Epicardial ablation of syncopal ventricular tachycardia. Utility of the electrocardiogram

Abstract

We describe the case of a young man with syncopal ventricular tachycardia, normal left ventricular ejection fraction, normal coronary arteries, and a left ventricular aneurysm. The ECG during tachycardia suggested an epicardial origin. The arrhythmia was successfully treated using a non-surgical transthoracic epicardial approach.

Introduction

Right bundle branch block (RBBB) and superior axis ventricular tachycardia (VT) in patients with apparently normal hearts may originate from the endocardium¹ or epicardium of the left ventricle (LV).² In the case of an endocardial origin, the Purkinje network surrounding the left posterior fascicle is a crucial part of the circuit, and endocardial radiofrequency ablation is easy to perform via retrograde transaortic access.¹ In the case of an epicardial origin, the arrhythmia may be related to the presence of an aneurysm in the posterior left ventricular wall,² and radiofrequency ablation may be performed by a transthoracic epicardial approach. Conventional 12 lead surface ECG may be useful in identifying these two different VT origins and help in deciding on the approach for radiofrequency ablation.

Case Report

A 23-year-old male was admitted to hospital because of a syncopal episode while driving resulting in a traffic accident. Previously, the patient had multiple near syncopal episodes after intense effort. The patient had neither cardiovascular risk factors nor familial history of sudden cardiac death. The conventional 12 lead surface ECG showed small q waves in the inferior leads of the frontal plane (II, III, aVF), slight elevation of the ST segment in these leads and premature ventricular complexes with RBBB morphology and superior axis (Figure 1). An echocardiogram showed neither structural nor functional anomaly and the ejection fraction of the LV was normal. During continuous monitoring, monomorphic sustained VT at a rate of 220 bpm, runs of non-sustained VT and premature ventricular complexes with the same morphology, were recorded. A coronary arteriogram showed normal coronary arteries. Left ventricle angiography revealed normal ejection fraction, normal global contractility, and a single aneurysm in the infero-lateral wall (Figure 2).

Electrophysiological study

At the beginning of the study, the arrhythmia was incessant, with runs of monomorphic VT alternating with sinus rhythm. The morphology of the complexes (RBBB, superior axis) suggested an origin of ventricular activation at the infero-lateral wall of the LV, close to the location of the aneurysm. In addition, the VT met the recently published electrocardiographic criteria that suggest an epicardial origin of the ventricular activation (Figure 3) (pseudodelta wave ≥34 ms, intrinsicoid deflection in V2 ≥85 ms, and the shortest RS interval in precordial leads ≥121 ms).³

Therefore, the pericardial space was reached by a non-surgical transthoracic epicardial approach described in previous reports.^4–6 The epicardium of the left ventricular free wall was mapped with a standard mapping approach using 8 mm tip catheter and the aid of a conventional fluoroscopic system (Figure 2). Continuous 12 lead surface ECG and simultaneous bipolar electrograms of the epicardial ablation catheter were recorded in an EP-TRACER (Cardio Tek bv, Maastricht, The Netherlands). The catheter was freely moved and the tip was directed to the area of the aneurysm, in which fragmented diastolic low amplitude potentials were registered during sinus rhythm. During VT, the precocity of the local electrogram was 18 ms with respect to the pseudodelta wave on the surface ECG. At this site, radiofrequency energy was delivered (target temperature of 60°C and power limit of 55 W) and the VT stopped in a few seconds. Afterwards, the VT was no longer inducible. Holter monitoring during the next 24 h showed normal sinus rhythm. Exercise testing was normal with no documented arrhythmias. At 1-year follow-up, the patient is asymptomatic and no new episodes of VT have been documented using repeated 24 h Holter monitoring.

Discussion

From the initial reports, non-surgical transthoracic epicardial radiofrequency ablation has been demonstrated to be a safe, feasible, and effective alternative in patients with an unsuccessful endocardial ablation.^4,5 More recently, another report demonstrated that the epicardial origin of VTs may be identified by analyzing the conventional surface ECG.³ In addition, Ouyang et al.² described a new syndrome that consists of an exercise-induced subepicardial reentrant VT attributable to infero-lateral left ventricular aneurysm in patients with normal coronary arteriograms. Up to now, only four cases of this subepicardial aneurysm-related VT syndrome in individuals with apparent normal left ventricular ejection fraction have been published. In the present case, the VT was incessant, thus making an ablation attempt mandatory.

Aneurysm-related VTs have been demonstrated in association with congenital, ischaemic heart disease, idiopathic, and inflammatory LV cardiomyopathy.^6,7 In the present case, the age of the patient, the normal coronary arteriogram, and the normal global LV function make an inflammatory aetiology the most common likely cause.

The major interest of this case is to focus our attention on the ECG with the key features being (1) small q waves in inferior leads in sinus rhythm, (2) the morphology of the ventricular complexes (RBBB superior axis) that suggest an infero-lateral left ventricular free wall origin, and (3) the pattern that suggested an epicardial origin.

Conclusion

In patients with RBBB morphology, superior axis VTs and apparently normal hearts, the ECG may differentiate between fascicular and subepicardial aneurysm-related VTs.

References