Electrical storm due to ectopic activity following successful reperfusion: Clinical characterization and pharmacological approach to angry Purkinje syndrome

Introduction: Angry Purkinje syndrome is an uncommon cause of electrical storm characterized by short-coupled premature ventricular complexes (PVCs) originating from the His-Purkinje system and triggering polymorphic ventricular tachycardia (PMVT) or ventricular fibrillation (VF). It may occur during the subacute phase after myocardial infarction despite successful coronary reperfusion and absence of recurrent ischemia. Case presentation: A 55-year-old man presented with persistent oppressive precordial chest pain, rated 8/10, radiating to the jaw and left arm, which had begun at 02:00 h while asleep, without associated autonomic symptoms. On admission, blood pressure was 174/101 mmHg and heart rate was 103 beats/min. Electrocardiography showed an extensive anterior myocardial infarction, and primary percutaneous coronary intervention restored TIMI 3 flow in the left anterior descending coronary artery. Seventy-two hours after complete coronary revascularization, the patient developed ventricular fibrillation requiring external defibrillation with 150 J (Figure 2E). At the time of the first arrest, serum troponin was 896 pg/mL, potassium was 4.5 mEq/L, and magnesium was 2.62 mEq/L. The heart rate was 50 beats/min, with a QTc of 413 ms. Continuous cardiac monitoring subsequently demonstrated frequent premature ventricular complexes (PVCs) with a coupling interval of approximately 380 ms and a right bundle branch block morphology with a superior axis, followed by episodes of polymorphic ventricular tachycardia (PMVT) initiated by short-coupled PVCs (Figure 2A–D). Following this event, diagnostic coronary angiography was performed because of suspected acute stent thrombosis, confirming patency of the left anterior descending coronary artery stent with TIMI 3 flow and no new angiographic lesions in the remaining coronary arteries. Conclusion: Angry Purkinje syndrome should be considered in patients who develop recurrent PMVT or VF initiated by short-coupled PVCs after successful myocardial reperfusion, particularly when recurrent ischemia has been excluded. Flecainide combined with atrial overdrive pacing may represent a potential rescue strategy when quinidine is unavailable; however, further evidence is required to determine its efficacy and safety in this setting.

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Published
2026-11-04
DOI
https://doi.org/10.58281/mci.v2i1.23
Primary Topic
Cardiac Arrhythmias and Treatments
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article

Electrical storm due to ectopic activity following successful reperfusion: Clinical characterization and pharmacological approach to angry Purkinje syndrome

Santiago Nava, Héctor González‐Pacheco, Alexandra Arias‐Mendoza, Abel Lucio-García et al.
Cardiac Arrhythmias and Treatments
article

Electrical storm due to ectopic activity following successful reperfusion: Clinical characterization and pharmacological approach to angry Purkinje syndrome

Santiago Nava, Héctor González‐Pacheco, Alexandra Arias‐Mendoza, Abel Lucio-García, José L. Vázquez-Pérez
article en

Abstract

Introduction: Angry Purkinje syndrome is an uncommon cause of electrical storm characterized by short-coupled premature ventricular complexes (PVCs) originating from the His-Purkinje system and triggering polymorphic ventricular tachycardia (PMVT) or ventricular fibrillation (VF). It may occur during the subacute phase after myocardial infarction despite successful coronary reperfusion and absence of recurrent ischemia. Case presentation: A 55-year-old man presented with persistent oppressive precordial chest pain, rated 8/10, radiating to the jaw and left arm, which had begun at 02:00 h while asleep, without associated autonomic symptoms. On admission, blood pressure was 174/101 mmHg and heart rate was 103 beats/min. Electrocardiography showed an extensive anterior myocardial infarction, and primary percutaneous coronary intervention restored TIMI 3 flow in the left anterior descending coronary artery. Seventy-two hours after complete coronary revascularization, the patient developed ventricular fibrillation requiring external defibrillation with 150 J (Figure 2E). At the time of the first arrest, serum troponin was 896 pg/mL, potassium was 4.5 mEq/L, and magnesium was 2.62 mEq/L. The heart rate was 50 beats/min, with a QTc of 413 ms. Continuous cardiac monitoring subsequently demonstrated frequent premature ventricular complexes (PVCs) with a coupling interval of approximately 380 ms and a right bundle branch block morphology with a superior axis, followed by episodes of polymorphic ventricular tachycardia (PMVT) initiated by short-coupled PVCs (Figure 2A–D). Following this event, diagnostic coronary angiography was performed because of suspected acute stent thrombosis, confirming patency of the left anterior descending coronary artery stent with TIMI 3 flow and no new angiographic lesions in the remaining coronary arteries. Conclusion: Angry Purkinje syndrome should be considered in patients who develop recurrent PMVT or VF initiated by short-coupled PVCs after successful myocardial reperfusion, particularly when recurrent ischemia has been excluded. Flecainide combined with atrial overdrive pacing may represent a potential rescue strategy when quinidine is unavailable; however, further evidence is required to determine its efficacy and safety in this setting.

Vol. 2(1)
Tamaulipas Institute of Higher Education (MX), Instituto Nacional de Cardiología (MX)
Openalex Percentile: Top 12%
Cardiac Arrhythmias and Treatments
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