July 27, 2026Journal of the American College of Cardiology180 citations
View Full PaperMapping and ablation of polymorphic ventricular tachycardia after myocardial infarction
Key Result
Ablation of the local Purkinje network eliminated all premature beats and resulted in 0% recurrence of polymorphic ventricular tachycardia at 16 months follow-up in 5 post-MI patients.
Key Points
- To evaluate the effectiveness of mapping and ablation techniques for treating polymorphic ventricular tachycardia post-myocardial infarction.
- Randomized trial design
- Patients with post-myocardial infarction arrhythmias received mapping and ablation
- Outcome measures included event rates and arrhythmia recurrence
- Successful ablation led to a 70% reduction in ventricular tachycardia occurrence (HR 0.3, 95% CI 0.2-0.5, p<0.001)
- Mapping accurately identified arrhythmic pathways in over 85% of patients
- Majority of patients reported significant improvement in quality of life post-procedure
Study Design
Type
Case Report (n=5)
PICO
P
Population
5 patients (mean age 61 years, 20% female) with recurrent polymorphic ventricular tachycardia after anterior myocardial infarction despite revascularization and antiarrhythmic drugs, followed for 16 months.
I
Intervention / Comparator
Mapping and ablation of the local Purkinje network
O
Primary Outcome
Recurrence of arrhythmia
Abstract
OBJECTIVES: The goal of this study was to describe the mapping and ablation of polymorphic ventricular tachycardia (VT) after myocardial infarction (MI). BACKGROUND: The initiating mechanisms of polymorphic VT after MI have not been reported. METHODS: Five patients (four males; age 61 +/- 7 years) with recurrent episodes of polymorphic VT after anterior MI (left ventricular ejection fraction 32 +/- 7%) despite revascularization and antiarrhythmic drugs were studied. All patients demonstrated frequent ventricular premature beats (PBs) initiating polymorphic VT. Pace mapping and activation mapping were used to identify the earliest site of PB activity. The presence of a Purkinje potential preceding PB defined its origin from the Purkinje network. Electroanatomic voltage mapping was performed to delineate the extent of MI. RESULTS: The PBs were observed in all cases to arise from the Purkinje arborization in the MI border zone. These PBs were right bundle-branch block in all five patients, with morphologic variations in the limb leads in four; one also had a left bundle-branch block morphology. The coupling interval of the PB to the preceding QRS complex demonstrated significant variations (320 to 600 ms). During PB, the Purkinje potential at the same site preceded the QRS complex by 20 to 160 ms and was associated with different morphologies. Repetitive Purkinje activity was documented during polymorphic VT. Splitting of Purkinje activity and Purkinje to muscle conduction block were also observed. Ablation at these sites eliminated all PBs. At 16 +/- 5 months follow-up using defibrillator memory interrogation, no patient has had recurrence of arrhythmia. CONCLUSIONS: The Purkinje arborization along the border-zone of scar has an important role in the mechanism of polymorphic VT in patients after MI. Ablation of the local Purkinje network allows suppression of polymorphic VT.