Circulation, Vol 72, 596-611, Copyright © 1985 by American Heart Association
PI Gardner, PC Ursell, JJ Fenoglio Jr and AL Wit
The electrophysiologic and anatomic basis for fractionated electrograms
were investigated in superfused epicardial preparations from infarcted
canine hearts. Fractionated bipolar electrograms were frequently recorded
in preparations from infarcts 2 weeks to 18 months old but only rarely in
preparations from 5-day-old infarcts. The fractionated electrograms were
not caused by movement artifacts. They were not associated with depressed
transmembrane resting or action potentials (which were found in the
5-day-old infarcts), but rather transmembrane potentials recorded in the
vicinity of the bipolar electrodes were normal. Despite the normal
transmembrane potentials, activation time in regions where fractionated
electrograms occurred was prolonged. However, prolonged activation time by
itself did not cause fractionation, since fractionated electrograms were
not recorded from normal preparations in which conduction was markedly
slowed by a superfusate containing 16 mM potassium and epinephrine.
Unipolar electrograms recorded with glass microelectrodes (tip size 1 to 5
microns) showed that activation in regions where fractionated electrograms
were recorded was inhomogeneous. Prepotentials were found preceding the
upstrokes of some action potentials in regions where double potentials were
recorded, suggesting the possibility of electrotonic transmission across
high resistance or inexcitable gaps, but no electrotonic potentials were
seen in regions with multicomponent fractionated electrograms. Fractionated
electrograms were recorded in regions where infarct healing caused wide
separation of individual myocardial fibers while distorting their
orientation. The anatomic changes probably caused slow and inhomogeneous
activation.
ARTICLES
Electrophysiologic and anatomic basis for fractionated electrograms recorded from healed myocardial infarcts
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