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[Early after-depolarization in polymorphic ventricular tachycardia without QT prolongation]
K Böhringer1, V Kühlkamp, L Seipel
1Medizinische Universitätsklinik, Abteilung II, Tübingen.
Zeitschrift Fur Kardiologie
|May 1, 1995
Summary
Early afterdepolarizations (EADs) in the right ventricle caused polymorphic ventricular tachycardia (pVT) in a patient, suggesting a myocardial cell defect. Verapamil suppressed pVT, indicating calcium channel involvement and abnormal sympathetic innervation.
Area of Science:
- Cardiology
- Electrophysiology
- Molecular Cardiology
Background:
- Recurrent polymorphic ventricular tachycardia (pVT) can occur without QT prolongation.
- Early afterdepolarizations (EADs) are implicated in triggered arrhythmias.
Observation:
- Endocardial monophasic action potentials (MAP) revealed early afterdepolarizations (EAD) in the infero-septal wall during sinus rhythm.
- Programmed ventricular stimulation induced pVT, which rapidly progressed to ventricular fibrillation.
- Iodine-123-meta-iodobenzylguanidine (MIBG) scintigraphy showed defective sympathetic innervation in the left ventricle.
- Intravenous verapamil suppressed pVT despite causing sinus bradycardia.
Findings:
- The patient's pVT was likely triggered by EADs, suggesting an intrinsic myocardial cell defect affecting calcium channels.
- Abnormalities in sympathetic innervation may contribute to the regulation defect of ionic channels.
- Regionally restricted findings explain the absence of QT prolongation in this case.
- Verapamil's efficacy indicates bradycardia is not essential for pVT genesis.
Implications:
- This case supports the hypothesis that EAD-induced triggered activity, potentially linked to sympathetic dysfunction and calcium channel abnormalities, causes pVT.
- The findings highlight the role of localized repolarization dispersion in arrhythmogenesis.
- Targeting calcium channels may be a therapeutic strategy for specific pVT mechanisms.