Circulation, Vol 77, 589-606, Copyright © 1988 by American Heart Association
JM de Bakker, FJ van Capelle, MJ Janse, AA Wilde, R Coronel, AE Becker, KP Dingemans, NM van Hemel and RN Hauer
In this report we describe electrophysiologic and histologic findings in
hearts and endocardially resected preparations from patients with sustained
ventricular tachycardias in the chronic phase of myocardial infarction. We
recorded simultaneously from 64 endocardial sites during tachycardia in 72
patients that were operated on for medically intractable ventricular
tachycardias. Two other patients underwent heart transplantation, and
mapping was performed on the explanted isolated heart connected to a
Langendorff perfusion set-up. During operation 139 tachycardias with
different morphologies could be induced. Although the majority of evidence
supports the concept of a reentrant mechanism for these tachycardias, we
found that 105 tachycardias appeared to arise at a focal area of less than
1.4 cm2. In only three cases macroreentry around the infarction scar could
be detected. Of 21 tachycardias in which the "origin" appeared to be focal,
earliest subendocardial activation was preceded by discrete electrograms of
low amplitude (presystolic activity). In three tachycardias presystolic
activity was detected at several sites, permitting reconstruction of its
route. Histology of the endocardial resected preparation in one of these
cases revealed separate zones of viable myocardial fibers in areas in which
presystolic activity was recorded. These zones were located intramurally
and subendocardially, supporting the concept that reentry occurred via
isolated bundles of surviving myocytes at the border of the infarct and the
larger subendocardial muscle mass. Conduction velocity through the isolated
tracts was on the order of 25 cm/sec. Similar reentrant pathways were found
in the two isolated hearts. Extracellular and intracellular recordings were
made from 20 endocardial preparations that were excised from areas in which
tachycardia originated. Preparations were superfused in a tissue bath.
These experiments showed that action potentials were usually close to
normal, but occasionally action potentials with reduced amplitude and slow
upstrokes were found. In addition, there were cells that exhibited both
fast and slow upstrokes, depending on the direction of the wavefront.
Histology of seven resected preparations and the isolated hearts showed
subendocardially as well as intramurally located zones of viable
myocardium. Fractionation of extracellular electrograms and slow conduction
were found in areas where surviving muscle fibers and strands of fibrous
tissue were interwoven, and in zones where muscle fibers were oriented in
parallel but isolated by strands of connective tissue.(ABSTRACT TRUNCATED
AT 400 WORDS)
ARTICLES
Reentry as a cause of ventricular tachycardia in patients with chronic ischemic heart disease: electrophysiologic and anatomic correlation
Interuniversity Cardiology Institute of The Netherlands, Utrecht.
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