Circulation, Vol 88, 915-926, Copyright © 1993 by American Heart Association
JM de Bakker, FJ van Capelle, MJ Janse, S Tasseron, JT Vermeulen, N de Jonge and JR Lahpor
BACKGROUND. Ventricular tachycardias occurring in the chronic phase of
myocardial infarction are caused by reentry. Areas of slow conduction,
facilitating reentry, are often found in the infarcted zone. The purpose of
this study was to elucidate the mechanism of slow conduction in the chronic
infarcted human heart. METHODS AND RESULTS. Spread of activation was
studied in infarcted papillary muscles from hearts of patients who
underwent heart transplantation because of infarction. Recordings were
carried out on 10 papillary muscles that were superfused in a tissue bath.
High-resolution mapping was performed in areas revealing slow conduction.
Activation delay between sites perpendicular to the fiber direction and 1.4
mm apart could be as long as 45 milliseconds. Analysis of activation times
revealed that activation spread in tracts parallel to the fiber direction.
Conduction velocity in the tracts was between 0.6 and 1 m/s. Although
tracts were separated from each other over distances up to 8 mm, they often
connected with each other at one or more sites, forming a complex network
of connected tracts. In this network, wave fronts could travel
perpendicular to the fiber direction. Separation of tracts was due to
collagenous septa. At sites where tracts were interconnected, the
collagenous barriers were interrupted. CONCLUSIONS. Slow conduction
perpendicular to the fiber direction in infarcted myocardial tissue is
caused by a "zigzag" course of activation at high speed. Activation
proceeds along pathways lengthened by branching and merging bundles of
surviving myocytes ensheathed by collagenous septa.
ARTICLES
Slow conduction in the infarcted human heart. 'Zigzag' course of activation
Interuniversity Cardiology Institute of The Netherlands, Department of Experimental Cardiology, Academic Medical Center, Amsterdam.
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