Case description

A 72-year-old woman who had recently been diagnosed with anterior wall ST-elevation myocardial infarction (STEMI) and undergone left descending artery revascularization was recently referred to our hospital. One day later, the patient experienced ventricular fibrillation (VF) storm that was triggered by premature ventricular contraction (PVC) (Figure 1A). The patient required repeated cardiopulmonary resuscitation (CPR) and multiple defibrillations despite administering antiarrhythmic drugs (amiodarone, lidocaine), general anaesthesia, and overdrive pacing.

(A) Association between Purkinje triggered by premature ventricular contraction and ventricular fibrillation [arrows represent Purkinje spikes], mapping catheter in left ventricular (LV) septal position between the anterior and posterior fascicles], (B) earliest activation of premature ventricular contraction on 3D mapping system, (C) anatomical correlation between earliest activation and Purkinje network system, (D) 12-lead electrocardiogram showing Purkinje potential preceding (-104 ms) the target premature ventricular contraction on ablation catheter (arrow), (E) voltage map of the left ventricle with septal substrate and mark out of both anterior and posterior fascicles (yellow dots) and earliest activation (square), (F) anatomical correlation of septal substrate and purkinje network system, (G) ablation of earliest activation and substrate modification (red dots), (H) anatomical reflect of substrate modification on Purkinje network system (Purkinje de-networking). AF, anterior fascicle of LBB; AV, aortic valve; Cx, circumflex artery; LAD, left anterior descending artery; LBB, left bundle branch; LV, left ventricle; PF, posterior fascicle.
Figure 1

(A) Association between Purkinje triggered by premature ventricular contraction and ventricular fibrillation [arrows represent Purkinje spikes], mapping catheter in left ventricular (LV) septal position between the anterior and posterior fascicles], (B) earliest activation of premature ventricular contraction on 3D mapping system, (C) anatomical correlation between earliest activation and Purkinje network system, (D) 12-lead electrocardiogram showing Purkinje potential preceding (-104 ms) the target premature ventricular contraction on ablation catheter (arrow), (E) voltage map of the left ventricle with septal substrate and mark out of both anterior and posterior fascicles (yellow dots) and earliest activation (square), (F) anatomical correlation of septal substrate and purkinje network system, (G) ablation of earliest activation and substrate modification (red dots), (H) anatomical reflect of substrate modification on Purkinje network system (Purkinje de-networking). AF, anterior fascicle of LBB; AV, aortic valve; Cx, circumflex artery; LAD, left anterior descending artery; LBB, left bundle branch; LV, left ventricle; PF, posterior fascicle.

Extracorporeal membrane oxygenation (ECMO) was selected to provide urgent cardiac mechanical support, and the patient was immediately sent to our heart transplantation centre for evaluation for the necessity of a left ventricular (LV) assist device or bailout VF ablation.

Premature ventricular contractions had their origin between the anterior and posterior fascicles as identified by 12-lead electrocardiogram (ECG). These PVCs were responsible for inducing numerous episodes of VF resulting in VF storm.1 We decided to perform a bailout catheter ablation aiming for the elimination of the trigger PVCs and concomitant substrate modification of the ischaemic revascularized area.

Mapping was carefully carried out using a multipolar catheter (OctaRay, Biosense Webster) and a 3D navigation system (Carto3, Biosense Webster). An endocardial bipolar voltage map was performed which showed scarred tissue in the septal area affecting the conduction system and Purkinje network (Figure 1E and F). The earliest myocardial activation during PVCs was observed along the Purkinje network of the left bundle branch, too Figure 1B  and  C. This activation was consistently preceded by Purkinje potentials, which were followed by a PVC with the initiation of VF (Figure 1D). These findings confirmed that the scar-mediated PVC mechanisms were responsible for VF.2

Catheter ablation was conducted using a contact force sensing catheter (QDOT, Biosense Webster) implementing a temperature-controlled ablation mode (QMODE, 50W). Ablation resulted in sustained PVC elimination and persistent suppression of VF. Afterward, ischaemic LV scar was targeted in terms of substrate modification and Purkinje de-networking (Figure 1G and H).3 The patient remained free from any PVC and VF episodes and received a cardiac resynchronization therapy defibrillator (CRT-D) before discharge.

Acknowledgement

We acknowledge support by the DFG Open Access Publication Funds of the Ruhr-Universität Bochum.

Consent: The patient signed written informed consent for all treatment procedures. The journal consent form has been signed by the patient. Patient information in this case report is provided anonymously in accordance with the Committee on Publication Ethics (COPE) guidelines.

Funding: None declared.

Data availability

Data will be made available from the authors on reasonable request.

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Author notes

Conflict of interest: None declared.

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