The patient is a 79-year-old male with previous history of atrial fibrillation (AF). He was admitted for fatigue and weakness, and was found to have runs of sustained ventricular tachycardia (VT). Echo showed a mildly dilated left ventricle with an ejection fraction of 45%, moderately dilated left atrium, moderate mitral valve regurgitation, and dilated aortic root and ascending aorta. Blood works were unremarkable. As a part of workup, the patient underwent coronary angiogram that showed mild, non-significant coronary artery disease. The clinical VT had right bundle superior and left axis deviation morphology at a rate of 155 bpm (Figure 1). The VT appeared consistent with a fascicular VT arising from the left posterior fascicle.
The patient was brought into the EP lab, and prepared and draped in the usual sterile fashion. The procedure was performed under conscious sedation. Access to the right femoral vein and artery was obtained, and sheaths were inserted. A quadripolar catheter was inserted into the right ventricular apex and a THERMOCOOL F curve catheter (Biosense Webster, Inc., a Johnson & Johnson company) was inserted into the left ventricle (LV) using the retrograde approach. Since the patient had an enlarged aortic root, it was difficult to enter into the LV. For this reason, a braided SL1 sheath was inserted via the right artery and used to obtain more support. Heparin was administered to maintain an ACT of ≥250 seconds. Electroanatomic mapping of the LV was performed using the CARTO® 3 mapping system (Biosense Webster, Inc., a Johnson & Johnson company). At baseline, the patient was in AF with frequent runs of spontaneous VT. We started activation mapping. Along the posterior-inferior wall, we found diastolic, prolonged pre-Purkinje potentials. However, placing the ablation catheter in this area terminated the VT and we were not able to re-induce. In sinus rhythm there were very late, low-amplitude electrograms after the QRS (Figure 2). With ventricular bursts, we induced few beats of non-sustained VT and found the diastolic pre-Purkinje potentials (Figure 3). Radiofrequency energy was delivered at 40W for 60 seconds, for a total of five lesions (Figure 4 and 5). Following ablation, there was no more spontaneous VT. We were also not able to induce VT despite ventricular bursts, down to 200 msec, during isoproterenol infusion at 3 mcg/min. Heparin was reversed with protamine and all sheaths were removed. The patient tolerated the procedure well and was transferred out of the EP lab in stable condition.
Idiopathic fascicular left VT is the most common idiopathic ventricular tachycardia of the LV.1 Zipes et al first described fascicular VT in 1979.2 Fascicular VT has specific electrocardiographic features and therapeutic options. VT is characterized by a relatively narrow QRS complex and right bundle branch block pattern. Depending on which fascicle is involved in the reentry, two different QRS axis morphologies have been classified: left axis deviation is noted with left posterior fascicular VT, and right axis deviation with left anterior fascicular VT. A third and more rare morphology with narrow QRS and normal or right axis deviation has also been described: the upper septal fascicular VT. Response to verapamil is an important feature of fascicular tachycardia.3
Fascicular VT can be induced by programmed atrial or ventricular stimulation. Isoproterenol infusion may be required to facilitate the induction. However, Lin et al reported that this arrhythmia is not inducible in a significant percentage of patients.4 During VT, two distinct potentials can be registered before the ventricular electrogram, specifically the presystolic Purkinje potential (P2) and the diastolic pre-Purkinje potential (P1).5 The Purkinje potential is a high frequency and sharp potential which precedes the QRS onset by 5-25 ms and reflects the activation of the left posterior fascicle or the Purkinje fibers in close proximity to the left posterior fascicle. The pre-Purkinje potential is a slow, lower frequency potential which anticipates the QRS onset by 30-70 ms and is related to the excitation at the entrance of the specialized zone in the ventricular septum with decremental properties and verapamil sensitivity.6,7
Catheter ablation can be performed either during VT or sinus rhythm. During VT, Nagakawa et al targeted the P2 potential to guide the ablation.6 Radiofrequency is delivered at the site of the earliest P2 potential. It has been reported a mean of 18 ± 6 ms between the P2 and the QRS onset at the site of successful ablation. Differently, Nogami et al targeted the P1 potential to guide the ablation.7 The P1 potential is recordable in an area proximal to P2. The interval between P1 and the QRS onset at the site of successful ablation is 60 ± 29 ms. After successful ablation, P1 is recorded after the QRS complex in sinus rhythm. However, this can also be evident at baseline or after an insufficient RF delivery.8
In patients with non-sustained or non-inducible VT, catheter ablation can be performed in sinus rhythm. In the ablation of fascicular VT, pace mapping could be misleading. Indeed, Nogami et al demonstrated that pacing at a site of successful ablation showed a morphology match in only 9.6 ± 2.1 of the 12 ECG leads. This may be related to the capture of adjacent myocardium not included in the reentry circuit.7 Electroanatomic mapping systems have facilitated the ablation of fascicular VT in sinus rhythm. In patients with non-inducible and non-sustained VT, using the CARTO electroanatomic mapping system, Lin et al created a linear lesion between the apex and the base of the septum.
Catheter ablation is the therapy of choice for left ventricular idiopathic fascicular VT. Although the inability to reliably induce VT is critical for achieving a successful ablation, the success rate is >90% with a low rate of complications. Ablation during VT is feasible in most patients. However, in case of non-inducible VT, ablation can be effectively performed in sinus rhythm.
Disclosures: The authors have no conflicts of interest to report regarding the content herein.
- Aliot EM, Stevenson WG, Almendral-Garrote JM, et al. EHRA/HRS Expert Consensus on Catheter Ablation of Ventricular Arrhythmias. Europace. 2009;11:771-817.
- Zipes D, Douglas PR, Troup PJ, et al. Atrial induction of ventricular tachycardia: reentry versus triggered automaticity. Am J Cardiol. 1979;44:1-8.
- Belhassen B, Rotmensch HH, Laniado S. Response of recurrent sustained ventricular tachycardia to verapamil. Br Heart J. 1981;46:679-682.
- Lin D, Hsia HH, Gerstenfled EP, et al. Idiopathic fascicular left ventricular tachycardia: linear ablation lesion strategy for noninducible or nonsustained ventricular tachycardia. Heart Rhythm. 2005;2:934-939.
- Nogami A, Naito S, Tada H, et al. Demonstration of diastolic and presystolic Purkinje potentials as critical potentials in a macroreentry circuit of verapamil-sensitive idiopathic left ventricular tachycardia. J Am Coll Cardiol. 2000;36:811-823.
- Nagakawa H, Beckman KJ, McClelland JH, et al. Radiofrequency catheter ablation of idiopathic left ventricular tachycardia guided by a Purkinje potential. Circulation. 1993;88:2607-2617.
- Tsuchiya T, Okumura K, Honda T, et al. Significance of late diastolic potential preceding Purkinje potential in verapamil-sensitive idiopathic left ventricular tachycardia. Circulation. 1999;99:2408-2413.
- Ouyang F, Cappato R, Ernst S, et al. Electroanatomic substrate of idiopathic left ventricular tachycardia: unidirectional block and macroreentry within the Purkinje network. Circulation. 2002;105:462-469.