Extra‐cardiac vagal stimulation: Clinical utility of a novel diagnostic and therapeutic tool in supraventricular tachycardia

Figures

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  FIGURE 1. Illustration and effects of extracardiac vagal stimulation (ECVS). (A) Typical parameters of the ECVS, including pulse duration, frequency, and amplitude (B) Schematic of the ECVS procedure showing the catheter inside the internal jugular vein, without direct contact with the vagus nerve. (C) Transverse section of the neck illustrating the proximity between the internal jugular vein and the vagus nerve. (D) x‐ray image of the ECVS catheter in the posteroanterior (PA) view. (E) Normal effect of ECVS on the sinus node, evidenced by a sinus pause. (F) Effect of ECVS on AV conduction during atrial pacing, showing a transient vagal‐induced AV block. This is normal behavior, indicating no abnormal AV pathways. (G) Effect of ECVS on VA conduction during ventricular pacing, with the induction of transient VA block. This normal response helps rule out abnormal VA pathways.

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  FIGURE 2. This flowchart illustrates the distribution of patients of this study. Six hundred twenty‐five cases were initially considered. ECVS was successful in 611 (98%) patients, and it was not achieved in 14 patients (2%). Special Focus: 90 patients with concentric VA conduction were further analyzed with ECVS to distinguish between atypical AVNRT and septal AP. Para‐septal AP was found in 57 cases. This detailed breakdown highlights the distribution of patients across different types of SVT and the success rate of ECVS, providing an overview of the study's scope and focused areas. The red box indicates the group for which ECVS has the highest differential diagnostic value.

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  FIGURE 3. (A) Typical AVNRT (short VA) and (B) Atypical ANVRT (long VA) patients preablation. The ECVS typically induces VA block both before and after ablation.

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  FIGURE 4. ECVS in AVRT. (A) Persistent VA conduction during ECVS with VP suggests the presence of AP. (B) ECVS showing dual VA conduction; (B1) By AV node and AP before the ECVS; (B2) Under VP the ECVS changed the VA conduction pattern, with the VA interval suddenly increasing from 73 ms to 198 ms. This change occurred because of sudden VA nodal conduction block, maintaining VA conduction through the AP only. (C) After AP ablation, there is normal VA conduction through the AV node during VP. However, during ECVS, there is an immediate vagal‐induced VA block, indicating the absence of ectopic VA conduction and confirming the successful AP ablation.

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  FIGURE 5. (A) Example of typical nodal reentrant tachycardia induced during an electrophysiological study, quickly reverted with just 1 s of ECVS application. This maneuver is quite helpful since, in some cases, during ablation procedures, there are various spurious inductions of tachycardia. (B) Example of atypical AVNRT reverted with a short ECVS of 0.5 s. (C) Wide QRS nodal reentrant tachycardia reverted with 3 s of ECVS. (D) Different from AVNRT and AVRT, atrial tachycardia or atrial flutter not dependent on the AV node, instead of reversion, typically shows a long period of high‐degree AV block.

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  FIGURE 6. ECVS in two patients with APs. Shaded areas represent the ECVS. (A) Patient 1, with no delta wave despite having a history of intermittent WPW. (B) Sinus arrest induced by vagal effect. (C) Atrial pacing showing 2:1 AV conduction via the AP revealed by the AV node block. In these cases, ECVS commonly reveals the anomalous pathway by blocking the AV node and allowing the alternative abnormal passage (D) Patient 2, with manifest AP (WPW) preablation during atrial stimulation. (E) The ECVS shows an increase in QRS aberrancy, observed because of AV node block with ventricular activation via AP. (F) Patient 2 postablation with atrial pacing, without delta wave and with a narrow QRS. (G) During ECVS, high‐degree AV block is observed because of vagal AV node block. This maneuver is very important to show that the anterograde anomalous conduction of the AP has been completely eliminated and there are no remaining active abnormal bundles. (H) Patient 2 preablation during VP showing 1:1 VA conduction. (I) The ECVS shows persistence of 1:1 VA conduction resistant to vagal action. The lack of VA block during ECVS denotes the presence of anomalous VA conduction. (J) Patient 2 postablation…

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  FIGURE 7. ECVS in a patient with Mahaim fiber tachycardia. (A) Preablation: Atrial pacing demonstrating an AV interval of 170 ms. During ECVS, first‐degree AV block is observed (AV = 240 ms) with QRS widening displaying a complete left bundle branch block morphology. This is attributed to AV node block by the vagal effect of ECVS, which predominantly affects the AV node more than the Mahaim fiber, which maintains ectopic anterograde conduction. (B) Preablation: Right ventricular pacing shows 1:1 VA conduction via the AV node, which is completely abolished by ECVS. (C) Atrial pacing postablation: Normal AV conduction solely through the AV node. ECVS plus atrial pacing demonstrates total AV block following the elimination of the Mahaim fiber. (D) Right ventricular pacing postablation: Normal VA conduction through the AV node, completely blocked by the vagal effect induced by ECVS. This patient exhibited complete right bundle branch block which was not visible on the ECG as the Mahaim fiber masked it during the preablation phase. (E) Preablation showing possible sensitivity of the Mahaim fiber to acetylcholine. ECVS showing complete anterograde block of the AV node and intermittent AV block…