Tissue characterization of acute lesions during cardiac magnetic resonance-guided ablation of cavo-tricuspid isthmus-dependent atrial flutter: a feasibility study.

CMR-guided ablation T1 mapping atrial flutter ablation cardiac magnetic resonance imaging interventional MRI tissue characterization

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:
29 Dec 2023
Historique:
received: 11 08 2023
revised: 18 10 2023
accepted: 28 11 2023
medline: 29 12 2023
pubmed: 29 12 2023
entrez: 29 12 2023
Statut: aheadofprint

Résumé

To characterize acute lesions during cardiac magnetic resonance (CMR)-guided radiofrequency (RF) ablation of cavo-tricuspid isthmus (CTI)-dependent atrial flutter by combining T2-weighted imaging (T2WI), T1 mapping, first-pass perfusion, and late gadolinium enhancement (LGE) imaging. CMR-guided catheter ablation offers a unique opportunity to investigate acute ablation lesions. Until present, studies only used T2WI and LGE CMR to assess acute lesions. Fifteen patients with CTI-dependent atrial flutter scheduled for CMR-guided RF ablation were prospectively enrolled. Directly after achieving bidirectional block of the CTI line, CMR imaging was performed using: T2WI (n = 15), T1 mapping (n = 10), first-pass perfusion (n = 12), and LGE (n = 12) imaging. In case of acute reconnection, additional RF ablation was performed. In all patients, T2WI demonstrated oedema in the ablation region. Right atrial T1 mapping was feasible and could be analysed with a high inter-observer agreement (r = 0.931, ICC 0.921). The increase in T1 values post-ablation was significantly lower in regions showing acute reconnection compared with regions without reconnection [37 ± 90 ms vs. 115 ± 69 ms (P = 0.014), and 3.9 ± 9.0% vs. 11.1 ± 6.8% (P = 0.022)]. Perfusion defects were present in 12/12 patients. The LGE images demonstrated hyper-enhancement with a central area of hypo-enhancement in 12/12 patients. Tissue characterization of acute lesions during CMR-guided CTI-dependent atrial flutter ablation demonstrates oedema, perfusion defects, and necrosis with a core of microvascular damage. Right atrial T1 mapping is feasible, and may identify regions of acute reconnection that require additional RF ablation.

Identifiants

pubmed: 38156446
pii: 7491178
doi: 10.1093/ehjci/jead334
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Maastricht University Medical Centre+
Organisme : Nederlandse Vereniging voor Wetenschappelijk Onderzoek

Informations de copyright

© The Author(s) 2023. Published by Oxford University Press on behalf of the European Society of Cardiology.

Déclaration de conflit d'intérêts

Conflict of interest: J.S. is an employee of Philips Healthcare. The other authors have no conflicts of interest relating to this article.

Auteurs

G P Bijvoet (GP)

Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Universiteitssingel 50, 6229 ER, Maastricht, The Netherlands.
Department of Cardiology, Maastricht University Medical Center, P.Debyelaan 25, PO Box 5800, 6202 AZ Maastricht, The Netherlands.

H M J M Nies (HMJM)

Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Universiteitssingel 50, 6229 ER, Maastricht, The Netherlands.
Department of Radiology and Nuclear Medicine, Maastricht University Medical Center, Maastricht, The Netherlands.

R J Holtackers (RJ)

Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Universiteitssingel 50, 6229 ER, Maastricht, The Netherlands.
Department of Radiology and Nuclear Medicine, Maastricht University Medical Center, Maastricht, The Netherlands.

B M Martens (BM)

Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Universiteitssingel 50, 6229 ER, Maastricht, The Netherlands.
Department of Radiology and Nuclear Medicine, Maastricht University Medical Center, Maastricht, The Netherlands.

J Smink (J)

Department of Clinical Research, Philips Healthcare, Best, The Netherlands.

D Linz (D)

Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Universiteitssingel 50, 6229 ER, Maastricht, The Netherlands.
Department of Cardiology, Maastricht University Medical Center, P.Debyelaan 25, PO Box 5800, 6202 AZ Maastricht, The Netherlands.
Faculty of Health and Medical Sciences, Department of Biomedical Sciences, University of Copenhagen, Copenhagen, Denmark.
Department of Cardiology, Radboud University Medical Center, Nijmegen, The Netherlands.

K Vernooy (K)

Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Universiteitssingel 50, 6229 ER, Maastricht, The Netherlands.
Department of Cardiology, Maastricht University Medical Center, P.Debyelaan 25, PO Box 5800, 6202 AZ Maastricht, The Netherlands.

J E Wildberger (JE)

Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Universiteitssingel 50, 6229 ER, Maastricht, The Netherlands.
Department of Radiology and Nuclear Medicine, Maastricht University Medical Center, Maastricht, The Netherlands.

R Nijveldt (R)

Department of Cardiology, Radboud University Medical Center, Nijmegen, The Netherlands.

S M Chaldoupi (SM)

Department of Cardiology, Maastricht University Medical Center, P.Debyelaan 25, PO Box 5800, 6202 AZ Maastricht, The Netherlands.

C Mihl (C)

Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Universiteitssingel 50, 6229 ER, Maastricht, The Netherlands.
Department of Radiology and Nuclear Medicine, Maastricht University Medical Center, Maastricht, The Netherlands.

Classifications MeSH