Key result
Post-infarction ventricular tachycardia originates from reentrant circuits across surviving myocyte bundles.
Why the study?
The electrophysiologic and anatomic mechanisms underlying sustained ventricular tachycardias in the chronic phase of myocardial infarction were not fully characterized.
Observational (n=74)
Electrophysiologic mapping and histology in patients with chronic ischemic heart disease demonstrate that ventricular tachycardia is often caused by reentry through isolated bundles of surviving myocytes at the infarct border.
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Supports reentry via surviving myocytes in ischemic VT; hypothesis-generating for mapping refinements pending larger studies.
Bakker et al. (1988) conducted an observational in Sustained ventricular tachycardias in chronic ischemic heart disease (n=74). Electrophysiologic mapping and histologic examination was evaluated on Mechanism of ventricular tachycardia. Electrophysiologic mapping and histologic examination of induced tachycardias in patients with chronic ischemic heart disease supported a reentrant mechanism via isolated bundles of surviving myocytes.
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