Background-Substrate-guided ablation of ventricular tachycardia (VT)

Current clinical LGE-CMRI scar imaging protocols produce ICD artifacts that affect >50% of the LV myocardium and correlate with the ICD-heart distance. This significantly limits the application of CMRI for image-guided VT ablation.

The integration of myocardial scar models in 3-dimensional (3D) mapping systems may provide a novel way of helping to guide ventricular tachycardia (VT) ablations. This study assessed the value of 201 Tl SPECT perfusion imaging to define ventricular myocardial scar areas and to characterize electrophysiology voltage-derived myocardial substrate categories of scar, border zone (BZ), and normal myocardium regions. Scar and BZ regions have been implicated in the genesis of ventricular arrhythmias. Methods: Ten patients scheduled for VT ablation underwent 201 Tl SPECT before the ablation procedure. 3D left ventricular (LV) scar models were created from the SPECT images. These scar models were registered with the LV voltage maps and analyzed with a 17-segment cardiac model. Scar location and scar burden were compared between the SPECT scar models and voltage maps. In addition, 201 Tl SPECT uptake was quantified using a 68-segment cardiac model and compared among voltage-defined scar, BZ, and normal segments. Results: 3D models of LV myocardium and scar were successfully created from 201 Tl SPECT images and integrated in a clinical mapping system. The surface registration error with the electrophysiology voltage map was 4.4 6 1.0 mm. The 3D scar location from SPECT matched in 72% of the segments with the voltage map findings. All successful ablation sites were located within the SPECTdefined scar or within 1 cm of its border, with 73% of the successful ablation sites within 1 cm of the scar border. Voltage measurements in SPECT-defined scar and normal areas were 1.2 6 1.7 and 3.4 6 2.8 mV, respectively (P , 0.001). The fractional SPECT scar burden area (18.8% 6 5.2%) agreed better with the abnormal (scar plus BZ) voltage area (20.8% 6 15.7%) than with the scar voltage area (5.8% 6 5.8%). Mean normalized 201 Tl uptake was 55% 6 21% in the voltage-defined scar, 63% 6 20% in BZ, and 79% 6 17% in normal myocardial segments (P , 0.05 for scar or BZ vs. normal). Conclusion: 3D SPECT surface models of LV scar were accurately integrated into a clinical mapping system and predicted endocardial voltage-defined scar. These preliminary data support the possible use of widely available 201 Tl SPECT to facilitate substrateguided VT ablations. Pat ients with internal cardiac defibrillators (ICD) may present with frequent shocks for ventricular tachycardia (VT) that are an appropriate response to the arrhythmia. Radiofrequency ablation of VT is required in many of these patients because of the side effects and decreasing longterm efficacy of antiarrhythmic medications. A substrateguided approach is required in 60%-90% of patients because of the multiple morphologies and hemodynamic intolerance of VT (1,2). In these approaches, linear ablation lines are placed across and along the myocardial scar and its border zone (BZ) to interrupt conducting channels of surviving myocardium (1,3,4). The current gold standard of scar delineation consists of voltage mapping, which is limited by catheter contact, mapping density, and inability to ...

oltage mapping is the primary tool for identifying sites for substrate-guided ventricular tachycardia (VT) ablation, but there are limitations in its application. Delayed-enhanced cardiac MRI (DE-CMRI) can facilitate VT ablations by providing complementary detail about myocardial scar location and geometry. We present the case of a patient with recurrent VT with left bundle branch block (LBBB)-right-side inferior axis morphology and a challenging voltage map. CaseThe patient was a 76-year-old man with a history of hypertension, type 2 diabetes mellitus, atrial fibrillation, and newly diagnosed dilated nonischemic cardiomyopathy (ejection fraction, 30%). He was transferred to our facility because of multiple episodes of monomorphic VT with a heart rate of 160 beats/min and an LBBB-right-side inferior axis morphology ( Figure 1) consistent with an origin in the right ventricular outflow tract (RVOT). He required 2 episodes of electric cardioversion and amiodarone therapy, but the VT was refractory to amiodarone, so the patient underwent a VT ablation procedure.CMRI with a 1.5-T Siemens Avanto scanner was performed in multiple anatomic planes using T1-weighted and cine steady-state free precision sequences. Gadoliniumenhanced sequences to evaluate early myocardial perfusion and delayed myocardial enhancement were also performed, using 0.1 mL/kg gadobenate dimeglumine. DE-CMRI demonstrated midmyocardial scar in the anteroseptal region of the RVOT (Figure 2), which raised the possibility of a substratemediated VT.Reformatted 2D slices using Amira software allowed the reconstruction of 3D models of the right ventricle (RV) and left ventricle (LV) anatomy with embedded myocardial scar. These were exported as 3D Carto-readable mesh files and allowed the identification of mapping point positions on the corresponding 2D images. MRI surfaces were uploaded into the clinical CartoMERGE system (Biosense).RV and LV voltage maps were created using the CartoMERGE system and a 3.5-mm Navistar cooled-tip catheter (Biosense Webster) with a filling threshold of 15 mm. The 3D DE-CMRI reconstructions were coregistered as previously described, using the commercial visual alignment and surface registration algorithms. 1 Standard clinical voltage criteria were used to define scar (Ͻ0.5 mV), border zone (0.5-1.5mV), and normal (Ͼ1.5 mV) myocardium. 2 A bipolar endocardial RV and LV voltage map revealed no endocardial scar (Figure 3).Using programmed electric stimulation, VT was easily inducible, with a tachycardia cycle length of 418 ms (LBBB-right-side inferior axis morphology). Activation mapping demonstrated earliest activation in the high septal outflow tract but was limited because of self-termination. The normal LV and RV voltage maps and 12-lead VT morphology raised the question of a more benign RVOT tachycardia mechanism occurring coincidentally in this patient with newly diagnosed nonischemic cardiomyopathy. However, the integrated scar substrate in the anteroseptal RVOT suggested a scar-mediated reentrant VT and directed the pac...