© 2003 by European Society of Cardiology
Coincidence of idiopathic ventricular outflow tract tachycardia and atrioventricular nodal reentrant tachycardia
ihák
ura
níkDepartment of Cardiology, Institute for Clinical and Experimental Medicine Prague, Czech Republic
Manuscript submitted 3 July 2002. Accepted after revision 29 March 2003.
Correspondence: Josef Kautzner, Department of Cardiology, Institute for Clinical and Experimental Medicine, Víde
ská 1958/9, 140 21 Prague 4, Czech Republic. Tel.: +4202-4172-20-11; Fax: +4202-4172-82-25; E-mail: josef.kautzner{at}medicon.cz
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Abstract |
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BACKGROUND: Tachycardia-induced tachycardia appears to be a relatively rare condition. In such cases an important question arises whether catheter ablation of one arrhythmia may prevent the occurrence of another. This paper reviews single-centre experience with coincident idiopathic outflow tract ventricular tachycardia (VT) and atrioventricular (AV) nodal reentry tachycardia (AVNRT), and strategy of treatment.
METHODS AND RESULTS: Seven of 46 patients (15%) with clinically documented idiopathic outflow tract VT were found to have reproducibly inducible AVNRT at the time of an electrophysiological study. There were two men and five women (mean age 35±9 years, range 20–44) without structural heart disease. During the study, AVNRT spontaneously triggered VT in three cases. Radiofrequency catheter ablation of the slow pathway did not suppress subsequent inducibility of VT in any of them. Successful catheter ablation of VT did not prevent clinical recurrence of AVNRT in one patient, and led to transition of VT into typical AVNRT in another.
CONCLUSION: Coincidence of idiopathic outflow tract VT and AVNRT was found in 15% of cases of clinically documented idiopathic VT. Catheter ablation of one arrhythmia substrate did not prevent inducibility or clinical recurrence of the other. These data support the strategy of performing catheter ablation of both arrhythmia substrates during one session.
Key Words: Idiopathic ventricular tachycardia, AV nodal reentry, radiofrequency catheter ablation
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Introduction |
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Tachycardia-induced tachycardia, or the so-called double tachycardia, has rarely been reported in the literature. An association between supraventricular and ventricular tachycardias (VT) was first noticed either in the setting of digitalis intoxication and/or in left ventricular dysfunction[1
–3]. More recently, both atrioventricular (AV) reentry and AV nodal reentry tachycardias (AVNRT) have been anecdotally observed to trigger paroxysms of idiopathic VT[4–7]. However, our observations over a 4-year period suggest that such coincidence between the two latter tachycardias may be more frequent than expected. There is a lack of knowledge whether catheter ablation of both arrhythmia substrates should be performed in these cases at once or whether elimination of the triggering effect of one arrhythmia may prevent the occurrence of the other[6]. The aim of this paper is to report single-centre experience with coincident idiopathic outflow tract VT and AV nodal reentry, and to describe the effect of radiofrequency (RF) catheter ablation of one arrhythmia substrate on inducibility of the other arrhythmia. |
Methods |
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Patient characteristics
In a series of 46 consecutive patients with clinically documented idiopathic outflow tract VT referred for an electrophysiological study and RF ablation over a 4-year period (April 1997–April 2001), seven were found to have reproducibly inducible AVNRT at the time of the study. Clinical characteristics of the study patients are listed in Table 1. There were two men and five women (mean age 35±9 years, range 20–44). None of them had either a history of cardiovascular disease or significant structural heart disease detected during routine diagnostic assessment. Of note is that only two of them presented with two distinct forms of palpitations. Two other patients with fast VTs had a history of presyncopal episodes.
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In order to estimate the occurrence of idiopathic VT in patients referred for RF ablation of documented supraventricular tachycardia, we reviewed a series of 400 cases that were found to have AVNRT during the electrophysiological study in our centre over the identical time period.
Electrophysiological study and ablation
None of the patients was receiving antiarrhythmic medication at the time of the investigation. Quadripolar electrode catheters were placed in the right ventricular apex and in the His bundle region. A 7-Fr, 4 -mm-tip, ablation catheter (Celsius, Cordis-Webster, Baldwin Park, CA) was used for mapping of VT within the right ventricular outflow tract (RVOT). Whenever mapping in the RVOT and ECG morphology of VT suggested an alternative location of arrhythmia origin, another ablation catheter was introduced retrogradely into the left ventricular outflow tract (LVOT) and a 2-Fr mapping catheter (Pathfinder, Cardima, Fremont, CA) was placed in the great cardiac vein, respectively. Both incremental atrial and ventricular pacing was used in all patients at baseline. Provided VT was not initiated, programmed ventricular stimulation was performed and finally, isoprenaline was used. In patients with inducible AVNRT, an additional 7-Fr, deflectable, deca- or octapolar catheter (Cordis-Webster, Baldwin Park, CA) with a 2-mm interelectrode distance and 10 -mm space between each electrode pair was introduced into the coronary sinus. AVNRT was diagnosed using the following criteria: demonstration of dual AV nodal refractory curves in response to atrial pacing and/or atrial premature beats with initiation of AVNRT dependent on critical AH interval during slow pathway conduction (except Case 7), the presence of retrograde atrial activation and retrograde P within the QRS complex, and proof that neither atria nor ventricles are required for maintenance of AVNRT using pacing manoeuvres[8].
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Results |
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During the electrophysiological study, AVNRT was reproducibly induced by atrial pacing in five patients at the beginning of the study. In three of them, AVNRT was readily inducible only after isoprenaline administration aimed at induction of clinically documented outflow tract VT. In another patient (Case 5), symptomatic AVNRT was first noticed following RF-induced termination of VT (Fig. 1), and was reproducibly inducible during atrial pacing on isoprenaline. In the last patient (Case 7), AVNRT was only inducible during ventricular pacing on isoprenaline following successful RF ablation of VT. Induced AVNRT was sustained in all patients, and often required termination by pacing. AVNRT was observed to trigger runs of VT spontaneously and repeatedly in three cases (Fig. 2). Although the cycle length of both arrhythmias was practically identical in two of them (Cases 1 and 4), triggered VT was faster in the remaining patient (Case 6). On the contrary, VT was not documented to initiate AVNRT.
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Early in our experience (Case 1), only successful catheter ablation of VT was performed during the first session as AVNRT was not clinically documented on ECG. However, it did not prevent subsequent paroxysms of palpitations with ECG recording suggestive of AVNRT. RF ablation of the slow pathway was performed 7 months later, leading to complete cure of the patient. Similarly, the second patient with a history of two forms of palpitations (Case 2) had clinically documented only paroxysms of VT suggestive of its origin in the RVOT. However, the only inducible arrhythmia at the time of electrophysiological study was atypical AVNRT that was perceived by the patient as her clinical symptoms. Despite successful RF ablation of the slow pathway, the patient continued to have paroxysms of different palpitations documented as RVOT VT. Subsequent RF ablation of the arrhythmogenic focus during clinical VT abolished all symptoms. In another patient (Case 5), termination of RVOT VT during RF application led to transition into rapid typical AVNRT. Subsequent study confirmed functional AV nodal duality and easily inducible AVNRT. After obtaining informed consent from the patient, successful RF ablation of the slow pathway was performed. Ablation of the slow AV nodal pathway during the same procedure was selected as the first step in the remaining three patients with inducible AVNRT, mainly because easy inducibility of AVNRT interfered with mapping of clinical VT. All these patients accepted the procedure. In one of them, VT was also triggered by accelerated junctional rhythm during RF ablation of the slow pathway (Fig. 3). Importantly, ablation of the slow AV nodal pathway did not suppress subsequent inducibility of VT in any of these patients. Successful ablation of VT was performed in one of them in the pulmonary valve cusp. VT was not ablated in two other patients due to subepicardial location of the arrhythmogenic focus. Both patients had predominantly negative QRS in lead I, and R wave transition before V3. Finally, in one patient with recurrence of VT from the RVOT after previous RF ablation (Case 7), symptomatic typical AVNRT was repeatedly induced during ventricular stimulation (CL of 353 ms) on isoprenaline after successful re-ablation of VT. The patient was willing to undergo slow pathway RF ablation at the same time and remains symptom-free during long-term follow-up (28 months).
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None of 400 cases of AVNRT who underwent RF ablation of the slow pathway in our centre over an identical time period had inducible VT during the electrophysiological study. More importantly, VT was not induced in any of them despite routine testing with intravenous infusion of isoproterenol.
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Discussion |
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Despite very rare reports of an association between idiopathic VT originating in the RVOT and AVNRT in the literature[4]
, our data on seven cases collected over a 4-year period suggest that such coincidence may be more common. In this respect, it appears to be the largest cohort of patients with double tachycardia of any nature. On the contrary, no such association has been described in previously reported larger series on outflow tract VTs[9–12]. The reasons for such a striking difference are not easy to explain. It may reflect consistent use of isoprenaline and incremental atrial pacing plus programmed atrial stimulation in all our VT patients before and after RF ablation. Under such circumstances, one can expect increased probability to induce a so-far latent arrhythmia. Alternatively, regional variations in the incidence of specific arrhythmias might contribute to apparent difference.
Surprisingly frequent inducibility of AVNRT in patients with documented idiopathic VT in our series may even imply that this is not just a random coexistence. However, this notion does not appear to be supported by data on different mechanisms of both types of arrhythmia. While AVNRT is a typical reentrant tachycardia arising from the AV nodal and perinodal tissue[13], it is believed that both paroxysmal and repetitive forms of outflow tract VT result from c-AMP mediated triggered activity[14]. Such activity is typically induced from Purkinje fibres, and possibly from the M cells, localized in the deep layer of ventricular wall and interventricular septum[14,15]. The mechanism of triggered activity is also supported by demonstration of a relatively narrow range of cycle lengths for induction of the arrhythmia and is consistent with experimental data showing a decrease in the amplitude of delayed afterdepolarizations at cycle lengths above and below the specific induction window[16]. This is consistent with our observation of the triggering effect of AVNRT of similar cycle length on outflow tract VT. On the other hand, observed high occurrence of AVNRT among subjects with documented idiopathic outflow tract VT may suggest that these patients have more abundant specialized myocytes both in the perinodal area[17] and in the outflow tract[18]. Some support for this hypothesis comes from experimental data on development of the embryonic heart and the incorporation of the flanking, slow-conduction segments in the definitive ventricles[19]. In this respect, conduction tissue-specific markers were found expressed in the outflow tract during cardiac development[20]. The above view seems to be further substantiated by observation of thermal sensitivity of the tissue in either region. Local thermal stimulus in the perinodal area is traditionally known to induce accelerated junctional rhythm. Similarly, temperature-dependent initialization and/or acceleration of the outflow tract VT were observed when heating in the close proximity to the arrhythmogenic focus[21]. Furthermore, it is intriguing that three of seven patients with coincident idiopathic VT and AVNRT in our series presented with the arrhythmogenic focus localized either in uppermost part of the interventricular septum or more epicardially, in close proximity to the great cardiac vein. Whether such a less usual location of the focus might reflect the presence of specialized tissue in abnormal sites or simply a larger mass of such tissue remains unknown.
No inducible VT was observed in a much larger series of patients with AVNRT, despite administration of isoprenaline in all of them. This observation may suggest that VT is generally easier to induce and therefore, patients with a coincident substrate for VT are identified clinically as having repetitive runs or paroxysms of VT. AVNRT may also trigger VT shortly after its origin, so that ECG recordings at the time of presentation show only VT. We observed the phenomenon of triggering VT in three of our patients.
From the practical point of view, our data seem to confirm that catheter ablation of one arrhythmia substrate does not influence inducibility and/or clinical occurrence of the other arrhythmia. Although it is hard to extrapolate what clinical relevance of inducible AVNRT might be for the patient, we decided to perform ablation of the slow AV nodal pathway during the same session in all but the first two patients. The reason for this approach was mainly easy inducibility of AVNRT that interfered with mapping and ablation of idiopathic VT. In some patients, AVNRT was perceived as clinical symptoms. All patients received explanation of the situation and potential risks, and accepted the suggested approach. We could not find any previous reports on this topic except one anecdote of successful control of concurrent arrhythmia following catheter ablation of the slow AV nodal pathway[6]. However, concurrent arrhythmia in this case was of different mechanism (idiopathic fascicular VT), and its control was apparently achieved only because both arrhythmias were reentrant in origin and with frequent spontaneous transformations from one tachycardia to the other.
In conclusion, we report seven cases of coincidence of two tachycardias with apparently separate mechanisms of origin—idiopathic outflow tract VT and AVNRT. Although one tachycardia may trigger the other, catheter ablation of one arrhythmia substrate was not found to influence either inducibility or clinical occurrences of the concurrent tachycardia. These data support the strategy of performing catheter ablation of both arrhythmia substrates during one session.
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