Three-dimensional transmural mapping to guide ventricular arrhythmia ablation

Idiopathic ventricular arrhythmias (VAs) lead to cardiomyopathy and worsened outcomes whether symptomatic or not^1,2 and are commonly treated by ablation. While VAs from the right and left outflow tracts are straightforward to ablate, this is not true for all locations.² In particular, arrhythmias from the left ventricular summit or interventricular septum, which constitute ~10% of all idiopathic cases, are more difficult to map and ablate.² Accordingly, there is great interest in novel approaches to guide intervention in such patients.

In this issue of Heart Rhythm Journal, Pothenini et al³ report a rigorous approach to transmurally map septal outflow tract and left ventricular summit VAs by combining endocardial recordings, epicardial recordings via the anterior interventricular vein with a 4-F decapolar catheter, and intramural mapping from septal perforating coronary venous branches with a 2-F octapolar catheter. This use of bipolar recording eliminates far-field signals noted on unipolar recordings in a previous report by the same group.⁴ In 4 well-characterized patients, the authors created 3-dimensional (3D) transmural electroanatomic maps of voltage and activation by merging these multisurface mapping data. The resulting elegant electroanatomic maps allowed the authors to directly map endocardial, mid-myocardial, and epicardial activation patterns; better understand arrhythmia circuits; and guide ablation. Each case was acutely successful, although long-term follow-up was not reported.

The authors should be congratulated on their meticulous and thoughtful study. While mid-myocardial mapping using the coronary venous system has been previously reported,⁵ this report extends that literature by creating 3D transmural electroanatomic maps in this limited anatomical region. Notably, the approach revealed intramural sites that could be ablated endocardially or epicardially, yet which likely would not have been detected from those surfaces. In 1 case, intramural electrogram fractionation and scar identified the candidate site that was ablated endocardially, even though the corresponding endocardial signals were recorded after the QRS onset of the premature ventricular complex (and epicardial signals were not early). In cases 2, 3, 4 of this report, ablation at endocardial sites nearest to intramural circuits eliminated arrhythmia, yet these endocardial sites also did not harbor clear arrhythmia signatures.

A major limitation of the report is that it does not outline a strategy to translate these data to definitively guide endocardial or epicardial ablation. For instance, in case 2, a mapped subepicardial focus was treated by endocardial ablation that altered its exit, yet epicardial ablation was required to eliminate it. Mechanistically, this highlights our lack of understanding of the spread of ventricular activation from intramural compared with endocardial or epicardial sources. This may reflect patient-specific fiber angles or breakouts or distributions of scar and likely vary with prematurity of ectopy or rate. Accordingly, the authors’ default ablation approach appeared to be endocardial, followed by empirical determination of whether epicardial (or intramural) ablation would be required. Future work should better define how to use these data to guide ablation.

The authors reported that a distance of mid-myocardial circuits to the endocardium of <8 mm and shorter timing delay from the earliest great cardiac vein to left ventricular endocardial activation were associated with successful endocardial ablation. Others have reported an electrocardiographic Q-wave ratio of <1.45 in lead aVL/aVR and an anatomical distance of <13.5 mm,⁶ a temporal interval of <7 ms between earliest activation in the great cardiac vein and left ventricular endocardium,⁷ and an abrupt V₃ transition on the surface electrocardiogram⁸ as predictors of successful left ventricular endocardial ablation from the aortic interleaflet triangle for arrhythmias with early activation in the distal coronary veins.

Other limitations of the approach are that it can be unwieldy for infrequent premature ventricular complex, like any activation mapping approach. Transmural 3D voltage maps may help guide substrate ablation in these cases. The technique is also limited by the location of the septal branches and their proximity to the site of origin of VA and by epicardial access using coronary vessels (although this could be extended using direct epicardial puncture). These are selected cases, and larger series may better predict cases where the closest endocardial site might not be successful and where other techniques such as half-normal saline irrigation,⁹ bipolar ablation,¹⁰ alcohol injection,¹¹ or intramural needle ablation¹² might be more effective.

In summary, Pothenini et al elegantly illustrated a systemic approach to map septal outflow tract and left ventricular summit VAs to create 3D transmural electroanatomic maps. They illustrated the utility of this technique to guide successful ablation at the nearest endocardial site, even if bereft of sites of early activation, or epicardially in the anterior interventricular vein. This mapping approach could be extended to map epicardially via a direct epicardial puncture and to guide ablation with other techniques such as alcohol injection and intramural needle radiofrequency ablation. They should be congratulated on this work.