Septal contraction predicts acute haemodynamic improvement and paced QRS width reduction in cardiac resynchronization therapy.


Journal

European heart journal. Cardiovascular Imaging
ISSN: 2047-2412
Titre abrégé: Eur Heart J Cardiovasc Imaging
Pays: England
ID NLM: 101573788

Informations de publication

Date de publication:
01 08 2020
Historique:
received: 15 06 2019
revised: 08 11 2019
accepted: 10 12 2019
pubmed: 12 1 2020
medline: 29 6 2021
entrez: 12 1 2020
Statut: ppublish

Résumé

Three distinct septal contraction patterns typical for left bundle branch block may be assessed using echocardiography in heart failure patients scheduled for cardiac resynchronization therapy (CRT). The aim of this study was to explore the association between these septal contraction patterns and the acute haemodynamic and electrical response to biventricular pacing (BIVP) in patients undergoing CRT implantation. Thirty-eight CRT candidates underwent speckle tracking echocardiography prior to device implantation. The patients were divided into two groups based on whether their septal contraction pattern was indicative of dyssynchrony (premature septal contraction followed by various amount of stretch) or not (normally timed septal contraction with minimal stretch). CRT implantation was performed under invasive left ventricular (LV) pressure monitoring and we defined acute CRT response as ≥10% increase in LV dP/dtmax. End-diastolic pressure (EDP) and QRS width served as a diastolic and electrical parameter, respectively. LV dP/dtmax improved under BIVP (737 ± 177 mmHg/s vs. 838 ± 199 mmHg/s, P < 0.001) and 26 patients (68%) were defined as acute CRT responders. Patients with premature septal contraction (n = 27) experienced acute improvement in systolic (ΔdP/dtmax: 18.3 ± 8.9%, P < 0.001), diastolic (ΔEDP: -30.6 ± 29.9%, P < 0.001) and electrical (ΔQRS width: -23.3 ± 13.2%, P < 0.001) parameters. No improvement under BIVP was observed in patients (n = 11) with normally timed septal contraction (ΔdP/dtmax: 4.0 ± 7.8%, P = 0.12; ΔEDP: -8.8 ± 38.4%, P = 0.47 and ΔQRS width: -0.9 ± 11.4%, P = 0.79). Septal contraction patterns are an excellent predictor of acute CRT response. Only patients with premature septal contraction experienced acute systolic, diastolic, and electrical improvement under BIVP.

Identifiants

pubmed: 31925420
pii: 5700482
doi: 10.1093/ehjci/jez315
doi:

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

845-852

Commentaires et corrections

Type : CommentIn

Informations de copyright

Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2020. For permissions, please email: journals.permissions@oup.com.

Auteurs

Stian Ross (S)

Department of Cardiology, Center for Cardiological Innovation, Oslo University Hospital, Rikshospitalet, Sognsvannveien 20, Pb 4950 Nydalen, 0424 Oslo, Norway.
University of Oslo, Faculty of Medicine, Institute of Clinical Medicine, Pb 1072 Blindern, 0316 Oslo Norway.

Eirik Nestaas (E)

Department of Cardiology, Center for Cardiological Innovation, Oslo University Hospital, Rikshospitalet, Sognsvannveien 20, Pb 4950 Nydalen, 0424 Oslo, Norway.
University of Oslo, Faculty of Medicine, Institute of Clinical Medicine, Pb 1072 Blindern, 0316 Oslo Norway.
Department of Pediatrics, Vestfold Hospital Trust, Pb 2168, 3103 Tonsberg, Norway.

Erik Kongsgaard (E)

Department of Cardiology, Center for Cardiological Innovation, Oslo University Hospital, Rikshospitalet, Sognsvannveien 20, Pb 4950 Nydalen, 0424 Oslo, Norway.
University of Oslo, Faculty of Medicine, Institute of Clinical Medicine, Pb 1072 Blindern, 0316 Oslo Norway.

Hans H Odland (HH)

Department of Cardiology, Center for Cardiological Innovation, Oslo University Hospital, Rikshospitalet, Sognsvannveien 20, Pb 4950 Nydalen, 0424 Oslo, Norway.
University of Oslo, Faculty of Medicine, Institute of Clinical Medicine, Pb 1072 Blindern, 0316 Oslo Norway.

Trine F Haland (TF)

Department of Cardiology, Center for Cardiological Innovation, Oslo University Hospital, Rikshospitalet, Sognsvannveien 20, Pb 4950 Nydalen, 0424 Oslo, Norway.
University of Oslo, Faculty of Medicine, Institute of Clinical Medicine, Pb 1072 Blindern, 0316 Oslo Norway.

Einar Hopp (E)

Department of Cardiology, Center for Cardiological Innovation, Oslo University Hospital, Rikshospitalet, Sognsvannveien 20, Pb 4950 Nydalen, 0424 Oslo, Norway.
Division of Radiology and Nuclear Medicine, Oslo University Hospital, Rikshospitalet, Sognsvannveien 20, Pb 4950 Nydalen, 0424 Oslo, Norway.

Kristina H Haugaa (KH)

Department of Cardiology, Center for Cardiological Innovation, Oslo University Hospital, Rikshospitalet, Sognsvannveien 20, Pb 4950 Nydalen, 0424 Oslo, Norway.
University of Oslo, Faculty of Medicine, Institute of Clinical Medicine, Pb 1072 Blindern, 0316 Oslo Norway.

Thor Edvardsen (T)

Department of Cardiology, Center for Cardiological Innovation, Oslo University Hospital, Rikshospitalet, Sognsvannveien 20, Pb 4950 Nydalen, 0424 Oslo, Norway.
University of Oslo, Faculty of Medicine, Institute of Clinical Medicine, Pb 1072 Blindern, 0316 Oslo Norway.

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