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

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.

Myocardial electrical propagation in patients with idiopathic dilated cardiomyopathy.

“…5). The amplitudes of 4 and 'mnin during transverse propagation at the same sites (Fig. 6 D), however, are much smaller and have multiple low amplitude deflections (fractionation) (50,61 ).…”

“…In these studies reentry has been shown to be an important mechanism of arrhythmias, and abnormalities ofconduction appear to play a principal role in their genesis (4). Much less is known about arrhythmia mechanisms in patients with IDC.…”

Correlation of Scar in Cardiac MRI and High‐Resolution Contact Mapping of Left Ventricle in a Chronic Infarct Model

“…Activation mapping is not possible for the majority of the tachycardias (unmappable), either because of hemodynamic instability during the tachycardia or because the tachycardia is not sustained, not reinducible, or changes to another tachycardia before mapping can be completed 1. The substrate for the multiple reentrant circuits is the interconnecting network of surviving myocardial bundles within the scar 2. Substrate mapping to identify the abnormal low‐voltage areas and the critical components of possible VT circuits (surviving myocardial bundles) is an effective strategy and often the only method available.…”

Endocardial Mapping of Electrophysiologically Abnormal Substrates and Cardiac Arrhythmias Using a Noncontact Nonexpandable Catheter

“…Most infarcts (and other remodeling processes) involve the three-dimensional myocardium, as do most reentrant circuits that underlie clinical VT. [25][26][27] In previous studies we used similar methodology (ECG imaging [ECGI]) to reconstruct noninvasively EP information on the epicardial surface of the heart from body surface potentials in the presence of an infarct 18 and during reentrant VT. 25,28 Combined application of ECGI and noncontact catheter mapping can provide potentials, electrograms, and isochrones on both surfaces of the heart during a single beat. Availability of such detailed EP information on the epicardium and endocardium simultaneously will permit determination of electrical activity in the three-dimensional myocardium in a way that currently is not possible in the EP laboratory.…”