Tissue characterisation of acute ablation lesions in the right atrium during CMR-guided atrial flutter ablation
Authors: Bijvoet G P , Nies H M J M , Holtackers R J , Martens B M , Smink J , Linz D , Vernooy K , Wildberger J E , Nijveldt R , Chaldoupi S M , Mihl C 
Published: June 2023

Abstract

Funding Acknowledgements
Type of funding sources: None.

Background
Cardiac magnetic resonance (CMR)-guided ablation therapy offers a unique opportunity and incentive to investigate acute ablation lesions. Until present, human studies only used T2-weighted imaging (T2WI) and late gadolinium enhancement (LGE) to assess acute ablation lesions.

Purpose
To investigate the tissue characteristics of acute ablation lesions during CMR-guided atrial flutter ablation, by combining T2WI and LGE with first-pass perfusion and T1 mapping.

Methods
Thirteen patients with typical isthmus-dependent atrial flutter were prospectively enrolled and treated with CMR-guided ablation. Pre-ablation tissue characterisation consisted of T2WI and T1 mapping. Postablation imaging was performed directly after application of the primary ablation lesions and included T2WI (n=12), first-pass perfusion (n=9), LGE (n=9) and T1 mapping (n=7). For analysis of T2WI an edema ratio (ER; i.e. the signal intensity ratio between myocardium and reference skeletal muscle) &gt; 2.0 was considered indicative of edema. Post-processing comprised native T1 measurements in three regions of the ablation line (near the tricuspid annulus, mid region, near the caval vein) on pre- and post-ablation images by two independent observers. For each region, the change in T1 value was expressed as the absolute increase (in ms) and the relative increase (in %). A third observer, blinded to the CMR results, reviewed which region(s) had required additional RF lesions after post-ablation CMR imaging.

Results
In 12 out of 13 patients CMR-guided atrial flutter ablation was successful, resulting in bidirectional conduction block. In 1 patient the ablation procedure was completed in the conventional electrophysiology lab, hampering acute post-ablation imaging. In all patients T2WI demonstrated edema in the ablation region. The ER increased from 1.6 ± 0.3 to 3.3 ± 0.5 post-ablation (p&lt;0.001). Perfusion defects were present in 9/9 patients. The LGE images demonstrated hyperenhancement with a central area of hypo-enhancement in 9/9 patients, suggestive of ablation necrosis and previously reported areas of microvascular damage and hemorrhage. Right atrial T1 mapping was feasible in 20/21 regions (in 1 case artifacts from the adjacent catheter hampered analysis) and reproducible (r 0.981, ICC 0.939). The post-ablation increase in T1 value was significantly different between regions that did (n=10) and did not (n=10) require additional RF lesions, T1 increase was 46 ± 90ms versus 133 ± 69ms (p = 0.026), and 4.7 ± 9.1% versus 13.2 ± 6.8% (p = 0.028) respectively.

Conclusion
CMR tissue characterisation of acute ablation lesions during CMR-guided atrial flutter ablation demonstrates edema, perfusion defects, and necrosis with a core of microvascular damage. Atrial T1 mapping of the acute ablation lesion is feasible and reproducible, and might distinguish regions that require additional RF applications.