Expect the unexpected

Pierre Groussin, Melvyn Dezecot, Philippe Mabo, Raphaël P Martins

► To cite this version:

Pierre Groussin, Melvyn Dezecot, Philippe Mabo, Raphaël P Martins. Expect the unexpected. Journal of Electrocardiology, 2025, 90, pp.153902. 10.1016/j.jelectrocard.2025.153902. hal-04981987

HAL Id: hal-04981987

https://hal.science/hal-04981987v1

Submitted on 7 Mar 2025

HAL is a multi-disciplinary open access
archive for the deposit and dissemination of sci-
entific research documents, whether they are pub-
lished or not. The documents may come from
teaching and research institutions in France or
abroad, or from public or private research centers.

L'archive ouverte pluridisciplinaire HAL, est
destinée au dépôt et à la diffusion de documents
scientifiques de niveau recherche, publiés ou non,
émanant des établissements d'enseignement et de
recherche français ou étrangers, des laboratoires
publics ou privés.

<figure><img src="image_1.png" /></figure>
# Expect the unexpected

Pierre Groussin*, Melvyn Dezecot, Philippe Mabo, Raphaël P. Martins

Univ Rennes, CHU Rennes, INSERM, LTSI – UMR 1099, F-35000 Rennes, France

## ECG challenge

A 73-year-old man was admitted to the intensive cardiac care unit for an electrical storm. His medical history included dilated cardiomyopathy with a left ventricular ejection fraction of 35 % and persistent atrial fibrillation. A dual-chamber implantable cardioverter defibrillator was implanted 6 years ago for secondary prevention of sudden cardiac death. Left ventricular ejection fraction was 35 %. The baseline antiarrhythmic treatment included bisoprolol 2.5 mg and amiodarone (100 mg), with clinical stability in terms of rhythm control.

No triggering factors were identified to explain the onset of the electrical storm. Multiple ventricular tachycardia (VT) episodes were interrupted with anti-tachycardia pacing and electrical shocks delivered by the implantable cardioverter defibrillator. Due to repetitive episodes of VT leading to hemodynamic compromise, the patient was referred for catheter ablation. During the procedure, two different VTs were reproducibly induced (Fig. 1).

**Question:** Where do VT1 and VT2 originate from?

* Answer 1: VT1 – Posterior right ventricular outflow tract / VT2 – Inferolateral LV

* Answer 2: VT1 - Left coronary cusp / VT2 – Inferoseptal LV

* Answer 3: VT1 - Right coronary cusp / VT2 – Inferobasal LV

* Answer 4: VT1 - Septal right ventricular outflow tract / VT2 – lateral LV

* Answer 5: VT1 - Parahisian / VT2 – Inferoapical LV

The correct answer is Answer 3: VT1 - Right coronary cusp / VT2 – Inferobasal LV.

## Response to the ECG challenge

Various algorithms have been developed to help clinicians determine the site of origin of VT. For the first arrhythmia (VT1), the QRS complex has a left bundle branch block morphology with an inferior axis,

suggesting a potential outflow tract region origin. Based on Enriquez et al.'s algorithm [1], the most likely site of origin is suspected to be the right coronary cusp. This hypothesis is supported by an early precordial transition in lead V3, positive deflection in lead I, negative deflection in lead aVL and V2S/V3R index <1,5.

In contrast, for the second VT (VT2), the QRS complex shows a right bundle branch block pattern, with a superior axis and late reverse precordial R wave progression According to the Miller et al. algorithm [2], this pattern suggests an inferobasal LV origin. Furthermore, several ECG markers suggest an epicardial origin for VT2, including the presence of a pseudo-delta wave, a maximum deflection index ≥0.59 in precordial leads, and a Q wave in lead I.

During VT ablation, both VTs were inducible, sustained and well-tolerated, allowing VT activation mapping. Surprisingly, 3D mapping revealed that both VT1 and VT2 shared a common isthmus located in the laterobasal region, but with opposite directions of activation for both tachycardias (Fig. 2). After verifying the absence of coronary arteries or the phrenic nerve on the target, radiofrequency ablation lesions were delivered in the mid-isthmus, rendering both VTs non-inducible.

The mechanism of monomorphic ventricular tachycardias has been elucidated by computer modeling and experimental studies in animals and humans. These studies demonstrated that ventricular tachycardias are sustained by narrow isthmuses of viable myocardial tissue with slow conduction, which forms the critical component of a reentrant circuit. These isthmuses are typically bordered by scar, infarcted myocardium or other anatomical barriers. Later studies expanded this understanding using 3D mapping, showing that a single critical isthmus could sustain multiple ventricular tachycardias in some cases [3].

Localization of ventricular tachycardias remains a diagnostic and therapeutic challenge, particularly in cases involving complex reentrant circuits. Although ECG-based algorithms provide valuable initial clues about the likely exit sites of ventricular tachycardias, these tools should be used cautiously, as they do not reliably identify the critical isthmus sustaining the reentrant circuit. In this case, the successful identification and ablation of a common isthmus contributing to both VT1 and VT2

<footnote>Abbreviations: VT, ventricular tachycardia; LV, left ventricular.</footnote>

<footnote>* Corresponding author at: Service de Cardiologie et Maladies Vasculaires, CHU de Rennes, 2 rue Henri Le Guilloux, 35000 Rennes, France.</footnote>

<footnote>E-mail addresses: pierre.groussin@chu-rennes.fr (P. Groussin), raphael.martins@chu-rennes.fr (R.P. Martins).</footnote>
<figure><img src="image_2.png" /><figcaption>**Fig. 1.** : Twelve-lead electrocardiogram showing clinical ventricular tachycardia 1 with a left bundle branch block inferior axis pattern (panel A) and clinical ventricular tachycardia 2 with a right bundle branch block superior axis pattern (panel B).</figcaption></figure>

<figure><img src="image_3.png" /><figcaption>**Fig. 2.** : The 3D mapping revealing that both VT1 and VT2 shared a common isthmus located in the laterobasal region, but with opposite directions of activation for the two tachycardias.</figcaption></figure>

underscores the importance of integrating ECG findings with invasive mapping techniques to optimize the treatment for complex ventricular arrhythmias.

Supplementary data to this article can be found online at https://doi.org/10.1016/j.jelectrocard.2025.153902.

### CRediT authorship contribution statement

**Pierre Groussin**: Writing – original draft, Conceptualization.
**Melvyn Dezecot**: Validation, Supervision.
**Philippe Mabo**: Supervision.
**Raphaël P. Martins**: Supervision, Conceptualization.

### Declaration of competing interest

None.

### References

[1] Enriquez A, Baranchuk A, Briceno D, Saenz L, Garcia F. How to use the 12-lead ECG to predict the site of origin of idiopathic ventricular arrhythmias. Heart Rhythm 2019 Oct;16(10):1538-44.

[2] Miller JM, Marchlinski FE, Buxton AE, Josephson ME. Relationship between the 12-lead electrocardiogram during ventricular tachycardia and endocardial site of origin in patients with coronary artery disease. Circulation 1988 Apr;77(4):759-66.

[3] Anter E, Kleber AG, Rottmann M, Leshem E, Barkagan M, Tschabrunn CM, et al. Infarct-related ventricular tachycardia: redefining the electrophysiological substrate of the isthmus during sinus rhythm. JACC Clin Electrophysiol 2018 Aug;4(8):1033-48.