Narrow QRS Regular Tachycardia With VA Dissociation: What Is the Mechanism?

A 40-year-old female was referred for catheter ablation of narrow QRS regular tachycardia. At baseline, atrio-His (AH) and His-ventricular (HV) intervals were 105 and 35 ms, respectively. Atrial extra stimulation revealed antegrade dual AV nodal physiology and ventricular extra stimulation (VES) showed single VA conduction with decremental property. The earliest atrial activation site during ventricular pacing was recorded at the proximal coronary sinus (CS). Supraventricular tachycardia (SVT 1) was induced with atrial extra stimulation accompanied by AH jump and the atrial sequence during the tachycardia was identical to that during ventricular programmed stimulation (Figure 1). A V-A-V response was observed after right ventricular (RV) overdrive pacing during the tachycardia, and the difference between post pacing interval (PPI) and tachycardia cycle length was 154 ms. SVT 1 was diagnosed with slow-slow type atrioventricular nodal reentrant tachycardia (AVNRT), and radiofrequency (RF) energy application within the proximal CS rendered SVT 1 non-inducible. Ventricular programmed stimulation after RF ablation revealed VA conduction with the earliest activation site at His region suggesting a retrograde fast pathway. Although SVT 1 was eliminated, spontaneous SVT 2 occurred. As shown in Figure 2, VA dissociation was observed during SVT 2. What is the mechanism of SVT 2? When VA block is observed during SVT, the differential diagnosis includes AVNRT with upper common pathway block, nodoventricular (NV) pathway or nodofascicular (NF) pathway mediated orthodromic reciprocating tachycardia (ORT), and junctional tachycardia (JT) (Figure 3). Since sinus beat could reset or terminate SVT 2 in the current case (Figure 4), JT was unlikely [1]. Differentiating NV or NF pathway-mediated ORT from AVNRT is challenging especially when VA conduction is inconsistent during tachycardia. Recent studies have shown multiple diagnostic observations of NV/NF mediated ORT which are useful to differentiate these tachycardias from AVNRT [2, 3]. Higuchi et al. reported the usefulness of differential RV overdrive pacing (RV apex vs. RV base) or His-refractory VES which could reset or terminate tachycardia without conducting to the atrium in a case of NV/NF mediated tachycardia. Since SVT2 was reproducibly terminated by sinus beats and VA was completely dissociated even after isoproterenol infusion, the diagnostic pacing maneuver was challenging in the current case. Although His-refractory VES still could have been diagnostic, delivering VES at an appropriate timing was difficult since sinus beats reproducibly reset or terminated SVT2. Furthermore, tachycardia reset by His-refractory VES is not universally observed in cases of AVNRT with bystander NV pathway [4] which is hard to differentiate from NV/VF mediated ORT. Although the type of VA block tends to be different between NV/NF mediated ORT and AVNRT and VA dissociation is rare in AVNRT, it cannot be diagnostic by itself. Of note, the HV interval was shortened during atrial extra stimulus in this case (Figure 5), indicating antegrade NV pathway conduction though there was no evidence that the pathway served as a retrograde limb during SVT2. By expecting both the slow pathway and NV/NF pathway which we assumed connected to the slow pathway would be eliminated, conventional slow pathway ablation was performed in the end accompanied by junctional beats during RF energy application and no tachycardia became inducible. As shown in the Supplemental Figure, the ablation site for SVT 2 was apart from the targeted site for SVT 1 (within the proximal CS) The patient became free from palpitation after ablation. The data that support the findings of this study are available from the corresponding author upon reasonable request. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.

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Journal
Pacing and Clinical Electrophysiology
Published
2024-09-27
DOI
https://doi.org/10.1111/pace.15079
Primary Topic
Cardiac Arrhythmias and Treatments
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article

Narrow QRS Regular Tachycardia With VA Dissociation: What Is the Mechanism?

Yasuhiro Shirai, Tatsuaki Kamata, Kaoru Okishige, Mihoko Kawabata et al.
Pacing and Clinical Electrophysiology
Cardiac Arrhythmias and Treatments
article

Narrow QRS Regular Tachycardia With VA Dissociation: What Is the Mechanism?

Yasuhiro Shirai, Tatsuaki Kamata, Kaoru Okishige, Mihoko Kawabata, Kenzo Hirao
article en

Abstract

A 40-year-old female was referred for catheter ablation of narrow QRS regular tachycardia. At baseline, atrio-His (AH) and His-ventricular (HV) intervals were 105 and 35 ms, respectively. Atrial extra stimulation revealed antegrade dual AV nodal physiology and ventricular extra stimulation (VES) showed single VA conduction with decremental property. The earliest atrial activation site during ventricular pacing was recorded at the proximal coronary sinus (CS). Supraventricular tachycardia (SVT 1) was induced with atrial extra stimulation accompanied by AH jump and the atrial sequence during the tachycardia was identical to that during ventricular programmed stimulation (Figure 1). A V-A-V response was observed after right ventricular (RV) overdrive pacing during the tachycardia, and the difference between post pacing interval (PPI) and tachycardia cycle length was 154 ms. SVT 1 was diagnosed with slow-slow type atrioventricular nodal reentrant tachycardia (AVNRT), and radiofrequency (RF) energy application within the proximal CS rendered SVT 1 non-inducible. Ventricular programmed stimulation after RF ablation revealed VA conduction with the earliest activation site at His region suggesting a retrograde fast pathway. Although SVT 1 was eliminated, spontaneous SVT 2 occurred. As shown in Figure 2, VA dissociation was observed during SVT 2. What is the mechanism of SVT 2? When VA block is observed during SVT, the differential diagnosis includes AVNRT with upper common pathway block, nodoventricular (NV) pathway or nodofascicular (NF) pathway mediated orthodromic reciprocating tachycardia (ORT), and junctional tachycardia (JT) (Figure 3). Since sinus beat could reset or terminate SVT 2 in the current case (Figure 4), JT was unlikely [1]. Differentiating NV or NF pathway-mediated ORT from AVNRT is challenging especially when VA conduction is inconsistent during tachycardia. Recent studies have shown multiple diagnostic observations of NV/NF mediated ORT which are useful to differentiate these tachycardias from AVNRT [2, 3]. Higuchi et al. reported the usefulness of differential RV overdrive pacing (RV apex vs. RV base) or His-refractory VES which could reset or terminate tachycardia without conducting to the atrium in a case of NV/NF mediated tachycardia. Since SVT2 was reproducibly terminated by sinus beats and VA was completely dissociated even after isoproterenol infusion, the diagnostic pacing maneuver was challenging in the current case. Although His-refractory VES still could have been diagnostic, delivering VES at an appropriate timing was difficult since sinus beats reproducibly reset or terminated SVT2. Furthermore, tachycardia reset by His-refractory VES is not universally observed in cases of AVNRT with bystander NV pathway [4] which is hard to differentiate from NV/VF mediated ORT. Although the type of VA block tends to be different between NV/NF mediated ORT and AVNRT and VA dissociation is rare in AVNRT, it cannot be diagnostic by itself. Of note, the HV interval was shortened during atrial extra stimulus in this case (Figure 5), indicating antegrade NV pathway conduction though there was no evidence that the pathway served as a retrograde limb during SVT2. By expecting both the slow pathway and NV/NF pathway which we assumed connected to the slow pathway would be eliminated, conventional slow pathway ablation was performed in the end accompanied by junctional beats during RF energy application and no tachycardia became inducible. As shown in the Supplemental Figure, the ablation site for SVT 2 was apart from the targeted site for SVT 1 (within the proximal CS) The patient became free from palpitation after ablation. The data that support the findings of this study are available from the corresponding author upon reasonable request. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.

Pacing and Clinical ElectrophysiologyVol. 47(11)
Yokohama Municipal Minato Red Cross Hospital (JP)
Zero hunger
Openalex Percentile: Top 71%
Cardiac Arrhythmias and Treatments
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