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Review
. 2024 Mar-Apr;24(2):84-93.
doi: 10.1016/j.ipej.2024.02.002. Epub 2024 Feb 8.

Epicardial ablation of ventricular tachycardia in ischemic cardiomyopathy: A review and local experience

Affiliations
Review

Epicardial ablation of ventricular tachycardia in ischemic cardiomyopathy: A review and local experience

Henri Roukoz et al. Indian Pacing Electrophysiol J. 2024 Mar-Apr.

Abstract

Myocardial scar in ischemic cardiomyopathy is predominantly endocardial, however, between 5% and 15% of these patients have an arrhythmogenic epicardial substrate. Percutaneous epicardial ablation should be considered in patients with ICM and VT especially if they failed an endocardial ablation. Simultaneous epicardial and endocardial ablation of VT in ICM may reduce short- and medium-term VT recurrence compared with an endocardial only approach. Cardiac imaging could be used to help guide patient selection for a combined epi-endo approach. Complications related to epicardial access can happen in up to 7% of patients. Epicardial ablation in these patients should be referred to experienced tertiary centers. We review the literature and share interesting cases.

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Conflict of interest statement

Declaration of competing interest Dr Roukoz has received no disclosures related to the content of this manuscript. Dr.Tholakanahalli has no relevant disclosures.

Figures

Fig. 1
Fig. 1
Patient 1 with ICM and VT with 2 previous failed ablations referred to our center for repeat ablation. (A) Intracardiac electrograms during endocardial mapping of VT. A1 shows a presystolic signal, A2 shows a mid-diastolic signal and A3 shows an early diastolic signal. All signals are in the inferior scar. (B) Activation map of the VT, inferior view. (C) Voltage map of the left ventricle, inferior view. Diligent mapping of the small signals (seen in A) within the scar and appropriate annotation generated the activation map in B. Note the far field nature of the early diastolic signal in A3. Entrainment could not be achieved in the isthmus area due to lack of capture even at high output. Ablation at that level terminated the VT but after 15 s of radiofrequency application. The VT could still be induced at slower rate and less sustained about 15 min after.
Fig. 2
Fig. 2
Patient 1's endocardial activation map with endocardial ablation lesions (A) and epicardial voltage map (B). During voltage mapping of the epicardium in sinus rhythm, we could locate a long channel opposing the isthmus mapped endocardialy on the epicardium, shown as late potentials using a decapolar mapping catheter (C). The late potentials are marked with the light blue dots on the voltage map (B).
Fig. 3
Fig. 3
Patient 1's continued epicardial mapping. Two VTs could be induced intermittently but were less sustained. The clinical VT (A) with right bundle branch block morphology and the second left bundle branch morphology VT (B) proves to be the antidromic and orthodromic activation of the same epicardial isthmus as demonstrated by the activation sequence on the decapolar catheter situated on the isthmus previously described (arrows). There is also demonstration of intra-isthmus delay in the proximal end of the isthmus corresponding to an increase in the VT cycle length (C). Ablation within the described channel terminated the VT promptly and rendered it non-inducible.
Fig. 4
Fig. 4
Patient 2 with ICM and VT referred for repeat ablation after one previous failed endocardial ablation. (A) shows the activation map of the VT and (B) shows the voltage map. A potential isthmus (yellow star) is demonstrated between the inferior scar and the mitral valve annulus (MA) septaly. The endocardial signals were far field and could not be entrained at high output. Epicardial access in this case would be limited by the coronary vasculature and basal epicardial fat. We mapped the proximal end of the middle cardiac vein and found an epicardial signal that demonstrated concealed entrainment with low output. The intracardiac echocardiography at the location of the ablation catheter is shown in (D). The ablation catheter tip (arrow) was inserted through the coronary sinus (CS) into the middle cardiac vein and opposing the endocardial far field signal mapped between the inferior scar/aneurysm (white star) and the mitral annulus. Ablation at that level terminated tachycardia promptly and achieved non-inducibility. LV: left ventricle. RA: right atrium.
Fig. 5
Fig. 5
Epicardial access. The skin entry is in general 3 cm under the left xiphoid-sternal juncture, allowing for access through Larrey's space. (A) shows the angles of approach for an anterior and posterior epicardial access in a patient with a BMI of 23. (B) In patients with higher BMI, the point of entry will have to be moved more caudal as illustrated by the yellow lines, even with compressing the epigastric area down for a smoother angle. Larrey's space is the space within the triangle delineated by the yellow lines.
Fig. 6
Fig. 6
Patient 3 with surgical epicardial ablation. The surgical approach was done using video-assisted thoracoscopic surgery and mini-thoracotomy. Mapping was done both endocardialy and epicardialy (A). Ablation was done using a radiofrequency surgical pen on the epicardial surface (B). Mapping of late potentials and homogenization of the epicardial scar was also carried out rendering the patient non-inducible.

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