Optimal Threshold and Interpatient Variability in Left Atrial Ablation Scar Assessment by Dark-Blood LGE CMR.

BACKGROUND

Dark-blood late gadolinium enhancement (LGE) cardiac magnetic resonance (CMR) has better correlation with bipolar voltage (BiV) to define ablation scar in the left atrium (LA) compared to conventional bright-blood LGE CMR.

OBJECTIVES

This study sought to determine the optimal signal intensity threshold of dark-blood LGE CMR to identify LA ablation scar.

METHODS

In 54 patients scheduled for atrial fibrillation ablation, image intensity ratios (IIRs) were derived from preprocedural dark-blood LGE CMR. In 26 patients without previous ablation, the upper limit of normal was derived from the 95th and 98th percentiles of pooled IIR values. In 28 patients with previous atrial fibrillation ablation, BiV was compared with the corresponding IIR. Receiver-operating characteristics analyses were employed to determine the optimal IIR threshold (ie, the point with the smallest distance to the upper left corner of the receiver-operating characteristics) for LA ablation scar (BiV ≤0.15 mV).

RESULTS

Upper limit of normal corresponded to IIR values 1.16 and 1.21, yielding low sensitivities of 0.32 and 0.09 to detect LA ablation scar. Receiver-operating characteristics analysis of IIR and BiV comparison achieved a median area under the curve of 0.77. Median optimal IIR threshold for LA ablation scar was 1.09, with an average sensitivity of 0.73, specificity of 0.75, and accuracy of 0.71. Median IIR thresholds of 1.00 and 1.10 corresponded to 80% sensitivity and 80% specificity, respectively. There was considerable interpatient variability: optimal IIR thresholds per patient ranged from 1.01 to 1.22.

CONCLUSIONS

The optimal IIR threshold to identify LA ablation scar by dark-blood LGE CMR is 1.09. Because of interpatient variability, the investigators recommend using a lower (1.00) and upper (1.10) threshold to prevent over- or underestimation of ablation scar.

Informations de copyright

Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Funding Support and Author Disclosures This work was supported by the Netherlands Heart Foundation (grant CVON2014-09, RACE V [Reappraisal of Atrial Fibrillation: Interaction Between Hypercoagulability, Electrical Remodeling, and Vascular Destabilisation in the Progression of AF], and grant 01-002-2022-0118, EmbRACE [Electro-Molecular Basis and the Therapeutic Management of Atrial Cardiomyopathy, Fibrillation and Associated Outcomes]), the European Union (grant 860974, ITN Network Personalize AF [Personalized Therapies for Atrial Fibrillation: A Translational Network]; grant 965286, MAESTRIA [Machine Learning Artificial Intelligence Early Detection Stroke Atrial Fibrillation]; and grant 952166, REPAIR [Restoring Cardiac Mechanical Function by Polymeric Artificial Muscular Tissue]). Dr Wildberger has received institutional grants via Clinical Trial Center Maastricht from Bard, Bayer, Boston, Brainlab, GE, Gleamer, Philips, and Siemens; and has received speaker fees via Maastricht UMC+ for serving on the Speakers Bureaus of Bayer and Siemens. Dr Schotten has received consulting fees or honoraria from Università della Svizzera Italiana, Roche Diagnostics, EP Solutions Inc , Johnson & Johnson Medical Limited, and Bayer Healthcare; and is cofounder and shareholder of YourRhythmics BV, a spin-off company of the University Maastricht. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.