What is the clinical evidence from this study?

Study design: Other. Population: Extensive myocardial infarction (n=9). Intervention: Electrophysiologic and histologic mapping. Primary outcome: Mechanism of activation delay during ventricular tachycardia.

What question did this study set out to answer?

The research aims to investigate the relationship between the arrangement of surviving cardiac fibers and the occurrence of ventricular tachycardia in infarcted human hearts.

June 28, 2026

Ventricular tachyrdia in the infarcted, Langendorff-perfused human heart: Role of the arrangement of surviving cardiac fibers

Key Result

Electrophysiologic mapping of 9 explanted infarcted human hearts revealed that ventricular tachycardia activation delay is caused by a zigzag route over branching bundles of surviving myocytes.

Key Points

The research aims to investigate the relationship between the arrangement of surviving cardiac fibers and the occurrence of ventricular tachycardia in infarcted human hearts.
Electrophysiologic and histologic studies were conducted on Langendorff-perfused human hearts from transplant patients with extensive infarction.
Induced sustained ventricular tachycardias were mapped via epicardial and endocardial electrical activity.
Histologic examinations assessed the arrangement of viable myocardial tissue in relation to activation timing during tachycardia.
Fifteen episodes of sustained ventricular tachycardia were induced in nine hearts, revealing variable activation patterns.
In hearts with small time gaps between activations, surviving tissue formed a continuous tract across the infarct.
In hearts with larger time gaps, surviving myocytes were arranged in separate bundles, affecting electrical conductivity.

Structured PICO

Population

9 explanted human hearts from patients who underwent heart transplantation due to extensive infarction, studied ex vivo.

Exposure

Programmed stimulation to induce ventricular tachycardia, followed by epicardial and endocardial mapping and histologic examination

Outcome

Electrophysiologic and histologic characteristics of the infarcted area during induced ventricular tachycardiasurrogate

Surviving myocardial tissue in infarcted human hearts forms complex branching bundles that cause activation delay and facilitate ventricular tachycardia via a zigzag route of activation.

Abstract

Electrophysiologic and histologic studies were performed on Langendorff-perfused human hearts from patients who underwent heart transplantation because of extensive infarction. In nine hearts, 15 sustained ventricular tachycardias could be induced by programmed stimulation. In all hearts, mapping of epicardial and endocardial electrical activity during tachycardia was carried out. Histologic examination of the infarcted area between the site of latest activation of one cycle and the site of earliest activation of the next cycle revealed zones of viable myocardial tissue. In two hearts in which the time gap between latest and earliest activation was small, surviving myocardial tissue constituted a continuous tract that traversed the infarct. In three other hearts in which the time gap was large, surviving tissue consisted of parallel bundles that coursed separately over a few hundred micrometers, then merged into a single bundle and finally branched again. The direction of the fibers within the bundles was perpendicular to the direction of the activation front in that area. A similar type of inhomogeneous anisotrophy and activation delay was found in an infarcted papillary muscle removed from one of the explanted hearts and studied in a tissue bath during basic stimulation. Histologic examination of this preparation revealed that the delay was caused by a zigzag route of activation over branching and merging bundles of surviving myocytes separated by connective tissue.

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