Aalst, Aalst, Belgium.

M Penicka (M)

Cardiovascular Center Aalst, OLV Clinic Aalst, Aalst, Belgium. Electronic address: martin.penicka@olvz-aalst.be.

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