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Atrial-His-atrial and atrial-His-His-atrial responses during slow–fast atrioventricular nodal reentrant tachycardia

Open AccessPublished:January 19, 2023DOI:https://doi.org/10.1016/j.hrcr.2023.01.005

      Keywords

      Introduction

      Distinguishing junctional tachycardia (JT) from slow–fast atrioventricular nodal reentrant tachycardia (AVNRT) is challenging during electrophysiologic testing. Both rhythms have similar intracardiac electrogram activation patterns and earliest atrial activation sites with catheter mapping. Atrial pacing at a rate slightly faster than the tachycardia cycle length (TCL) [i.e., atrial overdrive pacing (AOP)] from the high right atrium (HRA) or the proximal coronary sinus (CS) during a tachycardia could quickly differentiate JT from AVNRT. Previously, JT was identified with an atrial-His-His-atrial (AHHA) response in 100% (8/8) of cases, whereas AVNRT was identified with an atrial-His-atrial (AHA) response in 100% (14/14) of cases.
      • Fan R.
      • Tardos J.G.
      • Almasry I.
      • Barbera S.
      • Rashba E.J.
      • Iwai S.
      Novel use of atrial overdrive pacing to rapidly differentiate junctional tachycardia from atrioventricular nodal reentrant tachycardia.
      We presented a rare case of slow–fast AVNRT, wherein the response to AOP from the HRA exhibited an AHHA response, whereas that from the proximal CS exhibited an AHA response.

      Case presentation

      A 65-year-old man presented to the emergency department due to repetitive episodes of palpitations. A 12-lead electrocardiogram (ECG) showed a normal sinus rhythm, and a regular narrow QRS complex tachycardia was identified during the palpitations (Supplementary Figure 1). After obtaining the patient’s informed consent, an electrophysiological study and catheter ablation of the tachycardia were performed. Under local anesthesia, four electrode catheters were inserted into the femoral and brachial veins and positioned in the right atrial appendage, His bundle region, CS, and right ventricular apex (Supplementary Figure 2A). At baseline, the atrio-His (AH) and His-ventricular intervals were 72 and 41 ms, respectively. Dual atrioventricular nodal physiology was observed during programmed double atrial extrastimuli. Programmed ventricular stimulation exhibited decremental ventriculoatrial conduction with the earliest atrial activation site located on the His electrograms (Supplementary Figure 2B). Para-Hisian pacing showed a retrograde AV nodal pattern. After infusion of isoproterenol, SVT with a fixed 1:1 AV relationship was induced by double atrial extra-stimuli, revealing an AH jump (Supplementary Figure 2C). During the tachycardia, the AH and His-atrial intervals were 430 and 64 ms, respectively. The cycle length oscillations of <15 ms were observed during the tachycardia. The atrial activation sequence during the tachycardia was identical to that during right ventricular pacing. Premature ventricular complexes during His refractoriness did not perturb the tachycardia. After the right ventricular overdrive pacing, the first return electrogram resulted in a ventricular–atrial–ventricular response, but the TCL after the pacing became altered by the pacing; thus, we could not evaluate the post-pacing interval. Instead, we confirmed that the atrial timing was perturbed after the transition zone. From those findings, the tachycardia was diagnosed as slow–fast AVNRT. However, the response to AOP from the HRA was an AHHA pattern (Figure 1A), whereas that from the proximal CS was an AHA pattern (Figure 1B).
      Figure thumbnail gr1
      Figure 1Different responses to atrial overdrive pacing (AOP) were observed during the tachycardia. A: AOP from the HRA (TCL 489 ms, PCL 475 ms) exhibited an atrial-His-His-atrial response, which was presumably caused by the simultaneous atrioventricular nodal conduction: one conducting via the fast pathway (red solid arrows) and the other via the slow pathway (red dotted arrows). PPI–TCL was 138 ms, which suggested that the HRA was far from the tachycardia circuit. The His electrograms immediately after the stimulus (H1) were directly activated by pacing, whereas the subsequent His electrograms (H2) were activated after penetrating the slow conduction zone. The H1H2 interval was shorter than the TCL. B: AOP from the proximal CS (TCL 489 ms, PCL 475 ms) exhibited an atrial-His-atrial response. PPI–TCL was 66 ms, which suggested that the proximal CS was near the tachycardia circuit. The last captured His (H1) electrograms were the second beat after the stimulus, suggesting the His bundle electrograms were orthodromically captured. The H1H2 interval was similar to the TCL. HB, His bundle; CS, coronary sinus; HRA, high right atrium; RVA, right ventricular apex; TCL, tachycardia cycle length; PCL, pacing cycle length; PPI, post-pacing interval.
      As described in the Discussion section, an AHHA pattern would be possible in slow–fast AVNRT with a double ventricular response. Thus, radiofrequency energy was applied to the slow pathway potentials in the posteroseptal region. With a gradual titration increase of the radiofrequency energy from 15 W to 30 W, a steady junctional rhythm was confirmed during the application. After antegrade slow pathway modification, any evidence of dual AV nodal physiology (absence of an AH jump or echo beat) with and without isoproterenol was absent. During the 6-month follow-up, there was no recurrence of any symptomatic arrhythmias.

      Discussion

      The response to AOP during the tachycardia is important to distinguish AVNRT from JT. We described a case of slow–fast AVNRT that exhibited AHHA and AHA responses to AOP from the HRA and proximal CS, respectively. Inconsistent results can mislead the diagnosis, and the underlying mechanism should be cleared to prevent unnecessary ablation.
      In principle, an AHHA response is observed in JT (Figure 2A), whereas an AHA response is observed in AVNRT (Figure 2B).
      • Fan R.
      • Tardos J.G.
      • Almasry I.
      • Barbera S.
      • Rashba E.J.
      • Iwai S.
      Novel use of atrial overdrive pacing to rapidly differentiate junctional tachycardia from atrioventricular nodal reentrant tachycardia.
      Thus, the mechanism of why the slow–fast AVNRT exhibited an AHHA response should be explained. A double ventricular response resulting from simultaneous antegrade conduction over the fast and slow pathways of the AV node clears this phenomenon.
      • Kim S.S.
      • Lal R.
      • Ruffy R.
      Paroxysmal nonreentrant supraventricular tachycardia due to simultaneous fast and slow pathway conduction in dual atrioventricular node pathways.
      When the tachycardia terminates during AOP and the last atrial pacing simultaneously propagates over the fast and slow pathways (i.e., double ventricular response), the last atrial paced beat can result in two His signals. When an antegrade conduction via a slow pathway could retrogradely activate the fast pathway and re-initiate the tachycardia, an AHHA response is observed even in AVNRT cases (Figure 2C).
      • Alasti M.
      • Mirzaee S.
      • Machado C.
      • et al.
      Junctional ectopic tachycardia (JET).
      Figure thumbnail gr2
      Figure 2The possible mechanism of atrial-His-His-atrial (AHHA) and atrial-His-atrial (AHA) responses after an atrial overdrive pacing (AOP) in JT and AVNRT. H1 and H2 are defined as the last captured His electrograms with a PCL and the subsequent His electrograms, respectively. A: AOP during JT will transiently suppress the arrhythmia after pacing cessation and the tachycardia will resume with a junctional beat, beginning with a His signal. This will result in an AHHA response, and the H1H2 interval would be longer than the TCL due to the overdrive suppression in automatic cells. B: Contrarily, during AOP of the slow–fast AVNRT, the tachycardia will be entrained, and the anterograde atrioventricular nodal conduction propagates only through the slow pathway because the fast pathway is refractory from the retrograde conduction. After pacing cessation, the tachycardia will resume after the last paced beat. The last atrial paced beat during typical AVNRT should conduct anterograde down the slow pathway and exit into the His-Purkinje system while echoing up the fast pathway and exiting into the atrium. This would result in an AHA response. In this scenario, the tachycardia would continue during AOP, and the H1H2 interval would be similar to the TCL. C: However, if AOD terminates the tachycardia and the last atrial pacing simultaneously propagates over the fast and slow pathways (i.e., double ventricular response), the last atrial paced beat can result in two His signals. When an antegrade conduction via a slow pathway could retrogradely activate the fast pathway and re-initiate the tachycardia, an AHHA response is observed even in slow-fast AVNRT.
      • Alasti M.
      • Mirzaee S.
      • Machado C.
      • et al.
      Junctional ectopic tachycardia (JET).
      The H1H2 interval would be shorter than the TCL, because it corresponds to the difference between antegrade fast and slow pathway conductions. However, if the PCL is much shorter than the TCL, the decremental property of the slow pathway can make the H1H2 interval equal or longer than the TCL. A, atrium; AVNRT, atrioventricular nodal reentrant tachycardia; FP, fast pathway; JT, junctional tachycardia; SP, slow pathway; TCL, tachycardia cycle length; PCL, pacing cycle length.
      A previous study examining slow–fast AVNRT reported a different pacing site-dependent response in the His bundle potentials during AOP. An orthodromic capture of the atrial electrograms at the recording site of the His bundle was observed during AOP from the proximal CS in 5/7 (71%) patients, whereas an antidromic capture was observed during AOP from the HRA in 4/4 (100%),
      • Satoh M.
      • Miyajima S.
      • Koyama S.
      • Ishiguro J.
      • Okabe M.
      Orthodromic capture of the atrial electrogram during transient entrainment of atrioventricular nodal reentrant tachycardia.
      probably because the proximal CS pacing penetrated more easily into the upstream of the slow conduction, compared to the HRA pacing. When the pacing exhibits manifest entrainment and orthodromic capture of the earliest activation site (EAS), the entrance of the slow conduction zone is located between the pacing site and EAS.
      • Okumura K.
      • Olshansky B.
      • Henthorn R.W.
      • Epstein A.E.
      • Plumb V.J.
      • Waldo A.L.
      Demonstration of the presence of slow conduction during sustained ventricular tachycardia in man: use of transient entrainment of the tachycardia.
      Thus, in typical AVNRT, the entrance of the slow conduction zone (probably equivalent to the antegrade slow pathway) would be located between the proximal CS and His bundle regions (Figure 3).
      Figure thumbnail gr3
      Figure 3Schematic representations of the activation wavefront during (A) slow–fast AVNRT and during atrial overdrive pacing (AOP) from (B) the proximal CS and (C) HRA. A: In typical AVNRT, the proximal CS is presumably located on the entrance side of the slow conduction zone (i.e., slow pathway). B: The AOP from the entrance side of the slow conduction zone may allow the continuous resetting of the AVNRT by creating an excitable gap in the downstream myocardium. The antidromic wavefront of the first stimulus collides with the tachycardia, whereas its orthodromic counterpart advances the circuit. With the continuation of pacing, the orthodromic wavefront (N-1) after penetrating the slow conduction zone continuously collides with the antidromic wavefront of the subsequent pacing (N). C: Conversely, the HRA is presumably located on the exit side of the slow conduction zone. The antidromic wavefront (antegrade conduction via a fast pathway) would easily collide with the tachycardia wavefront and terminate the AVNRT. Then, the pacing wavefront would easily penetrate the His bundle electrograms via antegrade fast pathway conduction. These phenomena may make the continuation of the tachycardia difficult during AOP. AVNRT, atrioventricular nodal reentrant tachycardia; CS, coronary sinus; HRA, high right atrium.
      The pacing from the entrance side of the slow conduction zone would allow an orthodromic penetration (conduction via the antegrade slow pathway) of the last pacing impulse down to the His electrograms, resulting in an AHA response (Figure 3B). Conversely, an antidromic penetration (conduction via the antegrade fast pathway) from HRA pacing may terminate the tachycardia during AOP (Figure 3C). When the last atrial pacing propagates over the fast pathway alone, the tachycardia does not recur after AOP. However, when the last atrial pacing simultaneously propagates over the fast and slow pathways (i.e., double ventricular response), the antegrade conduction via the slow pathway could retrogradely activate the fast pathway, restarting the tachycardia. In this situation, an AHHA response is observed, leading to the misdiagnosis of the rhythm as JT.

      Conclusions

      An AHHA response after cessation of AOP was possible even in patients with slow–fast AVNRT. Tachycardia termination during AOP, simultaneous fast and slow pathway conduction (i.e., double ventricular response) of the last pacing stimulus, and restarting the tachycardia are the possible mechanisms of this phenomenon. Although there may be individual variations, AOP from the entrance side of the slow conduction zone (the proximal CS in typical AVNRT) may be the most suitable pacing site to correctly activate the antegrade slow pathway without terminating the tachycardia.

      Acknowledgments

      We would like to thank the nursing staff, clinical engineers, radiological technologists, and office administrators at Sakurabashi Watanabe Hospital for their support in conducting this study. We also thank Mr. John Martin for his linguistic assistance with the manuscript.

      Supplementary data

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