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Review
. 2018 Sep 18:5:123.
doi: 10.3389/fcvm.2018.00123. eCollection 2018.

Mapping and Ablation of Idiopathic Ventricular Fibrillation

Affiliations
Review

Mapping and Ablation of Idiopathic Ventricular Fibrillation

Ghassen Cheniti et al. Front Cardiovasc Med. .

Abstract

Idiopathic ventricular fibrillation (IVF) is the main cause of unexplained sudden cardiac death, particularly in young patients under the age of 35. IVF is a diagnosis of exclusion in patients who have survived a VF episode without any identifiable structural or metabolic causes despite extensive diagnostic testing. Genetic testing allows identification of a likely causative mutation in up to 27% of unexplained sudden deaths in children and young adults. In the majority of cases, VF is triggered by PVCs that originate from the Purkinje network. Ablation of VF triggers in this setting is associated with high rates of acute success and long-term freedom from VF recurrence. Recent studies demonstrate that a significant subset of IVF defined by negative comprehensive investigations, demonstrate in fact subclinical structural alterations. These localized myocardial alterations are identified by high density electrogram mapping, are of small size and are mainly located in the epicardium. As reentrant VF drivers are often colocated with regions of abnormal electrograms, this localized substrate can be shown to be mechanistically linked with VF. Such areas may represent an important target for ablation.

Keywords: Purkinje; ablation; idiopathic ventricular fibrillation; localized substrate; mapping.

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Figures

Figure 1
Figure 1
Examples of ECGs in patients with IVF. The origin of premature ventricular complexes triggering VF may be the right ventricular outflow tract (A), the right Purkinje system (B), or the left anterior (C) or posterior (D) Purkinje system.
Figure 2
Figure 2
12 lead ECG with associated endocardial electrograms of a PVC arising from the posterior Purkinje network. Purkinje fascicular potentials precede QRS onset by 18 ms during sinus rhythm. During the PVC, Purkinje potentials precede QRS onset by 108 ms (blue arrows). Notice the presence of a concealed Purkinje potential (red arrow).
Figure 3
Figure 3
12 lead ECG (Left) with associated endocardial tracings (Right) showing spontaneous polymorphic PVCs from a patient with idiopathic VF. A wide PVC likely originating from the right ventricle is followed by a concealed retrograde Purkinje potential (red star). Purkinje potentials during sinus rhythm are shown by blue arrows. PVCs originating from the Purkinje fibers are preceded by Purkinje potentials with a different coupling interval (red arrows). Notice the modifications in PVC morphology which result from the complex arborization of the left Purkinje system.
Figure 4
Figure 4
Twelve lead ECG and activation maps of the first and second beats of spontaneously initiated VF in a 30-year-old man. The PVC initiating VF has a similar morphology as the previous PVC with subtle changes in the precordial leads (V2-V3). The PVC initiating VF is located at the antero-apical RV (white star). The subsequent beat is a figure of eight at the same site as the first PVC.
Figure 5
Figure 5
(A) 12 lead ECG of a 37 y.o man with IVF. (B) Anterior view of the heart showing an area of reentrant activity located at the anterior and lateral epicardial RV. Fragmented epicardial electrograms with long duration during sinus rhythm are identified close to the driver sites.
Figure 6
Figure 6
Summary of the current diagnostic, mapping and ablation approaches in patients with IVF.

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