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Stepwise Ablation Strategy for Post-myocardial infarction ventricular fibrillation: from Arrhythmia Suppression to Ablation

Open AccessPublished:November 09, 2022DOI:https://doi.org/10.1016/j.hrcr.2022.10.021

      Key Words

      INTRODUCTION

      Polymorphic ventricular arrhythmias (Ventricular fibrillation and polymorphic ventricular tachycardia VF/PMVT) are serious complications of acute myocardial infarctions (MI). These arrhythmias typically occur shortly after an MI and are a challenging situation due to the frequent progression to an electrical storm. The central role of surviving bundles from the Purkinje system in this condition has been previously demonstrated, namely by endocardial mapping and ablation.
      Although lifesaving, ablation procedures in this context remain complex and dangerous given the patients’ hemodynamic instability, the rapidly syncopal and lethal nature of these arrythmias and the need to precisely map the origin of the initiating premature ventricular complex (PVC) within the ischemic zone.
      In this case report, we present a stepwise workflow used to stabilize and ablate VF in a 60-year-old man after acute myocardial infarction.

      CASE REPORT

      A 60-year-old patient with no prior history of cardiac disease presented with out-hospital cardiac arrest due to ventricular fibrillation. After CPR and defibrillation, the patient was sedated, intubated and stabilized. Post-resuscitation ECG showed ST-segment elevation of the inferior and lateral leads. The patient was transferred to the catheterization laboratory and a coronary angiography was performed, demonstrating acute thrombosis of the circumflex artery as the only lesion. PCI was performed, with an estimated total occlusion time of 3 hours.
      Upon admission to the cardiac ICU, TTE showed a reduced ejection fraction of 40%.
      Sedations were lifted 5 days after hospital admission, and the patient evolved towards an electrical storm with recurrent PMVT/VF episodes. Sedations were resumed, the patient received IV amiodarone and lidocaine and was transferred to our institution.
      Despite increased drug therapy, the patient presented incessant episodes of polymorphic ventricular arrhythmias. All arrhythmic episodes were initiated by a similar short-coupled ectopic beat, the morphology of which was compatible with a Purkinje origin. The QTc interval was within normal range (425 ms), and heart rate was on average around 70 bpm.
      The patient was quickly fitted with a right-ventricular temporary pacemaker lead and overdrive pacing in the right ventricle with 100 beats/min was performed to suppress ventricular arrhythmias. Transient loss of ventricular capture or a decrease in pacing rates both led to an almost immediate VF recurrence. An urgent VF ablation procedure was planned the next day.

      PROCEDURE MANAGEMENT

      • 1)
        Using a transeptal approach, a left ventricular (LV) substrate map was performed while pacing the RV at 600 ms, visualizing an inferior and lateral scar.
      • 2)
        RV Pacing was transiently interrupted, leading to the immediate recurrence of monomorphic short-coupled PVCs. VF was eventually triggered, requiring immediate electrical cardioversion (Figure 1A).
        Figure thumbnail gr1
        Figure 1A- 12 leads ECG showing recurrence of short coupled PVCs and VF upon pacing interruption during the ablation procedure. This VF episode needed defibrillation. B- Pacing is stopped after placing high-density mapping catheter on the best pacemapping site. We observe monomorphic PVC recurrence, early Purkinje potentials are recorded. The earliest one is spotted on Penta 11-12, 102ms before ventricular exit. We can notice other less early purkinje potentials and an activation sequence (red arrow) from Penta 11-12, 3-4 and 1-2.
      • 3)
        The recorded PVC morphology was used as a template for pace-mapping in the electro-anatomical mapping system (Carto, Biosense webster, Diamond Bar, CA). Rapid RV-pacing was resumed using an external pacer to safely pacemap the left ventricle without arrhythmia recurrence. To avoid fusion while pacemapping, we programmed a VVI mode at a frequency of 80 beats/min on external pacer and paced from the ablation catheter at a frequency of 100 beats/min. Thus, the external pacer was inhibited when a stimulation was performed from the ablation catheter. The best matching QRS sites were located within the border zone of the inferior scar (Figure 2). The Purkinje network was also tagged when retrograde activation was visible.
        Figure thumbnail gr2
        Figure 2A- Correlation map obtained after pacemapping. The position of the high-density mapping catheter is concomitant with endocavitary recording in . Spots with earliest Purkinje potentials are tagged (green dots) and the previously described activation sequence is shown (black arrow). B- Baseline substrate map of the LV (RV pacing). C- On the left, ECG morphology of the best pacemap, to the right ECG morphology of the trigger PVC.
      • 4)
        A high-density mapping catheter (PentaRay, Biosense Webser, Diamond Bar, CA) was positioned on the area of best correlation and RV pacing was interrupted again, leading to PVC recurrence. Purkinje pre-potentials were recorded prior to the muscular exit of the PVC, with earliest potentials more than 100 ms before the onset of the PVC on the ECG (Figure 1B). This position was slightly more septal towards the conduction system, compared to the best correlation site.
      • 5)
        Based on previously published data, these pre-potentials were likely to be arising from the Purkinje system. Indeed, they were sharp, high frequency potentials, at the earliest activation sites of each PVC in the border zone of the myocardial scar. Moreover, their timing from the PVC and the preceding QRS was not consistent with late diastolic potentials related to slow conduction regions, which would most likely occur right after the end of the surface QRS.
      • 6)
        Ablation targeting this area led to an immediate and complete disappearance of the initial clinical PVC. Ablation was continued towards the area of the best pacemap and adjacent pre-potentials, in the direction of the purkinje system that we had previously mapped.
      • 7)
        Rapid pacing was stopped, and no recurrent arrhythmia was observed.
      After ablation, sedations were lifted. Antiarrhythmic drugs were discontinued, and post-MI medical therapy was initiated. An ICD was implanted, and the patient was discharged home a week after ablation. At 6 months follow-up, no recurrent arrhythmia was observed.

      DISCUSSION

      The term electrical storm broadly refers to recurrent life-threatening arrhythmias occurring over a short period of time. In the context of ischemic cardiomyopathy, electrical storms are generally due to recurrent episodes of scar-related monomorphic VTs and occur months or years after myocardial infarction (MI).
      In contrast, VF/PMVT storms shortly after myocardial infarction should be recognized as a distinct arrhythmic entity with a specific pathophysiology, time course and evolution.
      After revascularization, standard management of these storms includes adrenergic suppression (beta blocker therapy, stellate ganglion block and sedation), antiarrhythmic drug therapy (lidocaine, amiodarone and/or quinidine) and transient hemodynamic support. Nevertheless, these first line therapies may fail to suppress VF or be limited by contraindications or adverse effects. For this reason, VF storms after MI are often uncontrolled and associated with a high risk of death.
      Rapid pacing is a safe, fast and efficient method to control recurrent arrhythmia in post-MI VF/PMVT storms. In this case report, rapid pacing was used to transiently suppress arrhythmias and stabilize the patient until the ablation procedure. The mechanisms by which rapid pacing suppresses recurrent VF are incompletely understood. Stabilization of heart rate likely contributes to the antiarrhythmic effect, reducing action potential dispersion.
      Catheter ablation targeting the focal Purkinje-related triggers arising from the scar border zone is effective in suppressing recurrent VF after acute MI. Clinical mapping of PVCs in this context is particularly challenging, as these PVCs are frequently the first beat of a ventricular fibrillation episode.
      In this case report, we take advantage of the on/off nature of arrhythmia suppression using rapid pacing to allow us to record a template, safely identify the area of interest using pace-mapping and finalize mapping using a multi-electrode catheter in the area of interest. This combined approach allows us to perform an ablation with a strong endpoint while minimizing hemodynamic instability for the patient.

      CONCLUSION

      In VF electrical storms complicating acute myocardial infarction, rapid pacing seems efficient in suppressing VA recurrence. It can be used safely as bridge to ablation and transiently interrupted to allow safe mapping an efficient ablation of initiating PVCs using the proposed stepwise approach (Figure 3).

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