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Polymorphic ventricular tachycardia / ventricular fibrillation (VF) occurring shortly after myocardial infarction should be considered as a distinct entity. In those cases, early premature ventricular contractions arising from the Purkinje network are likely to be VF trigger.
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Rapid pacing is safe, fast, and efficient in reducing VF recurrence in this situation.
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The rapid pacing “ON/OFF” effect on arrhythmia occurrence can be used to identify safely and precisely the area of interest to ablate, using the proposed stepwise approach.
Introduction
Polymorphic ventricular arrhythmias (ventricular fibrillation [VF] and polymorphic ventricular tachycardia [PMVT]) are serious complications of acute myocardial infarction (MI). These arrhythmias typically occur shortly after an MI and are a challenging situation owing 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 arrhythmias, 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 MI.
Case report
A 60-year-old patient with no prior history of cardiac disease presented with out-of-hospital cardiac arrest due to VF. After cardiopulmonary resuscitation and defibrillation, the patient was sedated, intubated, and stabilized. Postresuscitation electrocardiogram (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. Percutaneous coronary intervention was performed, with an estimated total occlusion time of 3 hours.
Upon admission to the cardiac intensive care unit, transthoracic echocardiography showed a reduced ejection fraction of 40%.
Sedations were lifted 5 days after hospital admission, and the patient evolved toward an electrical storm with recurrent PMVT/VF episodes. Sedations were resumed, and the patient received intravenous 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 beats/min.
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
The procedure was managed as follows:
(1)
Using a transseptal approach, a left ventricular substrate map was performed while pacing the right ventricle (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 1A: Twelve-lead electrocardiogram showing recurrence of short coupled premature ventricular contractions (PVCs) and ventricular fibrillation (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 pace-mapping site. We observe monomorphic PVC recurrence, and early Purkinje potentials are recorded. The earliest one is spotted on Penta 11-12, 102 ms 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.
The recorded PVC morphology was used as a template for pace mapping in the electroanatomical mapping system (CARTO; Biosense Webster, Diamond Bar, CA). Rapid RV pacing was resumed using an external pacer to safely pace map the left ventricle without arrhythmia recurrence. To avoid fusion while pace mapping, 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 2A: Correlation map obtained after pace mapping. The position of the high-density mapping catheter is concomitant with endocavitary recording in Figure 1B. 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 left ventricle (right ventricle pacing). C: On the left, electrocardiogram (ECG) morphology of the best pace map; to the right, ECG morphology of the trigger premature ventricular contraction.
A high-density mapping catheter (PentaRay; Biosense Webster, Diamond Bar, CA) was positioned on the area of best correlation and RV pacing was interrupted again, leading to PVC recurrence. Purkinje prepotentials 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 toward the conduction system, compared to the best correlation site.
these prepotentials 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 toward the area of the best pace map and adjacent prepotentials, 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 implantable cardioverter-defibrillator 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 ventricular tachycardias and occur months or years after MI.
In contrast, VF/PMVT storms shortly after MI 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 VF 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 multielectrode 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 MI, rapid pacing seems efficient in suppressing ventricular arrhythmia recurrence. It can be used safely as bridge to ablation and transiently interrupted to allow safe mapping and efficient ablation of initiating PVCs using the proposed stepwise approach (Figure 3).
The management of recalcitrant polymorphic ventricular arrhythmias following acute myocardial infarction (MI) can represent one of the most challenging clinical scenarios faced in critical care. Post-MI electrical storm often requires a multitiered, multidisciplinary approach to manage the complex interplay of arrhythmic triggers, ischemic substrate, and the hyperadrenergic state. It requires a combination of antiarrhythmic drug therapy, sympathetic nervous system modulation, and other case-specific interventions to obtain stability (Table 1).
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