Ventricular fibrillation ablation in cardiomyopathies and arrhythmic storm

Abstract

Sudden cardiac death (SCD) is a relevant contributor to cardiovascular mortality, often occurring as a dramatic event. It can be the consequence of a ventricular tachycardia/fibrillation (VT/VF), a common and life-threatening arrhythmia. The underlying mechanisms of this catastrophic arrhythmia are poorly known. In fact, it can occur in the presence of a structural heart condition which itself generates the suitable substrate for this arrhythmia. Nevertheless, a VF may cause SCD also in young and otherwise healthy individuals, without overt structural abnormalities, generating difficulties in the screening and prevention of these patients. The implantable cardioverter-defibrillator represents the only therapy to contrast SCD by treating a VT/VF; however, it cannot prevent the occurrence of such arrhythmias. Catheter ablation is emerging as an essential therapeutic tool in the management of patients experiencing ventricular arrhythmias.

Keywords: Ablation; BrS; Idiopathic VF; PVC; Purkinje; Substrate.

Figure 1

(A) Continuous one-lead electrocardiogram recording in the intensive care unit showing repetitive, isolated, and short-coupling monomorphic premature ventricular complexes triggering incessant ventricular fibrillation episodes successfully treated with external DC-shocks. (B) Electrocardiogram recording from the external cardioverter-defibrillator during plane transfer to our Hospital. Transient ST-segment elevation after DC-shock can also be observed.

Figure 2

Twelve-lead electrocardiogram showing premature ventricular complexes morphology. The two morphologies are shown in panels A and B, respectively. (C) The two premature ventricular complexes morphologies are superimposed (in green the first, in yellow the second). They are both narrow, due to their origin from the specialized fibres of the conduction system; the morphology on the horizontal plane is very similar, but the frontal axis is different, superior, and inferior respectively, reflecting their different origin in the context of the Purkinje network, posterior, and anterior fascicle, respectively. Apart from the premature ventricular complexes, the electrocardiogram is normal without signs of Brugada syndrome, early repolarization syndrome, or long-QT syndrome.

Figure 3

Three-dimensional electro-anatomical maps using CARTO3 system (Biosense Webster, CA, USA) showing the LV septum with a 22° caudal 33° right anterior oblique view. The His Bundle separating into the anterior and posterior fascicle are roughly tracked in yellow (lines and dots) according to the intracardiac recordings using the ablation catheter. Red dots indicate the sites of radiofrequency delivery. Twelve-lead electrocardiogram (200 mm/s) with the potentials recorded at the ablation sites are shown on the right. Top panel shows the ablation of the first premature ventricular complex morphology, whereas bottom panel indicates the ablation of the second one. In both cases, at the ablation sites, the local ventricular near field is clearly preceded by a discrete high-frequency potential, i.e. Purkinje potential (ablation catheter distal and proximal electrodes). The recording of such potentials is fundamental for the effective ablation in these cases.