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(Circulation. 1996;93:497-501.)
© 1996 American Heart Association, Inc.

Articles

Anatomic Substrate for Idiopathic Left Ventricular Tachycardia

Ranjan K. Thakur, MD; George J. Klein, MD; Chittur A. Sivaram, MD; Marco Zardini, MD; David E. Schleinkofer, MD; Hiroshi Nakagawa, MD; Raymond Yee, MD; Warren M. Jackman, MD

From the Arrhythmia Service, University Hospital, London, Canada (R.K.T., G.J.K., M.Z., R.Y.), and the Division of Cardiology, University of Oklahoma Health Sciences Center, Oklahoma City (C.A.S., D.E.S., H.N., W.M.J.).

Correspondence to R.K. Thakur, MD, Arrhythmia Service, Thoracic and Cardiovascular Institute, 405 W Greenlawn; Room 110, Lansing, MI 48910.

	Abstract

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Background Idiopathic left ventricular tachycardia (ILVT) characterized by QRS complexes with right bundle-branch block (RBBB) morphology and left axis deviation is a distinct clinical syndrome that also demonstrates a characteristic response to verapamil and inducibility from the atrium in patients without structural heart disease. A false tendon has been described in the left ventricle in a patient with ILVT in whom surgical resection of the false tendon resulted in cure. We hypothesized that the false tendon is responsible for the genesis of similar ventricular tachycardia (VT) in others.

Methods and Results We performed transthoracic (TTE) and/or transesophageal (TEE) two-dimensional echocardiograms in 15 patients undergoing catheter ablation for ILVT. There were 12 men and 3 women (mean age, 31±12 years, with average symptom duration of 11±9 years). The mean VT cycle length was 360±70 ms, and all had RBBB morphology with left axis deviation. Cardiac chamber sizes, left ventricular wall thickness, and wall motion were normal in all ILVT patients. TTE and/or TEE demonstrated a false tendon extending from the posteroinferior left ventricular free wall to the left ventricular septum in all ILVT patients. The false tendons were thick (2 mm maximal thickness) in 5 patients and thin (<2 mm maximal thickness) in 10 patients. We compared ILVT patients with a control group of 671 consecutive patients referred for echocardiography for other reasons. The mean age for the control group was 42 years. A false tendon was seen in the left ventricle in 34 of 671 (5%). In the control group patients with a false tendon, 2 patients had a history of VT (left bundle-branch block morphology) and 1 had ventricular fibrillation. The false tendons in the control patients were also oriented transversely across the ventricular cavity but were somewhat thinner (<2 mm maximal thickness in 32 of 34 patients). Catheter ablation with the use of radiofrequency and/or direct current applied to the posteroapical septum resulted in cure in 14 of 15 patients.

Conclusions A false tendon extending from the posteroinferior left ventricle to the septum is a consistent finding in patients with ILVT and probably is responsible for this unique arrhythmia. The mechanism by which the false tendon precipitates tachycardia is speculative, but possibilities include conduction through the false tendon or by producing stretch in the Purkinje fiber network on the interventricular septum.

Key Words: tachycardia • ablation • false tendon

	Introduction

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Idiopathic left ventricular tachycardia is a distinct clinical syndrome observed in patients without structural heart disease.^{1 2 3 4 5 6 7 8 9 10 11 12} It is characterized by QRS complexes with RBBB morphology and left axis deviation, precipitation by catecholamines and exercise, may be induced by programmed stimulation of the atrium, termination by intravenous verapamil and occasionally adenosine, and suppression by oral verapamil and ß-adrenergic blocking agents.^{1 2 3 4 5 6 7 8 9 10 11 12} Both reentry and triggered activity have been postulated as mechanisms.^{13 14 15 16 17 18 19} Gallagher et al²⁰ described a patient with ILVT cured by intraoperative Nd-YAG laser photocoagulation of an abnormal strand in the posteroinferior region of the left ventricle. Suwa et al²¹ described a false tendon in the left ventricle in a patient with ILVT cured by surgical resection of the false tendon and cryoablation in the posteroinferior left ventricular insertion site. We hypothesized that a false tendon extending from the posteroinferior left ventricle to the interventricular septum is responsible for similar VT in others and prospectively performed 2D transthoracic and/or TTE and/or TEE in patients referred to our two centers for evaluation and ablation of ILVT.

	Methods

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Clinical Evaluation
The study population consisted of 15 consecutive patients referred for evaluation and catheter ablation of medically refractory idiopathic sustained ventricular tachycardia exhibiting the clinical characteristics described above. Detailed clinical characteristics and the ablation experience from each center have been reported separately.^{22 23}

In addition to history and physical examination, all patients underwent evaluation with M-mode and 2D TTE and/or TEE in the standard views. Maximal exercise stress testing was performed on all patients at one center and only in patients with a history of VT with exertion at the other center. Coronary angiography with left ventriculography was performed on a selective basis.

To determine the incidence of left ventricular fibromuscular bands in the general population, a control group consisting of all patients undergoing 2D echocardiography during a 4-month period at one institution was selected. These echocardiograms were reviewed by the same echocardiographers specifically looking for false tendons.

Electrophysiological Evaluation
Electrophysiological evaluation and catheter ablation protocols were approved by the respective institutional review boards. After providing written informed consent, each patient was studied in the postabsorptive state under sedation with fentanyl and midazolam. Four or 5 multielectrode catheters were inserted percutaneously via the subclavian veins or the femoral veins and positioned in the coronary sinus, high right atrium, His-bundle recording position, and the right ventricular apex. Left ventricular endocardial mapping and ablation were performed using a 7F deflectable quadripolar or hexapolar electrode catheter with a 4-mm-tip electrode. This catheter was inserted into the right femoral artery and advanced retrogradely across the aortic valve. Intravenous heparin was administered in a bolus dose of 5000 to 10 000 U, and therapeutic anticoagulation was maintained throughout the procedure.

Bipolar intracardiac electrograms were recorded along with 5 to 12 surface ECG leads. Ventricular tachycardia was induced by ventricular or atrial programmed stimulation in the baseline state or with isoproterenol infusion at 1 to 5 µg/min if sustained tachycardia could not be induced in the baseline state. Endocardial mapping was performed using biplanar fluoroscopy to identify potential ablation sites with a presystolic potential.

Catheter Ablation
Ablation was performed through the same catheter used for mapping. Radiofrequency current as well as DC shock (London) were used for ablation. Radiofrequency energy was delivered from a commercially available generator as a continuous, unmodulated sinusoidal wave at 500 to 750 kHz between the distal electrode of the ablation catheter and a large skin electrode positioned over the left posterior chest. If DC shock ablation was chosen, general anesthesia was instituted with intravenous propofol. Two types of DC shocks were used: the standard defibrillator using a damped sinusoidal waveform and a short pulse-width defibrillator (National Heart Hospital Ablater) with a capacitive discharge (Cardiac Recorders, Ltd). Shocks of up to 150 J were delivered via the standard defibrillator (n=1) and shocks of 10 to 50 J were delivered via the short pulse-width defibrillator (n=5). With either ablation method, energy was delivered during ventricular tachycardia, if possible. Thirty minutes after ablation, programmed stimulation was repeated in the absence of any drugs and during an isoproterenol infusion, if isoproterenol was necessary to induce tachycardia before ablation.

Follow-up
After the procedure, patients were monitored for 2 to 6 days. Electrophysiological evaluation prior to discharge was performed in 2 patients, exercise stress testing was performed in 10 patients, and isoproterenol infusion (1, 3, and 5 µg/min for 5 minutes at each dose) challenge was performed in 8 patients prior to discharge. Patients received aspirin (325 mg/d) for 6 to 12 weeks. Patients were followed by the investigators or their referring physicians.

	Results

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Clinical Characteristics
There were 12 men and 3 women, ranging in age from 12 to 50 years (mean±1 SD, 31±12 years). The average symptom duration prior to catheter ablation was 11±9 years. The number of documented episodes ranged from 2 to >20 episodes. Tachycardia occurred with a mean frequency of 4±3 episodes per year per patient, ranging from 1 to 10 per year. Tachycardia episodes were sustained or nonsustained, lasting from several minutes to several days, and were relatively well tolerated. Syncope associated with tachycardia had occurred in 6 patients, and the remainder of the patients reported palpitations, dyspnea, fatigue, or weakness. Pharmacological control had been attempted in all patients with 2.3±1.3 antiarrhythmic agents. The documented clinical arrhythmia in all patients was ventricular tachycardia, with a mean cycle length of 360±70 ms with RBBB morphology QRS complexes and left axis deviation.

All patients had a normal physical examination. One patient had pulmonary sarcoidosis without evidence of cardiac involvement by magnetic resonance imaging. The resting 12-lead ECG was normal in 14 patients and showed incomplete RBBB in 1 patient. In 3 patients, the ECG showed transient nonspecific T-wave changes in the inferior and anterolateral leads after an episode of tachycardia. Coronary angiography with contrast left ventriculography was performed in 5 patients and was normal. Left ventricular function was normal in the remainder of the patients as assessed by 2D echocardiography or radionuclide angiography.

In contrast, the control group consisted of 671 consecutive patients referred to the echocardiography laboratory over a period of 4 months for various reasons. The age ranged from 15 to 89 years, with a mean age of 42 years. In 34 of these 671 patients, a false tendon was demonstrated by echocardiography (see below). Of these 34 patients, 2 patients had a history of ventricular tachycardia with left bundle-branch block morphology and 1 patient with ischemic heart disease had had ventricular fibrillation.

2D Echocardiography
Standard M-mode and 2D echocardiography with Doppler evaluation was performed on all patients prior to ablation. Biplane transesophageal echocardiography was performed on 8 patients. Cardiac chamber sizes were normal in all ILVT patients without any wall motion abnormalities or Doppler abnormalities. TTE and TEE demonstrated a false tendon in every patient. The false tendon was best seen in the parasternal long-axis view to extend transversely across the left ventricular cavity from the middle septum to the posteroinferior region of the left ventricular free wall (Fig 1). Thickness of the false tendon varied from a thin strand (<1 mm in thickness) to a well-defined structure (2 to 3 mm in thickness), as shown in Fig 1. The false tendons were arbitrarily defined as being thick if the maximal thickness was 2 mm. The false tendons were thick in 5 patients and thin in 10 patients with ILVT. In contrast, 34 of 671 patients (5%) in the control group demonstrated a left ventricular false tendon on transthoracic 2D echocardiography (Fig 2). These false tendons were thin in 32 patients and thick in 2 patients and were oriented transversely in 32 of 34 patients.

View larger version (133K): [in this window] [in a new window]   Figure 1. 2D echocardiogram from a patient with idiopathic left ventricular tachycardia. The heart is seen in the parasternal long axis view. Arrows point to the false tendon. Ao indicates aorta; LA, left atrium; LV, left ventricle; and RV, right ventricle.

View larger version (92K): [in this window] [in a new window]   Figure 2. 2D echocardiogram from a patient in the control group. The heart is seen in the apical four-chamber view. Arrow points to the false tendon. LA indicates left atrium; LV, left ventricle; RA, right atrium; and RV, right ventricle.

TEE was performed in 7 patients (all patients at one center) after catheter ablation.²² Mild mitral regurgitation was noted in 1 patient in whom the tip of the catheter was caught in a snare formed by the chorda that had two closely adjacent attachments to the papillary muscle. TEE in the other 7 patients, performed 18 to 48 hours after ablation, did not show any abnormalities.

Cardiac Mapping and Ablation
Fragmented or delayed potentials could not be identified in any patient, either during sinus rhythm or during ventricular tachycardia. During ventricular tachycardia, the earliest ventricular activation was recorded from the posteroapical septum.^{22 23} A high-frequency, presystolic potential (Purkinje potential) preceding the onset of the QRS by 5 to 42 ms was identified at the successful ablation site. DC shock was used in 5 patients because no ventricular electrogram earlier than the QRS onset could be identified or because the earliest ventricular electrogram preceding the QRS onset was not preceded by a Purkinje potential (London).²³ Mapping in these patients was limited by increasing difficulty in consistent induction of sustained ventricular tachycardia. DC shock was delivered during sinus rhythm in 2 patients and during ventricular tachycardia in 3 patients, resulting in termination.

Follow-up
During the immediate postprocedure monitoring period, patients who underwent DC shock ablation showed a transient period of frequent complex ventricular arrhythmias, including ventricular couplets and triplets (4 patients), accelerated idioventricular rhythm (2 patients), and nonsustained ventricular tachycardia with QRS morphology different from the clinical arrhythmia, at a rate of 150 beats per minute (1 patient). These arrhythmias resolved in all patients within 48 hours from the procedure.

Treadmill exercise test was performed in 10 patients. Ventricular tachycardia was observed in 1 patient in whom a preablation exercise test induced VT. The patient refused a second attempt at catheter ablation and was treated with sotalol, 160 mg every 12 hours, and has remained free of symptoms. During follow-up electrophysiology study performed in 3 patients, ventricular tachycardia was not inducible. One other patient developed recurrence of ventricular tachycardia and required therapy with verapamil. Prior to ablation, this patient's symptoms could not be controlled with verapamil, but after ablation she has been free of symptoms for more than 24 months. The remainder of the patients have been free of symptoms during a follow-up of 1 to 70 months.

	Discussion

Top Abstract Introduction Methods Results Discussion References

 
ILVT in patients without structural heart disease characterized electrocardiographically by QRS complexes with RBBB morphology and left axis deviation represents a distinct clinical syndrome.^{1 2 3 4 5 6 7 8 9 10 11 12} It is often precipitated during exercise or by catecholamines; it is inducible by programmed stimulation from the ventricle or the atrium; it responds to intravenous verapamil and occasionally to adenosine; and it may be suppressed by oral administration of verapamil and ß-adrenergic–blocking agents.^{1 2 3 4 5 6 7 8 9 10 11 12} Both reentry and triggered activity have been proposed as the mechanism of this tachycardia.^{1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19} Evidence supporting reentry as the mechanism includes induction and termination by programmed ventricular stimulation, an inverse relationship between the coupling interval of the ventricular extrastimulus and the first tachycardia return cycle, an increasing pattern of response during resetting of the tachycardia with premature ventricular stimuli, and tachycardia entrainment with progressive fusion with shorter pacing cycle lengths. Evidence supporting a local reentrant circuit seems to be supported by the observation that the ventricle can be captured by extrastimuli, without resetting the tachycardia, suggesting that the remainder of the ventricle does not participate in the arrhythmia circuit.^{2 8} Similarly, the observation that the His bundle can be activated antegradely without influencing the tachycardia excludes a macroreentrant circuit involving the His bundle.^{2 8} This unique tachycardia originates from the posteroapical left ventricular septum, as evidenced by endocardial mapping. This is further supported by several recent reports describing successful catheter ablation of this form of ventricular tachycardia in the posteroapical left ventricular septum.^{14 22 23 24 25 26 27 28}

A high-frequency Purkinje potential near the site of earliest endocardial activation preceding the surface QRS has been described and was observed in 12 of our patients.^{22 23} On the basis of observations that this tachycardia originates in the posteroapical septum and that the surface QRS during tachycardia is preceded by a Purkinje potential and of electrophysiological evidence supporting localized reentry as the mechanism, it has been postulated that the tachycardia circuit incorporates the Purkinje fiber network of the left posterior fascicle.^{2 4 5 8 22} However, these observations have an alternate explanation. Two surgical reports have described a false tendon extending from the posteroinferior left ventricle to the basal septum in patients with ILVT.^{20 21} Gallagher et al²⁰ recorded a bipolar high-frequency potential preceding the surface QRS during tachycardia from a false tendon under direct visualization. Laser photocoagulation of this band resulted in termination of the tachycardia.²⁰ Suwa et al²¹ described a patient with ILVT in whom a false tendon was found on transthoracic 2D echocardiography. This false tendon was resected, and cryoablation was performed at the posteroinferior left ventricle, resulting in cure. Histological examination of this band revealed Purkinje fibers within the band.²¹ Thus, observations from Gallagher et al and Suwa et al suggest a correlation between a false tendon, which is capable of rapid conduction (sharp bipolar potential, and Purkinje fibers on histology), and idiopathic left ventricular tachycardia syndrome.

We found a false tendon in all ILVT patients on TTE and/or TEE. In a control group of 671 consecutive patients referred to the echocardiography laboratory during a 4-month period, a left ventricular false tendon was observed in 5% of the patients. These false tendons were similar in thickness and orientation. The significance of false tendons in the control group is not clear, although a correlation between left ventricular false tendons and premature ventricular contractions has been reported.^{29 30} It is not known whether all such false tendons contain Purkinje fibers and are capable of rapid conduction or whether only the false tendons with Purkinje fibers predispose to ventricular tachycardia. Furthermore, while the false tendon was observed in every patient with ILVT, the mechanism by which the false tendon precipitates tachycardia is unknown. It is possible that conduction through the false tendon constitutes part of the ventricular tachycardia circuit or that the tendon may produce stretch in the Purkinje fiber network on the interventricular septum.

We recorded a bipolar high-frequency potential in 12 patients at the site of successful ablation. In the 3 patients in whom such a potential was not recorded, DC shock ablation was successful. In one such patient, tachycardia recurred during an exercise stress test the following day, suggesting that the ablation catheter had not been in close proximity to the substrate.²³ In another patient in whom tachycardia recurred, a sharp potential was observed fused with the local ventricular electrogram rather than preceding it by an isoelectric segment.²² The observation that a bipolar high-frequency potential was not recorded in 4 patients is still consistent with the hypothesis that a left ventricular false tendon is the necessary substrate for this unique tachycardia and may be a reflection of proximity of the ablation tip electrode to the false tendon. Demonstration of proximity of the ablation tip electrode to the false tendon by TEE was technically difficult. In one case we were able to demonstrate juxtaposition of the ablation catheter to the false tendon, and ablation at this site was successful (Figs 3 and 4).

View larger version (105K): [in this window] [in a new window]   Figure 3. Fluoroscopic images from a patient undergoing transesophageal echocardiography during catheter ablation. An octapolar catheter is shown at the His-bundle recording position (HB). A quadripolar catheter is positioned at the right ventricular apex (RV). The ablation catheter is positioned on the left ventricular septum (LV). The transesophageal probe is marked "Probe." RAO indicates right anterior oblique; LAO, left anterior oblique.

View larger version (167K): [in this window] [in a new window]   Figure 4. Image obtained from the transesophageal probe. The ablation catheter (ABL) is shown in the region of successful ablation in proximity to the false tendon (FT). LA indicates left atrium; LV, left ventricle; RA, right atrium; and RV, right ventricle.

Conclusions
A false tendon extending from the posteroinferior left ventricle to the septum is a consistent finding in patients with ILVT characterized by RBBB morphology QRS complexes and left axis deviation. On the basis of the direct surgical experience in two patients and our ablation experience as well as the observations of others, we postulate that the left ventricular false tendon is responsible for this tachycardia. The mechanism by which the false tendon precipitates tachycardia is speculative, but possibilities include conduction through the false tendon or by producing stretch in the Purkinje fiber network on the interventricular septum.

	Selected Abbreviations and Acronyms

 

2D = two-dimensional ILVT = idiopathic left ventricular tachycardia RBBB = right bundle-branch block TEE = transesophageal echocardiography TTE = transthoracic echocardiography VT = ventricular tachycardia

Received September 14, 1994; revision received August 9, 1995; accepted September 11, 1995.

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