Sustained and recurrent ventricular tachycardia (VT) presents a therapeutic challenge in patients with heart disease, with an implied overall increased morbidity and mortality. Although implantable cardioverter-defibrillators (ICD) confer a mortality benefit in these patients, it is not a cure for the arrhythmia.1-4 Recurrent VT is known to occur in up to 60% of the patients who receive a secondary prevention ICD; in patients with an ICD implanted for primary prevention, about 20% will experience a VT episode within 3-5 years of implant.2,5 Furthermore, recurrent VT with frequent ICD discharges is known to be associated with increased morbidity and mortality, hospitalization for congestive heart failure, and decreased overall quality of life.6
Successful catheter ablation of VT in patients with large substrates, such as those with myocardial infarction, may be affected by several factors including unmappable VT due to hemodynamic instability and poor patient intolerance, VT morphology change, or noninducibility. Several observational and randomized trials including SMASH-VT have shown that a substrate-based approach with an advanced three-dimensional cardiac mapping system may be a useful alternative for successful RF ablation of VT during sinus rhythm.1,7 Commonly applied substrate-based ablation techniques include linear ablation, short linear ablation, local abnormal ventricular activity (LAVA) ablation, late potential ablation, scar encircling, and scar dechanneling. Varying success and recurrence rates of up to 50% have been reported in literature for any selected technique. Successful electrophysiologic study and ablation relies heavily on accuracy, resolution, and fidelity of electroanatomic mapping alongside careful analysis of electrograms. Early mapping tools required a tedious point-by-point approach and increased the likelihood of missing smaller zones of abnormal conduction. More recently, with the advent of non-contact mapping with multielectrode arrays, multipolar catheters, and the improved accuracy of acquired shells, electrophysiologists have been able to cut down fluoroscopic exposure and procedure time with improved overall procedure efficacy.4,12
In this case, we discuss our use of the Rhythmia™ Mapping System (Boston Scientific) to enable more detailed scar and LAVA mapping to possibly increase the success of VT ablation.
A 71-year-old male with hypertension, diabetes mellitus, and hyperlipidemia was brought into the emergency room with multiple ICD shocks and sustained VT. The patient is an active smoker and has a significant cardiac history, including coronary artery bypass grafting in 1989, ischemic cardiomyopathy (ejection fraction 25%), ICD implant in 2013, and prior sustained VT episodes and VT ablation. The patient’s home medications included mexiletine 150 mg every 8 hours and amiodarone 200 mg daily. He previously failed sotalol. Device interrogation in the emergency room revealed multiple VT episodes within the last two months that had been terminated with antitachycardia pacing (ATP), and in the 48 hours prior to hospitalization, there were episodes of sustained VT unresponsive to ATP, which were subsequently shock terminated.
Laboratory data was unremarkable except for elevated pro-BNP levels and TSH levels (<0.02, Free T4 5.15, Free T3 6.98). Chest X-ray and CT scan were remarkable only for cardiomegaly and a moderate right and small left pleural effusion. Prior coronary angiography demonstrated triple vessel disease with a patent LIMA graft to the second obtuse marginal. The saphenous vein graft to right coronary artery was occluded, and there were chronic total occlusions of the mid left anterior descending and right coronary arteries.
The patient’s amiodarone was replaced by quinidine, as the patient was noted to have hyperthyroidism during this hospitalization. Despite quinidine and mexiletine, the patient continued to have frequent recurrences of hemodynamically unstable, sustained slow VT that required external defibrillation. A lidocaine infusion was initiated, and device zones were reprogrammed to a lower cutoff. The patient consented to VT ablation.
The patient was brought to the electrophysiology lab and prepared for procedure as per standard protocol. Right and left femoral vein accesses were obtained, and later on during the procedure, the right femoral artery was accessed for retrograde approach to the left ventricle for ablation. A decapolar catheter was placed in the coronary sinus and a quadripolar catheter was advanced to the right ventricular apex. A transseptal puncture was performed using a 10 French (Fr) ICE catheter, and heparin was administered to an ACT of >300 seconds. The IntellaMap Orion™ High Resolution Mapping Catheter (Boston Scientific) was introduced through a large curl sheath (Agilis™ NxT Steerable Introducer, St. Jude Medical) into the LA and then the LV. In a short amount of time, a 10,985-point map of the LV scar (Figures 1 and 2) was created. A distinct zone of late potentials (LP) (Figure 3) and fractionated electrograms were found on the apical anteroseptal region in the middle of a dense, anteroseptal scar. Activation in sinus rhythm was mapped (Figure 4). Ablation was performed using a Biosense Webster ThermoCool SF DF curve ablation catheter via the transseptal route as well as from a retrograde approach to ablate the late potential region. After ablation in this region, a verification map (vMap™, Boston Scientific) was performed with the Orion catheter in approximately 1 minute, and no further late potentials were detected (Figure 5). Programmed stimulation was performed from the RV apex at two cycle lengths up to triple extrastimuli. No VT was inducible.
The patient was monitored for 48 hours post procedure in telemetry, and had no further significant arrhythmias or ventricular ectopy. He was discharged home on quinidine 324 mg orally every 8 hours and mexiletine 200 mg orally every 8 hours, in addition to guideline-directed medical therapy for congestive heart failure. There has not been any further VT at two-month follow-up.
Electrogram analysis in combination with dense, high-fidelity electroanatomic mapping remains a vital step in identifying potential targets for substrate-guided VT ablation in patients with non-inducible or poorly tolerated VT. Scar-related reentry through areas of slowed conduction interspersed between viable myocardium and fibrosis is the most common mechanism of monomorphic VT in patients with ischemic heart disease. The critical part of the reentry circuit is the isthmus or the narrowest portion of the circuit. Other suggested mechanisms for VT induction in structurally abnormal hearts include gap junction abnormalities, autonomic nervous system imbalance, and loss of ion channel function. The substrate of VT in non-ischemic cardiomyopathy is less well described. Different markers of VT isthmus recognized during sinus rhythm or paced rhythms have been proposed targets of ablation. Prior studies on both endo- and epicardial mapping at the time of arrhythmia surgery have shown a high prevalence of low-amplitude fragmented electrograms and LPs during sinus rhythm in relation to VT occurrence and the resection of VT substrate resulting in abolition of these LPs.4,13 Although these late potentials electrograms were found to be very sensitive by some investigators, they had lower specificity as compared to LAVAs that when eliminated were associated with better outcomes.8
Mapping can be challenging in patients when VT is unstable. Point-by-point mapping with recreation of ventricular anatomy is commonly used alongside electrophysiological data. Potential sources of error or limitations include cardiac motion or non-visualization of finer anatomic details including papillary muscles. Pre-acquired CT or MRI mapping may allow for better definition of substrate at the cost of time and radiation exposure. Balloon or basket electrode arrays that sample from multiple sites simultaneously allow for activation maps to be constructed from a single beat or brief runs of VT are potential alternatives to allow for high-fidelity maps. Prior studies using standard mapping systems allowed for identification of myocardial scar with bipolar voltage (0.5 mV), normal myocardium (1.5 mV), and areas of intermediate voltage (0.5-1.5 mV) as border zone. The success rate of ablation and recurrence of VT has been shown to correlate with the number of late potential sites.2,4,9 Volkmer et al reported that Carto-guided mapping and ablation during VT or sinus rhythm in patients with coronary artery disease was successful long term in 75% of patients, but left about 23% at risk of developing fast VT/VF.15 This may partly be related to the fact that narrower bands of fibrosis within areas of normal myocardium can escape detection on the basis of very low amplitude. Thus, detailed mapping with higher point acquisition and lower bipolar voltage cutoff shows promise in terms of complete substrate isolation and successful RF ablation.
Although VT may be non-inducible in around 90% of cases when using late potentials as a guide to substrate ablation, studies have suggested that the recurrence of scar-related VT approaches 50% in patients at 6-12 months.14 Persistence of late potentials at the end of initial ablation correlated with VT recurrence and persistence during repeat mapping and ablation. Late potentials are described as any electrograms less than 1.5 mV with single or multiple continuous delayed electrical components, separated from the higher amplitude of the local ventricular electrogram by at least 20 msec and recorded after the end of surface QRS. These sensitive targets, as reported by Vergara et al, achieved 71% success in VT ablation after elimination of all late potentials.13 Arenal et al followed 59 post-MI patients who underwent complete endocardial VT substrate ablation during sinus rhythm. Targeting isolated components/late potentials and conduction channels, the authors reported an 81% freedom from VT at one-year follow-up and 58% freedom from VT at 39 months.9
Whereby sensitivity of late potentials may be limited by the requirement that the activity occurs after QRS, LAVA were proposed by the Bordeaux group as an alternative substrate target.8 The LAVA potentials are sharp, high-frequency and low-amplitude ventricular potentials, distinct from the far-field ventricular electrogram in sinus rhythm or before the far-field ventricular electrogram in sustained monomorphic VT that may be fractionated. LAVA is poorly coupled with the rest of the myocardium, and offers a broader substrate target for ablation with elimination documented using multipolar catheters correlating well with non-recurrence.4,8
Therefore, the role of dense substrate mapping in VT ablation is of the utmost importance, and mapping systems such as the Rhythmia Mapping System could prove to be highly valuable. Whereas conventional mapping systems with a bipolar voltage cutoff of 0.5 mV would have demonstrated dense scar, the Rhythmia Mapping System revealed viable tissue within dense scar using a cutoff of 0.1 mV. As demonstrated by this case, in which the patient had recurrences of VT ablation after a prior ablation, we were able to create a highly dense map and successfully ablate and eliminate late potential substrate. No VT was inducible at the end of the procedure, and the patient remains arrhythmia-free to date. Although early experience with this system is mostly in the form of preclinical data, individual reports from electrophysiologists suggest it to be an effective tool in generating highly accurate and detailed maps of cardiac chambers within minutes, quickly acquiring thousands of electrograms per map. The system is unique in that it generates high-resolution images with both magnetic-based and impedance-based localization using the IntellaMap Orion Basket Catheter with 64 imprinted electrodes.12 With further studies and clinical experience, we should be able to better delineate the targets of VT ablation, improve technology to assist identification, and achieve immediate and long-term procedural success.
Disclosure: The authors have no conflicts of interest to disclose.
- Reddy VY, Reynolds MR, Neuzil P, et al. Prophylactic catheter ablation for the prevention of defibrillator therapy. N Engl J Med. 2007;357:2657-2665.
- Stevenson WG, Soejima K. Catheter ablation for ventricular tachycardia. Circulation. 2007;115:2750-2760.
- Berruezo A, Fernández-Armenta J. Lines, circles, channels, and clouds: looking for the best design for substrate-guided ablation of ventricular tachycardia. Europace. 2014;16:943-945.
- Fernández-Armenta J, Penela D, Acosta J, Andreu D, Berruezo A. Approach to ablation of unmappable ventricular arrhythmias. Card Electrophysiol Clin. 2015;7(3):527-537.
- Schron EB, Exner DV, Yao Q, et al. Quality of life in antiarrhythmics versus implantable cardioverter-defibrillator trial: impact of therapy and influence of adverse symptoms and defibrillator shocks. Circulation. 2002;105:589-594.
- Komatsu Y, Maury P, Sacher F, et al. Impact of Substrate-Based Ablation of Ventricular Tachycardia on Cardiac Mortality in Patients with Implantable Cardioverter-Defibrillators. J Cardiovasc Electrophysiol. 2015 Sep 1. doi: 10.1111/jce.12825. [Epub ahead of print].
- Tilz RR, Makimotot H, Rilling A, et al. Electrical isolation of a substrate after myocardial infarction: a novel ablation strategy for unmappable ventricular tachycardias—feasibility and clinical outcome. Europace. 2014;16:1040-1052.
- Jaïs P, Maury P, Khairy P, et al. Elimination of local abnormal ventricular activities: a new end point for substrate modifications in patients with scar-related ventricular tachycardia. Circulation. 2012;125:2184-2196.
- Arenal A, Hernández J, Calvo D. Safety, Long-term results, and predictors of recurrence after complete endocardial ventricular tachycardia substrate ablation in patients with previous myocardial infarction. Am J Cardiol. 2013;111:499-505.
- Marchlinski FE, Callans DJ, Gottlieb CD, Zado E. Linear ablation lesions for control of unstoppable ventricular tachycardia in patients with ischemic and non-ischemic cardiomyopathy. Circulation. 2000;101:1288-1296.
- 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;8:353-361.
- Piccini JP. Innovations in Electroanatomic Mapping: Ultra-High Density Mapping. Emerging Technologies. EP Lab Digest. 2015;15(5):65-66.
- Vergara P, Trevisi N, Ricco A, et al. Late potentials abolition as an additional technique for reduction of arrhythmia recurrence in scar related ventricular tachycardia ablation. J Cardiovasc Electrophysiol. 2012;23:621-627.
- Silberbauer J, Oloriz T, Maccabelli G, et al. Noninducibility and late potential abolition: a novel combined procedural end point for catheter ablation of postinfarction ventricular tachycardia. Circ Arrhythm Electrophysiol. 2014;7(3):424-435.
- Volkmer M, Ouyang F, Deger F, et al. Substrate mapping vs. tachycardia mapping using CARTO in patients with coronary artery disease and ventricular tachycardia: impact on outcome of catheter ablation. Europace. 2006;8(11):968-976.