A new method for induction of atrioventricular nodal reentrant tachycardia in non-inducible cases

Abstract

Aim

In some patients with clinical paroxysmal supraventricular tachycardia (PSVT), who are candidates for radiofrequency (RF) catheter ablation, attempts for the induction of arrhythmia during the electrophysiological study (EPS) fail despite different stimulation protocols even during the isoproterenol infusion and atropine injection. The presence of an atrial-His interval (AH) jump during decremental pre-mature atrial stimulation is the only clue for slow pathway ablation in these patients; in occasional patients, however, the AH jump is an accidental finding and the real arrhythmia is not atrioventricularnodal reentrant tachycardia (AVNRT). We aimed to introduce a new method for the induction of AVNRT in these patients.

Methods and results

Ten patients (50% male, mean age=44.40 ± 12.80 years) with clinical PSVT who were referred to our department for the EPS and RF catheter ablation were selected. These patients had documented clinical PSVT with non-inducible arrhythmia during the EPS with different stimulation protocols even during the isoproterenol infusion and atropine injection but they only showed an AH jump. To induce AVNRT, low-watt (15–20), low-temperature (40–45°C) RF currents were delivered into the slow pathway area for a maximum of 40 s. Atrioventricularnodal reentrant tachycardia was inducible in five cases (50%, three male, mean age=45.80 ± 9.65 years). Induction of AVNRT occurred either during the RF current application after the occurrence of junctional ectopic beats or after another stimulation protocol.

Conclusion

A low-watt, low-temperature RF current application into the slow pathway area can be a provocative method for the induction of AVNRT probably by AV-junction warming and conduction-velocity augmentation.

Introduction

Patients with documented episodes of paroxysmal supraventricular tachycardia (PSVT) at times do not have inducible tachycardia in the electrophysiology laboratory (EP lab).^1,2 The presence of a dual atrioventricular (AV) node pathway, which serves as the substrate for atrioventricularnodal reentrant tachycardia (AVNRT), suggests a possible pre-dilection for this type of tachycardia.

Evidence of dual AV node pathways in patients with a history of PSVT who do not have inducible tachycardia in the EP lab can be an indication for slow pathway ablation.³ However, evidence of dual AV node pathways may be present in individuals who have never had PSVT.^4,5 On the other hand, sometimes the presence of dual AV node physiology is an accidental finding and the real arrhythmia is not AVNRT. The arrhythmias that can be encountered on this occasion are: automatic atrial tachycardia; intra-atrial reentrant tachycardia; atrial flutter with 1:1 or 2:1 conduction, in which the flutter waves are not apparent and mimic PSVT; and the junctional ectopic tachycardia. Therefore, it should not be assumed that slow pathway ablation will be therapeutic in all patients with dual AV node physiology and non-inducible arrhythmia.⁶

There are several ways to induce AVNRT: Previous studies have reported that in the low-hyperthermic range between 38 and 45°C, there was an increase in the maximal dv/dt of action potential.⁹ So we thought that low-temperature, low-watt RF current can be a provocative method for induction of AVNRT by conduction-velocity augmentation in the slow pathway area.

• The most common way is through the introduction of atrial or ventricular pre-mature depolarization beats. Double atrial stimuli can also be used.

• Continuous burst pacing or rapid incremental pacing in the right atrium (RA); the coronary sinus may induce the tachycardia.

• Decremental ramp atrial extra stimuli have also been shown as an effective method to induce AVNRT. To perform these, the total number in S1 drive train must be set to one and then S1, S2, S3, S4, S5, and S6 must be turned on at the following cycle lengths: S1: 600, S2: 550, S3: 500, S4: 450, S5: 400, and S6: 350 ms. Thus, a train consisting of a total of six atrial premature depolarizations (APD) at a decremental coupling interval of 50 ms from previous APDs is delivered from the high RA. If no supraventricular tachycardia is induced, S1 is programmed at 550 ms and subsequent APDs are also decreased by 50 ms, to a minimum of 300 ms.⁷

• If there is no success with the above pacing protocols, the operator can start pharmacological agents such as isoproterenol or atropine.

• Non-pharmacological manoeuvres such as hyperventilation and 45° head-up tilt posture during pacing have also been studied to facilitate the induction of AVNRT.⁸ In rare cases, in spite of using the above manoeuvres, AVNRT is still non-inducible.

We herein introduce a new method to use a low-temperature, low-watt radiofrequency (RF) current application into the slow pathway region to induce AVNRT.

Method

Ten patients (50% male, mean age=44.40 ± 12.80 years) with clinical PSVT who were referred to our department for the EP study and RF catheter ablation were studied.

These patients had recurrent episodes of PSVT documented by superficial electrocardiographic (ECG) recordings, but there was non-inducible arrhythmia in the EP lab despite the application of different stimulation protocols even after isoproterenol infusion (1→4 μg/min) and atropine injection (1 mg). There was no evidence of accessory pathway in these patients, but dual AV node physiology was observed.

Based on a physical examination, a 12-lead ECG, and an echocardiogram, none of these patients had any evidence of structural heart disease except for one patient with a history of coronary artery bypass graft surgery (Table 1).

The EP study was performed in post-absorptive state after written informed consent had been obtained and after anti-arrhythmic drug therapy had been discontinued for at least five half-lives. Three quadripolar catheters were inserted in a femoral vein and positioned in the high RA, the His bundle position, and the right ventricle, and one decapolar catheter was positioned into the coronary sinus.

Atrial and ventricular overdrive pacing and programmed stimulation were conducted to determine the conduction and refractoriness properties of the AV node, to rule out the presence of accessory pathway, and to induce supraventricular tachycardia.

Attempts to induce supraventricular tachycardia by atrial and ventricular overdrive pacing and programmed stimulation were repeated during 1–4 μg/min infusions of isoproterenol titrated to result in a sinus rate of 120–130 bpm, and again after the intravenous administration of 1 mg of atropine.

In spite of using the above manoeuvres, none of the patients had inducible SVT or evidence of accessory pathway; all the patients, however, had evidence of dual AV node pathway. This evidence consisted of dual AV node physiology, defined as an increment of 50 ms or more in the A2 H2 interval in association with a 10 ms decrement in the A1 A2 interval. There was no echo beat during the atrial-His interval (AH) jump.

In case of non-inducible arrhythmia and dual AV node physiology, low-watt (15–20 W), low-temperature (40–45°C) RF currents were delivered into the slow pathway area, using OSYPKA 7–60 ablating catheters for 40 s. The RF generator was OSYPKA HAT 300. This study has been approved by our institutional review board.

Follow-up

Patients undergoing electrophysiology study and RF catheter ablation were normally followed up by being visited in the electrophysiology outpatient clinic. Seven of our study patients were also visited in the clinic and underwent Holter monitoring for 24 h. Three patients were followed up by telephone questioning if they experienced any recurrence palpitation.

Statistical analysis was performed using a statistical package (SPSS 18.0, Chicago, IL, USA). The categorical variables were presented in numbers and percentages (%), and the continuous variables as mean ± standard deviation.

Results

The clinical characteristics of the patients in this study are depicted in Table 1. By applying the low-temperature, low-watt RF current, AVNRT was inducible in five (50%) cases (mean age=45.80 ± 9.65 years), three (60%) of whom were male. Among the patients in whom the induction of AVNRT was not successful (mean age=43.00 ± 16.49 years) by the same method, four (80%) were female. In all patients (inducible or non-inducible cases) slow pathway ablation was performed by applying RF current (25–40 W at 70°C).

Inductions of AVNRT occurred either during the RF current application and occurrence of junctional ectopic beats or after other stimulation protocols.

After mean follow-up of 4.90 ± 4.10 months (range: 1–15 months) none of the patients of either group (inducible or non-inducible group) had recurrence of arrhythmia (AVNRT) and no cases of AV block was observed, except for one patient with clinical PSVT, AH jump during decremental pre-mature atrial pacing, and non-inducible arrhythmia group who had one episode of atrial tachycardia.

Discussion

Nath et al⁹ examined action potential in vitro in a superfussed guinea pig papillary muscle preparation. In the low hyperthermic range between 38 and 45°C, there was an increase in the maximal dv/dt of action potential, indicating enhanced sodium channel kinetic. In the moderate hyperthermia range from 45 to 50°C, the maximal dv/dt decreased below the baseline values.

Simmers et al.^10,11 examined the effect of hyperthermia on impulse conduction in vitro in preparation of superfussed canine myocardium. Average conduction velocity at a baseline temperature of 37°C was 0.35 m/s. When the superfussed temperature was raised, conduction velocity increased to super normal values, reaching a maximum of 114% of the baseline at 42.5°C. At a temperature >45.4°C, the conduction velocity slowed, transient conduction block was observed between 49.5 and 51.5°C, and >51.7°C permanent block was observed.

It is obvious that the sole effect of the RF current on the electrophysiological properties of the myocardium is hyperthermic, but the effect of the RF current varies when the energy of the RF current is very weak. By applying (low-watt, low-temperature) RF currents, the net effect is the augmentation of the conduction velocity; and with higher power of the RF energy, permanent block is the result. Therefore, by applying low-watt, low-temperature RF currents into the slow pathway area, the conduction velocity of the slow pathway increases and junctional ectopic beats or pre-mature atrial beats are able to propagate more easily in this region and facilitate the induction of AVNRT without any danger to the AV node and producing permanent AV block, a complication about whose occurrence operators and patients are always concerned.¹²

After the induction of AVNRT, the operator can increase the power of RF energy for slow pathway ablation and complete the procedure with more confidence.

Conclusion

A low-watt, low-temperature RF current application into the slow pathway region can be a provocative method for the induction of AVNRT probably by AV-junctional warming and conduction-velocity augmentation. The operator can increase the power of the energy after the induction of AVNRT and perform slow pathway ablation more confidently afterwards.

Conflict of interest: none declared.

References