Asian Cardiovasc Thorac Ann 2006;14:284-288
© 2006 Asia Publishing EXchange Ltd
Coincident Atrioventricular Nodal Reentrant and Idiopathic Ventricular Tachycardia
Babak Kazemi, MD,
Arash Arya, MD,
Majid Haghjoo, MD,
Mohammad A Sadr-Ameli, MD
Department of Pacemaker and Electrophysiology, Rajaie Cardiovascular Center, Tehran, Iran
For reprint information contact: Babak Kazemi, MD Tel: 98 21 202 8313 Fax: 98 21 2204 8174 Email: bkazemia1966{at}gmail.com, Department of Pacemaker and Electrophysiology, Rajaie Cardiovascular Medical and Research Center, Mellat Park, Vali-e-Asr Avenue, Tehran, 1996911151 Iran.
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ABSTRACT
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Double tachycardia appears to be relatively rare. Our single-center experience of coincident typical atrioventricular nodal reentrant and idiopathic ventricular tachycardia was reviewed. Between September 2003 and February 2005, 40 patients with idiopathic ventricular tachycardia underwent catheter ablation for right ventricular outflow tract tachycardia in 20, left ventricular outflow tract tachycardia in 2, and left ventricular septal tachycardia in 18. In 5 patients (2 men and 3 women, aged 27–49 years) there was a combination of typical atrioventricular nodal reentrant tachycardia and idiopathic ventricular tachycardia. They had no structural heart disease. The presenting arrhythmia was supraventricular in one and ventricular in 4. There was no case of inducibility of one arrhythmia by the other (tachycardia-induced tachycardia), but an interaction was observed in one tachycardia in which inducibility was seen only after ablation of the other arrhythmia. Radiofrequency ablation of either arrhythmia did not prevent induction of the other.
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INTRODUCTION
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Double tachycardia is classically defined as the simultaneous occurrence of an atrial or junctional tachycardia with a ventricular tachycardia. This type of tachycardia has been described in digitalis intoxication, after exercise, or during catecholamine use. Recently, both atrioventricular nodal reentrant tachycardia (AVNRT) and atrioventricular reentrant tachycardia have been observed to trigger paroxysms of idiopathic ventricular tachycardia (VT), in addition to cases of idiopathic VT that merely accompany AVNRT.1–5 There is a divergence of opinion on whether catheter ablation of both arrhythmia substrates should be performed in a single session, or whether elimination of the triggering effect of one arrhythmia may prevent the occurrence of the other.3,4 The purposes of this study were to report a single-center experience of the prevalence of coincident AVNRT with various forms of idiopathic VT, to describe the electrophysiologic study (EPS) findings, and to define the interaction between these combined arrhythmias and the effect of radiofrequency ablation (RFA) of one arrhythmia on the inducibility of the other.
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PATIENTS AND METHODS
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Between September 2003 and February 2005, 40 patients with VT underwent RFA at our institute. There was right ventricular outflow tract (RVOT) tachycardia in 20 patients, left ventricular outflow tract tachycardia in 2, and left ventricular septal tachycardia in 18. In 5 of these patients (12.5%), there was both typical AVNRT and idiopathic VT (Figures 1
, 2, & 3). They were 2 men and 3 women aged 27–49 years (mean, 34 years). In all 5 patients, structural heart disease was excluded by physical examination and transthoracic echocardiography. Except for one patient, the baseline electrocardiogram and 24-hour Holter monitoring showed evidence of ventricular arrhythmias (premature ventricular contraction, non-sustained VT, sustained monomorphic VT). Therefore, the presumptive clinical diagnosis before EPS was VT in all except patient no. 4 (Table 1) whose presenting arrhythmia was supraventricular tachycardia (SVT).
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Figure 1. Intracardiac electrograms and surface electrocardiograms during (A) atrioventricular nodal tachycardia and (B) right ventricular outflow tract tachycardia. Black arrow heads and white arrows show His-bundle potentials during atrioventricular nodal tachycardia and right ventricular outflow tract tachycardia, respectively (patient no. 2). His = His bundle, HRA = high right atrium, RVA = right ventricular apex.
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Figure 2. (A) Intracardiac electrograms and selected surface electrocardiograms during typical atrioventricular nodal tachycardia; (B) Twelve-lead surface electrocardiogram during left ventricular outflow tract tachycardia; (C) Intracardiac electrograms and selected surface electrocardiograms during ablation of left ventricular outflow tract tachycardia (patient no. 5). Abl U1 = distal unipolar ablation catheter, Abl U2 = proximal unipolar ablation catheter, His = His bundle, HRA = high right atrium, RVA = right ventricular apex.
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Figure 3. Intracardiac electrograms and surface electrocardiograms during (A) typical atrioventricular nodal tachycardia and (B) left septal ventricular tachycardia. Arrows point to His bundle potentials during arrhythmias (patient no. 4). His = His bundle, HRA = high right atrium, RVA = right ventricular apex.
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All patients gave written informed consent for EPS and RFA, and the procedure was performed in a postabsorptive and non-sedated state. All antiarrhythmic drugs were withdrawn for at least 5 half-lives prior to the study. Three quadripolar 6F Daig catheters (St. Jude Medical, St. Paul, MN, USA) were introduced via the left femoral vein and positioned at the right ventricular apex (and RVOT), the bundle of His, and the high right atrium. A 7F steerable decapolar catheter (Marinr, Medtronic, Inc., Minneapolis, MN, USA) was introduced using a retrograde approach via the left femoral artery into the left ventricle in 2 patients with left septal VT. A 7F 4-mm tip ablation catheter (Conductr, Medtronic, Inc., Minneapolis, MN, USA) was used for mapping the VT. In all patients, programmed atrial and ventricular stimulation was carried out using 3 basic cycle lengths (600, 500, 400 msec) and up to 3 premature stimuli (
180 msec) with and without isoproterenol. Typical AVNRT was diagnosed using the following criteria: demonstration of a dual atrioventricular nodal response with programmed atrial stimulation and induction of tachycardia upon reaching a critical AH delay ( 50 msec increase in AH interval with 10 msec decrease in cycle length of the premature stimulus); a short ventriculoatrial interval (< 70 msec); and proof using pacing maneuvers that atria or ventricles were not required in the maintenance of the arrhythmia.6
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RESULTS
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The arrhythmia characteristics are shown in Table 2. At EPS, the first induced arrhythmia was typical AVNRT in 4 patients and RVOT-VT in one. All AVNRTs were induced by atrial extrastimulation. All VTs were induced by ventricular extrastimulation or ventricular overdrive pacing, except for one patient with RVOT-VT that was induced by atrial extrastimulation. In most cases, isoproterenol (up to 4 µg·min-1) was needed for arrhythmia induction. In all 5 cases, double tachycardia was diagnosed incidentally during EPS. In no case could we show inducibility of one arrhythmia by the other (tachycardia-induced tachycardia). However, there was an interaction between the 2 types of tachycardia in patient no. 5 who had a pre-study clinical diagnosis of VT and no ventricular arrhythmia could be induced until after successful slow-pathway ablation; only then was VT reproducibly inducible with ventricular overdrive pacing under isoproterenol infusion.
All ablation procedures were carried out in a single session, except in patient no. 4 whose second arrhythmia (left septal VT) was ablated in a separate session because of prolonged study and ablation time during the first one. Combined ablation of both clinical and non-clinical arrhythmias was performed because of the likely recurrence of the second arrhythmia (usually AVNRT) in the near future.4 All patients had successful ablation procedures. During follow-up, one patient (no. 1) who had multiple anterior jumps in the AH interval during the initial study, experienced recurrence of symptoms 4 months later and underwent successful repeat ablation of both arrhythmias (AVNRT and RVOT-VT). All others remained free of symptoms during the follow-up period.
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DISCUSSION
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The main findings of this study were: that AVNRT can coexist with all forms of idiopathic VT; there is a relatively high prevalence of AVNRT in idiopathic VT (12.5%); and RFA of one arrhythmia may not prevent the inducibility of the other, but there might be some interaction between these double tachycardias both before and after ablation. Although there have been several case reports of coincident idiopathic VT and AVNRT, a recent study on a relatively large patient population with idiopathetic VT (46 cases) reported a surprisingly high coincidence (15%) of AVNRT and RVOT-VT.1–5 Our study on 40 cases confirmed a high coincidence (12.5%). Cooklin and McComb1 suggested that this coincidence might be no more than a chance association, and several studies on large series of patients with idiopathic VT have failed to report any correlation between these arrhythmias.7 These suggestions appear to be supported by the presence of different mechanisms for each type of tachyarrhythmia. While AVNRT and left septal VT have a reentrant mechanism, outflow tract VT results mainly from catecholamine-mediated delayed after-depolarization and c-AMP-triggered activity.8,9 However, we believe that the relatively high coincidence of IVT and AVNRT among our cases and in the study by Kautzner and colleagues4 might be explained by the different EPS protocol used (systematic atrial and ventricular programmed electrical stimulation and consistent use of isoproterenol in all patients, both before and after ablation), and/or a difference in the patient population. On the other hand, these 2 different arrhythmias may actually have some points in common. It is interesting to note that the atrioventricular node and the outflow tracts are anatomically very close. Furthermore, the observed high occurrence of AVNRT among subjects with idiopathic outflow tract VT might be explained by the abundance of specialized myocytes both perinodal and in the outflow tract, or by the presence of autonomic dysfunction and catecholamine sensitivity of both arrhythmias.2,10–15
There are several reports of interactions of SVT with the inducibility of VT.1–4 We only observed this interaction in patient no. 5 who had a presumptive clinical diagnosis of VT but no ventricular arrhythmia could be induced until the slow pathway was successfully ablated. The reason for this may be the development of parasympathetic denervation by slow pathway ablation, and changing the sympathovagal balance in favor of sympathetic dominance, hence inducing a catecholamine-sensitive left ventricular outflow tract VT.16 Vagal postganglionic neurons to the sinus node are located in a fat pad adjacent to the right pulmonary vein, while the vagal postganglionic neurons to the atrioventricular node are located in an inferior vena cava-left atrial fat pad.17 Chiou and colleagues18 reported that the elimination of each fat pad with RFA selectively denervated the vagal input to the atria and to the sinus and atrioventricular nodes. Local parasympathetic denervation has been observed after ablation of SVT.16 If parasympathetic nerve innervation in humans is similar to the canine heart, a decrease in heart rate variability by energy delivered along the mitral or tricuspid annulus is likely because it interrupts parasympathetic fibers innervating the sinus node. Although there was a high coincidence of typical AVNRT and idiopathic VT among our cases and those of Kautzner and colleagues,4 it was most likely to be of chance occurrence.
We could not confirm the prognostic and clinical importance of the second non-clinical arrhythmia (usually AVNRT). However, according to the reported likely recurrence of this arrhythmia in the near future, we recommend performing combined ablation of both the clinical and non-clinical arrhythmias in the same session.4 In our patients, RFA of either arrhythmia did not prevent induction of the other. However, Wagshal and colleagues3 observed the opposite in their case report, and described the coincidence of left septal VT and AVNRT, and non-inducibility of the former with successful ablation of the later. Our data support the strategy of complete systematic programmed electrical stimulation in patients with AVNRT who have premature ventricular contraction morphology compatible with an outflow tract or left septal origin, or in patients with idiopathetic VT showing dual atrioventricular nodal physiology. RFA of both arrhythmia substrates is feasible in most patients during a single session.
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REFERENCES
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ABSTRACT
INTRODUCTION
