Percutaneous catheter ablation with a strategy of scar modification is a validated technique for management of ventricular tachycardia (VT) and is particularly advantageous in the setting of multiple hemodynamically unstable circuits. Homogenization and/or isolation of abnormal myocardium with fractionated electrograms and late potentials have been reported as successful approaches for improving substrate-based ablation outcomes.1 In patients with subendocardial or transmural scar and wall thinning, an endocardial approach is effective in the majority of patients.2 Epicardial access is typically utilized after a failed endocardial approach or during the index procedure in patients with arrhythmogenic cardiomyopathy or non-ischemic cardiomyopathy and subepicardial scar involving the free wall. The majority of patients with ischemic cardiomyopathy and VT can be successfully treated with endocardial VT ablation if the scar does not extend beneath the papillary muscles. However, the presence of mobile left ventricular endocardial thrombus is a contraindication for endocardial mapping and ablation, due to the increased risk for thromboembolism.
Preprocedural imaging with cardiac magnetic resonance (CMR) and/or multi-detector computed tomography (MDCT) can be helpful to identify the location and extent of scar, wall thinning, aneurysm, and important anatomical structures such as the coronary arteries.3 The identification of subepicardial scar can help in planning the procedure with an index epicardial approach. The integration of segmented MDCT or CMR images with electroanatomic mapping (EAM) can further contribute to recognition and elimination of arrhythmic substrates critical for maintenance of VT. We report a case of VT mapping and ablation with an epicardial-only approach in a patient with inferior transmural infarct, LV endocardial mobile thrombus, recent embolism, and recurrent shocks for monomorphic ventricular tachycardia (MMVT).
A 66-year-old male with a history of mild ischemic cardiomyopathy due to prior right coronary and distal left anterior descending occlusion, cerebrovascular accident without residual deficit, and chronic kidney disease, presented to the hospital with complaints of chest pain for three days. He was diagnosed with inferolateral ST elevation myocardial infarction (STEMI) and urgently underwent cardiac catheterization with placement of drug-eluting stents in the left circumflex (LCx) and large first obtuse marginal arteries. Chronic proximal occlusion of the right coronary artery was noted. During the hospitalization, the patient had episodes of hemodynamically unstable MMVT requiring external defibrillation. He was started on amiodarone 400 mg daily following a 10-gram loading protocol, and a dual-chamber defibrillator was implanted. The patient was optimized from a heart failure standpoint with guideline-directed medical therapy. Within 3 days of hospital discharge, he returned in VT storm requiring multiple rounds of antitachycardia pacing and 13 shocks. Amiodarone was reloaded, and mexiletine started. Due to continual episodes of VT requiring therapies, he was transferred to the Hospital of the University of Pennsylvania for catheter ablation. Concurrent to transfer, the patient developed severe abdominal pain and nausea. On arrival, mexiletine was discontinued and lidocaine initiated. Despite antiarrhythmic drug (AAD) therapy, he continued to have episodes of MMVT with right bundle block with right superior morphology (Figure 1A). Twelve-lead ECG during sinus rhythm revealed Q waves in the inferior leads and lateral T wave inversions (Figure 1B). CT abdomen, obtained due to worsening abdominal discomfort, revealed small bowel ischemia and ischemic colitis.
Transthoracic echocardiography (TTE) disclosed severe left ventricular dysfunction with akinesis and thinning of the entire inferior and inferolateral wall with an estimated left ventricular ejection fraction of 25% (left ventricular end-diastolic volume [LVEDV] 210 mL, left ventricular end-systolic volume [LVESV] 160 mL). A large (1.2 x 1 cm) mobile echogenic mass was also noted in the left ventricular apex consistent with thrombus (Figure 2A). The patient was started on anticoagulation with heparin.
Catheter ablation of VT was deferred due to metabolic acidosis and bowel ischemia, which required exploratory laparotomy with double-barrel jejunostomy for worsening obstruction. In this setting, he developed acute worsening of chronic kidney injury requiring continuous renal replacement therapy, and ultimately, hemodialysis. While recovering from surgery, he had recurrent VT episodes despite use of multiple other AADs including amiodarone, procainamide, and quinidine, requiring defibrillator therapies. He also underwent bilateral ultrasound-guided stellate ganglion block with transient decrease in VT burden. Due to the presence of persistent LV endocardial mobile thrombus and recurrent VT, the decision was made to proceed with epicardial-only VT ablation. A preprocedure contrast-enhanced MDCT revealed diffuse thinning at the apex with a 14 x 11 mm left ventricular apical thrombus along with diffuse thinning of the distal inferior and lateral wall of the LV consistent with prior infarction (Figure 2B). Image processing (ADAS 3D software, ADAS3D Medical) revealed hypoperfused and thinned myocardial regions in apical inferolateral LV and spared intervening tissue as candidate corridors for VT inner circuitry (see Video 1 at https://bit.ly/2L7KgsN). Importantly, CT imaging showed that the substrate could be reached from the epicardium, the septum was largely spared, and wall thickness in the substrate region was uniformly less than 5 mm.
Following informed consent, the patient underwent electrophysiologic study under general anesthesia using three-dimensional mapping (CARTO, Biosense Webster, Inc., a Johnson & Johnson company). An ACUSON AcuNav (Biosense Webster, Inc.) intracardiac ultrasound probe was advanced into the right atrium and ventricle to assist with ablation, assess anatomy, and monitor for complications. A 4 French (Fr) quadripolar catheter was advanced to the RV apex. Epicardial access was obtained with a Tuohy needle using an anterior approach under fluoroscopic guidance. After obtaining access with the Tuohy needle and Bentson Wire Guide (Cook Medical), a steerable 8.5 Fr epicardial sheath (Agilis EPI, Abbott) was introduced into the epicardial space, and 100 cc of blood (which accrued during access) was drained without further active bleeding. Electroanatomic mapping of the LV epicardium was performed using a multipolar catheter (PENTARAY, Biosense Webster, Inc.). Large areas of LV epicardial low voltage were present in the mid to apical inferior and apical regions, with late potentials and abnormal electrograms matching the distribution anticipated from CT image processing (Figure 3). Programmed stimulation was not performed due to pressor requirements with anesthesia and preference for avoidance of defibrillation in the setting of fresh thrombus and multiple recent emboli. Pacing at the threshold from the apical lateral aspect of the inferior scar resembled prior VT morphologies, with right bundle block with right superior morphology and long stimulus to QRS. Radiofrequency (RF) ablation, targeting a 15-20 ohm impedance drop with a maximum energy of 35-40 Watts for 20-30 seconds was performed, targeting epicardial late potentials and fractionation within scar and away from coronary vessels visualized by CT (Figure 4). Pacing within the scar post ablation showed the core to be completely inexcitable. During three months of follow-up to date, the patient has remained VT free of all AADs, has successfully undergone jejunostomy takedown and reanastomosis, and continues to recover at home.
Scar-related reentry is the most likely cause of MMVT in patients with ischemic heart disease. Regions of fibrosis within the surviving myocardium fibers can lead to unidirectional conduction block and slow conduction as substrates for reentry.4 RF catheter ablation of critical regions of heterogeneous myocardial tissue within scar has emerged as an important treatment option for patients with recurrent VT. Targeted ablation of the critical isthmus with RF following identification of diastolic activation coupled with favorable entrainment mapping is useful in patients with hemodynamically tolerated sustained MMVT.5 However, detailed activation and entrainment mapping is not always feasible when VT is hemodynamically not tolerated or cannot be induced. A substrate-based ablation strategy without entrainment mapping of the VT can be successful when multiple hemodynamically unstable circuits are present or when VT induction is not desired.6-8 However, success hinges upon the identification and elimination of the entire VT substrate.
Epicardial-only VT ablation has been previously reported to be feasible and associated with at least short-term favorable outcomes.9 It has been previously demonstrated that endocardial ablation can eliminate epicardial abnormal electrograms if wall thickness does not exceed 5 mm.2 Thus, there is a reasonable chance that epicardial ablation can also modify endocardial abnormal electrograms in patients with wall thinning. Preprocedural imaging with CT and/or CMR can identify the substrate as well as measure the wall thickness. The identification and definition of scar tissue prior to mapping, as in this case, can provide confidence that the arrhythmogenic substrate can be reached from the epicardium. In our case, we had detailed geometry of the infarct and scar prior to ablation using MDCT, showing the sparing of septum and myocardial thickness favorable for epicardial ablation. Registration of these pre-acquired images onto an electroanatomic map greatly enhanced the utility of this technology. The preprocedural imaging can also help identify “3D corridors” in the border zone in a complex scar prior to ablation as potential targets for ablation. Late potentials in the present case had excellent regional agreement to such corridors identified by CT imaging.
This case illustrates that an epicardial-only catheter ablation strategy targeting areas of late potentials and abnormal electrograms effectively suppressed VT in a patient with transmural scar, wall thinning, and arrhythmic substrate accessible from the epicardium as identified by preprocedural MDCT imaging.
The ADAS 3D software platform is designed by ADAS3D Medical SL. Circle Cardiovascular Imaging, Inc. (www.circlecvi.com) is the global distributor of the ADAS 3D software.
This article is published with support from Circle Cardiovascular Imaging, Inc.
Disclosures: Dr. Garg and Dr. Khoshknab have no conflicts of interest to report regarding the content herein. Dr. Nazarian reports consultant fees and honoraria for speaking from Circle Cardiovascular, software support from ADAS 3D, and grants from Biosense Webster relevant to the contents of the case report, as well as grants from Siemens, Imricor, and NIH/NHLBI outside the submitted work.
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- Tzou WS, Frankel DS, Hegeman T, et al. Core isolation of critical arrhythmia elements for treatment of multiple scar-based ventricular tachycardias. Circ Arrhythm Electrophysiol. 2015;8(2):353-361.
- Di Biase L, Santangeli P, Burkhardt DJ, et al. Endo-epicardial homogenization of the scar versus limited substrate ablation for the treatment of electrical storms in patients with ischemic cardiomyopathy. J Am Coll Cardiol. 2012;60(2):132-141.
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