Europace Advance Access originally published online on January 28, 2008
Europace 2008 10(3):289-293; doi:10.1093/europace/eun004
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ELECTROPHYSIOLOGY
His-Purkinje system re-entry in patients with clustering ventricular tachycardia episodes
Department of Cardiology, Swiss Cardiovascular Center Bern, University Hospital, CH-3010 Bern, Switzerland
Manuscript submitted 23 October 2007. Accepted after revision 28 December 2007.
* Corresponding author. Tel: +41 31 632 21 11; fax: +41 31 632 14 14. E-mail address: etienne.delacretaz{at}insel.ch
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Abstract |
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Aims: Multiple arrhythmia re-inductions were recently shown in His-Purkinje system (HPS) ventricular tachycardia (VT). We hypothesized that HPS VT was a frequent mechanism of repetitive or incessant VT and assessed diagnostic criteria to select patients likely to have HPS VT.
Methods and results: Consecutive patients with clustering VT episodes (>3 sustained monomorphic VT within 2 weeks) were included in the analysis. HPS VT was considered plausible in patients with (i) impaired left ventricular function associated with dilated cardiomyopathy or valvular heart disease; or (ii) ECG during VT similar to sinus rhythm QRS or to bundle-branch block QRS. HPS VT was plausible in 12 of 48 patients and HPS VT was demonstrated in 6 of 12 patients (50%, or 13% of the whole study group). Median VT cycle length was 318 ms (250–550). Catheter ablation was successful in all six patients.
Conclusion: His-Purkinje system VT is found in a significant number of patients with repetitive or incessant VT episodes, and in a large proportion of patients with predefined clinical or electrocardiographic characteristics. Since it is easily amenable to catheter ablation, our data support the screening of all patients with repetitive VT in this regard and an invasive approach in a selected group of patients.
Key Words: Bundle-branch re-entry, Ventricular tachycardia storm, Catheter ablation
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Introduction |
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In some reported or unpublished cases, re-entry in the His-Purkinje system (HPS) was found to be the mechanism of repetitive or incessant ventricular tachycardia (VT).1
,2 Intermittent right ventricular pacing or repeated ventricular premature beats may be responsible for multiple VT initiations in these patients.1,2 We hypothesized that some of the patients with HPS VT had a predisposition to repetitive VT initiations, and consequently that HPS VT was a frequent mechanism of repetitive or incessant VT. Since repetitive VT episodes may be life-threatening and may severely affect quality of life of ICD patients, diagnosis of the VT mechanism and prompt treatment are warranted. Moreover, HPS VT responds poorly to anti-arrhythmic drugs, and can be easily treated with catheter ablation.3,4 Diagnosis of HPS VT requests electrophysiological testing, but some important clinical features can be used to select patients likely to have HPS VT and might directly benefit from an invasive approach.3–8 Accordingly, the aim of the study was to test the efficacy of clinical screening in patients with repetitive or incessant VT and to analyse the incidence of HPS VT in this special group of patients. |
Methods |
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Consecutive patients with clustering VT episodes were investigated. VT cluster was defined as the occurrence of
3 sustained VT or 3 VT triggering adequate and successful ICD intervention within a 2-week period. Incessant VT with multiple re-initiations was also considered as a VT cluster. Patients with idiopathic infundibular VT were excluded. Electrophysiological testing was performed in presence of one of the following characteristics suggesting HPS VT as arrhythmia mechanism: (i) severely impaired left ventricular function associated with valvular heart disease or with dilated cardiomyopathy; (ii) ECG during VT showing typical left or right bundle-branch block or VT QRS morphology similar to sinus rhythm QRS. Electrophysiological study and catheter ablation were performed in a fasting and mildly sedated state, after informed consent was obtained. A seven French 4 mm-tip radiofrequency (RF) mapping/ablation catheter (CelsiusTM, Biosense Webster, Diamond Bar, CA) was used for mapping and ablation. One or two additional 6 F quadripolar or decapolar electrode catheters were used. A 5000 U bolus of heparin was administered intravenously, followed by 1000 U/h.
Diagnosis of His-Purkinje system ventricular tachycardia
His-Purkinje system VT was diagnosed with usual criteria, 3, 6, 7 including (i) QRS morphology with typical left or right bundle-branch block pattern; (ii) exclusion of supraventricular tachycardia with aberrancy; (iii) each ventricular activation preceded by a stable His electrogram during tachycardia with HV interval slightly longer than that recorded during sinus rhythm; (iv) spontaneous changes in the ventricular cycle length preceded by similar change in the His or bundle-branch potential; and (v) if HPS VT was suspected but demonstration was impossible: VT termination during RF energy delivery or VT rendered non-inducible after catheter ablation of right or left bundle-branch.
Ablation for His-Purkinje system ventricular tachycardia
After establishing the diagnosis of HPS VT, the ablation catheter was positioned along the right or left ventricular septum distal to His bundle, in order to record a right or left bundle-branch potential. RF energy was applied from the distal electrode during sinus rhythm or sustained HPS VT. RF was applied in the power controlled mode (max 30 W) with a preset maximal temperature of 65° using an EP-shuttle generator (Stockert GmbH, Freiburg, Germany). Control stimulation was performed at least 20 min after the ablation procedure. A maximum of three extra stimuli were delivered at two basic pacing cycle lengths (600 and 400 ms) with minimum coupling interval of 200 ms. Successful ablation was defined as inability to induce the HPS VT.
Statistical analysis
Results are expressed as means ± SD unless otherwise indicated.
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Results |
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Characteristics of the patients
During 3-year period, 48 patients with clustering VT episodes were identified. Mean patient age was 56 ± 14 years; the study group included seven women (14%), 29 patients with ischaemic heart disease (60%), nine patients with dilated cardiomyopathy (18%), four patients with arrhythmogenic right ventricular cardiomyopathy (8%), one patient with valvular heart disease (2%), and five patients with miscellaneous cardiac disease (10%). Mean left ventricular ejection fraction was 39 ± 15%; 45 patients had an ICD (94%), 38 patients (79%) were on beta-blocker therapy and 32 patients (67%) were treated with anti-arrhythmic drugs. An electrophysiological study was performed in 12 patients with one of the characteristics suggesting HPS VT as arrhythmia mechanism: (i) left ventricular dysfunction associated with dilated cardiomyopathy or with valvular heart disease; (ii) VT QRS morphology showing typical left bundle-branch block or similar to sinus rhythm QRS morphology (Table 1). No patient had typical right bundle-branch block.
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His-Purkinje system VT was identified in six patients (13%), that is 50% of those with characteristics suggesting HPS VT (Table 1, Figures 1–3). In four patients with a 12-lead ECG of the clinical tachycardia available, the morphology of the induced VT matched that of the clinical tachycardia (Figures 1 and 2). In the two patients without 12-lead ECG available, other criteria strongly suggested that the induced VT had the same mechanism than the clinical VT, principally the fact that VT was abolished by RF ablation of HPS VT. Two of the six patients with HPS VT also had one additional VT inducible with a shorter cycle length that was considered non-clinical and was not targeted with RF ablation. All six patients with HPS VT presented with severe symptoms, recurrent syncope, or recurrent appropriate ICD shocks. They were men with a median age of 62 years (range 43–72). Three patients had dilated cardiomyopathy, one patient had valvular heart disease, one patient had coronary artery disease, and one patient had mild impairment of left ventricular function and mild conduction abnormalities of unclear etiology. Median left ventricular ejection fraction was 26% (range 15–55%), median VT cycle length was 318 ms (range 250–550 ms). Four patients were treated with anti-arrhythmic drugs. Of the whole study group, only 22 of 48 patients (46%) had had an electrophysiological testing prior to ICD implantation. Electrophysiological testing before ICD implantation demonstrated the inducibility of intramyocardial re-entrant tachycardia in 18 patients and induction of polymorphic VT or VF in four patients. Only one of the 12 patients with features suggesting HPS VT had had an electrophysiological testing before ICD implantation, and he had inducible VT not consistent with HPS VT. None of the six patients with HPS VT had had electrophysiological testing before they presented with VT clusters.
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Patients with clustering VT episodes without clinical features suggesting HPS VT primarily received anti-arrhythmic drug therapy. Eight of these patients underwent RF ablation of intra-myocardial reentrant VT later in the follow-up (Table 2).
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Electrophysiological study
During sinus rhythm, four patients had LBBB (incomplete in one patient), one patient had RBBB, and one patient with valvular heart disease had complete heart block with ventricular paced rhythm (Figure 3). Electrocardiogram during VT showed typical bundle-branch block pattern in all six patients, left bundle-branch block in five patients (incomplete in one patient) and right bundle-branch block in one patient. VT QRS morphology matched the sinus rhythm QRS, except in the patient with ventricular paced rhythm. One patient had RBBB and right superior QRS axis during VT. All five patients with spontaneous AV conduction showed prolonged HV interval during sinus rhythm with a median HV interval of 60 ms (range 55–64 ms). HV interval during HPS VT was slightly longer than HV during sinus rhythm (median 67.5 ms, range 60–84 ms). HPS VT mechanism was a bundle-branch re-entry in five patients and an interfascicular re-entry in one patient (Table 3).
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Result of radiofrequency ablation
Radiofrequency ablation targeted the right bundle in five patients and the left bundle (left posterior fascicle) in one patient. RF ablation terminated VT in five patients and/or rendered VT non-inducible in all six patients. Complete heart block subsequent to catheter ablation occurred in two patients and one patient already had heart block before the procedure. Two of these three patients underwent a device upgrade with cardiac resynchronization therapy because of symptomatic hear failure. One patient had permanent right ventricular pacing from his ICD following the procedure. Finally, all patients were maintained on their pre-ablation oral medication, including anti-arrhythmic drug treatment. Five patients remained free of any arrhythmia during a mean follow-up of 2.2 ± 1.5 year. One patient with dilated cardiomyopathy presented isolated episodes of fast VT with a cycle length different from that of HPS VT.
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Discussion |
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Ventricular tachycardia involving the HPS was found in 6 of 48 patients (12.5%) with clustering episodes of VT and was diagnosed in 50% of the patients selected based on predefined screening criteria. Since HPS VT is easily amenable to catheter ablation, our data support the screening of all patients with repetitive VT in this regard and an invasive approach in a selected group of patients.
Clustering VT episodes or VT storm may affect as much as one-third of ICD recipients, may be life-threatening, may severely alter quality of life, and request prompt treatment. Identifying patients with HPS VT is important, because they often respond poorly to anti-arrhythmic drugs and can be easily treated by catheter ablation,6,8,9 whereas patients with scar-related re-entry tachycardia, for example, may better respond to anti-arrhythmic drug and may be less susceptible to VT ablation in centers without special experience. Our study supports the screening of all patients with clustering monomorphic VT. Those patients with dilated cardiomyopathy, the patients with a history of cardiac valve repair or replacement, and finally all those with QRS morphology during VT similar to sinus rhythm QRS should undergo an electrophysiological testing.
Our study was inspired by the observation of a few patients with HPS VT and very frequent or incessant VT. Other investigators showed that right ventricular pacing can induce HPS VT.1 Spontaneous arrhythmia induction may become frequent in patients who have developed the conduction abnormalities in the HPS supporting a re-entry,10 and a predisposition to multiple VT re-initiations may be present in some patients with HPS VT. This is supported by the relatively high prevalence of HPS VT in our patient population. However, we could not directly compare the incidence of HPS VT in patients with either repeated VT episodes or with isolated episodes, because only a minority of the latest group undergoes electrophysiological testing. In Lopera’s series, HPS VT was observed in 8.5% of patients with recurrent VT referred to VT ablation.8 In Chien’s series, 6.7% of 120 patients studied were found to have HPS VT.11 Thus, indirect comparisons suggest that HPS VT is more frequently found in patients with VT clusters than in patients with less frequent episodes of VT. This is possibly in relation with a propensity of HPS-VT to be easily re-initiated by extrasystoles or right ventricular pacing.
Currently, the majority of the patients undergoes implantation of a defibrillator without prior electrophysiological study. Therefore, it appears important to carefully screen patients who develop clustering VT and to perform electrophysiological testing in those patients with characteristics commonly seen related to HPS VT.12
Limitations
We cannot rule that some of the patients who did not undergo EP testing did have HPS VT, and the sensitivity of selection criteria is not known. For example, several publications have described HPS VT with QRS morphology different from sinus rhythm QRS, that may not have been selected for electrophysiological testing when using the diagnostic criteria proposed.13,14
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Conclusion |
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In conclusion, HPS VT is the arrhythmia mechanism in a relatively large number of patients with repetitive VT episodes, and patients with HPS-VT may be at risk of multiple VT re-initiations. Our data support the screening of all patients with repetitive VT in this regard and an invasive approach in a selected group of patients.
Conflict of interest: none declared.
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Funding |
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This work was supported by a grant from the Swiss National Foundation (632-66101.01) to E.D.
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References |
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