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VF is usually initiated by PVCs or by the transition from VT to VF. PVCs can originate from areas of scar and fibrosis, from the ventricular myocardium, or from the Purkinje system. The underlying mechanism can be early afterdepolarizations, late afterdepolarizations, or abnormal automaticity. Previous studies demonstrated that Purkinje ectopies are prominent triggers of VF in a wide spectrum of cardiac disease,1,2 and this role was confirmed by the efficacy of ablation of PVC triggers. PVCs triggering VF therefore represent the main target for ablation.

VF Maintenance

In animal models, VF is maintained by different mechanisms, including mother rotor reentry, multiple wavelets, and focal activities (mainly originating from the Purkinje system). Multiple wavelets are due to self-sustained wavelets resulting from dynamic instabilities associated with APD restitution properties and intracellular calcium dynamics.³ Mother rotors are rapid reentrant electrical sources that drive VF. It is classically defined as a stationary, persistent source that lasts ≥ 5 seconds and actively induces wavebreaks.³ The Purkinje system, in addition to initiating VF, also helps to maintain long-duration VF, usually lasting for at least 1 minute.

In humans, previous studies revealed that the early VF phase is maintained by a limited number of wavefronts and stable rotors4 that frequently anchor at scar borders. During this same period, there is no activation gradient between the endocardium and the epicardium, indicating transmural involvement.⁵

Preprocedural Planning for VF Ablation

Definition of the Underlying Heart Condition

Diagnosis of the underlying substrate is essential before selecting a treatment strategy. Briefly, on the basis of the published guidelines, we perform cardiac echocardiography, exercise testing, coronary angiography, MRI, and in some cases, cardiac CT. We also perform genetic screening, ajmaline testing, and isoprenaline testing.

According to the ACC/ESC guidelines,⁶ long QT syndrome (LQTS) is diagnosed in the presence of an LQTS risk score ≥ 3.5 and/or in the presence of an unequivocal mutation in one LQTS gene or, in the absence of a secondary cause of QT prolongation, in the presence of a QTc ≥ 500 ms in repeated 12-lead ECG. LQTS can be diagnosed in the presence of a QTc between 480–499 ms in a patient with unexplained syncope in the absence of a secondary cause of QT prolongation.

Short QT syndrome (SQTS) is a less common condition. It is diagnosed in the presence of a QTc ≤ 330 ms and can be diagnosed in the presence of a QTc < 360 ms and one or more of the following conditions: a pathogenic mutation, family history of SQTS, family history of SCD ≤ 40 years, or survival of VT/VF episode in the absence of heart disease.

Brugada syndrome (BrS) is diagnosed in patients with ST-segment elevation with type 1 morphology ≥ 2 mm in one or more of the right precordial leads, V₁ and V₂, positioned in the second, third, or fourth intercostal space. ST elevation may occur either spontaneously or after provocative drug testing with intravenous administration of class I antiarrhythmic drugs. It is also diagnosed in patients with type 2 or type 3 ST-segment elevation in the same leads when a provocative drug test induces a type 1 ECG morphology.

Catecholaminergic polymorphic VT (CPVT) is diagnosed in patients less than 40 years old with the a structurally normal heart, normal ECG, and unexplained exercise- or catecholamine-induced bidirectional VT or polymorphic PVC or VT. It is also diagnosed in the context of a normal heart when exercise-induced PVCs or bidirectional/polymorphic VTs are present, and a pathogenic mutation or a familial history of CPVT.

Early repolarization is diagnosed in the presence of J-wave elevation ≥ 1 mm in more than two inferior and/or lateral leads of a standard 12-lead ECG in a patient resuscitated from otherwise unexplained VF/polymorphic VT.

Indication for VF Ablation

Although implantation of an ICD remains the primary treatment for secondary and primary prevention of SCD, the underlying heart disease should be considered when deciding the most appropriate treatment strategy.

VF ablation is recommended in patients who have multiple recurrent episodes of VF, resistant to antiarrhythmic drugs, with frequent triggering PVCs. VF ablation can be proposed in patients with a history of electrical storm and appropriate ICD shocks. In our center, we have proposed VF ablation as a first-line treatment in a limited number of patients with electrical storm and multiple triggering PVCs. In all patients, we subsequently implanted an ICD.

Before ablation, it is essential to document on a 12-lead ECG the culprit PVCs that trigger VF. Their origin can be identified in the majority of the cases thanks to their morphology on the surface ECG. The coupling interval is typically variable and VF is usually triggered by short-coupled PVCs (Figure 49.1).¹

When originating from the left Purkinje system, the QRS duration is usually < 120 ms with a sharp and rapid onset. PVCs show a right bundle branch block (RBBB) morphology and right or left axis deviation when coming from the anterior or posterior distal Purkinje systems, respectively. PVCs originating from the right Purkinje system are wider and show a left bundle branch block (LBBB) morphology (Figure 49.2). PVCs arising from the RVOT usually have an inferior axis. PVCs with epicardial origin are usually large and have a slow initial component.

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