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Can dark core lesions on cardiac MRI shed some light on recurrence after VT ablation?

Catheter ablation of ventricular tachycardia (VT) has been shown to reduce the burden of VT and implantable cardioverter‐defibrillator (ICD) shocks in patients with structural heart disease. The role of this procedure in the management of VT has continued to develop rapidly, due to advances in ablation technology and imaging techniques, in conjunction with an evolving understanding of the underlying arrhythmogenic substrate. However, despite modern ablation techniques, VT recurrence remains common (rates of up to 40%). There are three fundamental reasons for recurrence after ablation including misidentification of critical portions of the VT circuit, ineffective ablation of those components (i.e., deep intramural substrate), or evolution of the substrate itself. Indeed, the precise localization of critical components of the VT re‐entrant circuit can be challenging, at times due to hemodynamic intolerance of VT, inability to induce VT, or inability to record signals from these critical sites. As a result, there has been increasing interest in the development and integration of advanced imaging technologies, such as cardiac magnetic resonance (CMR) imaging, to identify potential arrhythmogenic substrates without the need for VT induction or mapping. Prospectively identifying VT substrate may improve the safety and efficacy of these procedures, as well as potentially make them more focused and streamlined. Gadolinium contrast agents have a molecular size that permits their distribution in the extracellular space without entering myocardial cells. Compared to normal myocardium, scar tissue contains more extracellular space due to increased collagen deposition, which leads to reduced clearance of gadolinium. When magnetic resonance imaging (MRI) images are obtained after a short delay, hyperenhancement or late gadolinium enhancement (LGE) of areas with increased extracellular space is seen, a finding which has been correlated to scar tissue histologically. The acute myocardial response to radiofrequency ablation results in myocardial necrosis and disruption of blood vessels, a phenomenon known as microvascular obstruction. On CMR, this microvascular obstruction leads to dark areas within the bright hyperenhanced areas of LGE. Previously, evaluations of CMR findings of chronic changes postablation were performed in animal models or in normal myocardium, and not in diseased hearts. Recently, however, Dabbagh et al. described the CMR characteristics of chronic ablation lesions in 17 patients with ischemic cardiomyopathy referred for a second VT ablation. The authors showed that in areas of prior VT ablation, the CMR LGE images (performed on average 30 months after the ablation) showed a dark, confluent core located on the endocardial aspect of the myocardial scar, which they termed dark core lesions (DCLs). These lesions closely correlated with the size of the non‐excitable areas during the repeat ablation (R = .98, p < .001). This study provided a proof‐of‐concept that prior ablation lesions may be visualized using CMR but was unable to explain why chronic ablation lesions in diseased myocardia retain the appearance of microvascular obstruction seen acutely after ablation in normal hearts. Furthermore, this study did not examine the clinical and procedural outcomes of incorporating this data into subsequent ablations. In this issue of the Journal of Cardiovascular Electrophysiology, Ghannam et al. aimed to implement this interesting CMR technique to identify ablation lesions from prior VT ablations and to subsequently correlate this with sites of recurrent VT during repeat ablation. They evaluated 19 patients (94% men) with a history of ischemic VT who underwent a second VT ablation with a CMR performed between the index ablation and the repeat procedure and compared outcomes with 14 patients who had a second ablation but did not undergo CMR. CMRs were performed in close temporal proximity to the second ablation (average of 21 days prior) and were performed on clinical grounds and not as part of the study. The CMRs were analyzed using proprietary software developed at the University of