Circulation, Vol 88, 250-263, Copyright © 1993 by American Heart Association
RB Schuessler, T Kawamoto, DE Hand, M Mitsuno, BI Bromberg, JL Cox and JP Boineau
BACKGROUND. Since the atria are thin-walled structures, most studies that
have examined the spread of activation in the atria have assumed that they
behave electrophysiologically as a two-dimensional surface. It was the
objective of this study to determine whether or not this assumption is true
by simultaneously mapping the epicardial and endocardial activation
sequences in the right atrium. METHODS AND RESULTS. Identical precisely
superpositioned epicardial and endocardial electrode templates with 250
unipolar electrodes each were used to map the isolated canine right atrium
(n = 8) during continuous perfusion and superfusion with Krebs-Henseleit
buffer. Data were recorded during control conditions (normal sinus rhythm),
continuous pacing (S1S1 = 300 msec), and premature stimulation (S1S2 =
effective refractory period + 5 msec). Pacing was performed at two sites,
one located on the inferior crista terminalis and one lateral to the crista
terminalis on a pectinate muscle. Tachyarrhythmias were induced by a single
extrastimulus during the continuous perfusion of acetylcholine (10(- 3.5)
mol/L). Individual electrode sites were correlated with the gross anatomy
and histology. Activation time differences were calculated between each two
corresponding epicardial and endocardial sites. There were differences in
the activation times between the epicardium and endocardium during all
experimental conditions. However, the average difference for each condition
was < 1 msec, suggesting that overall activation did not spread faster
on either the epicardium or the endocardium, even though in certain regions
one surface could lead the other. The dispersion of time differences was
smallest during normal sinus rhythm and continuous pacing (SD = 5.6-5.8
msec) and largest after premature stimulation (SD = 6.3 msec for crista
pacing, p < 0.05; SD = 8.1 msec for pacing lateral to the crista, p <
0.001). Differences in the activation sequence correlated with the
underlying anatomic architecture. The largest differences in activation
times between the epicardium and endocardium were associated with those
regions of the atrium where pectinate muscles ran below the epicardial
surface. The pectinate muscles in those areas were often discontinuous with
the epicardial surface and facilitated the discordant epicardial-
endocardial activation. The discordant activation was also found in regions
where the atrial wall thickness was < 0.5 mm and correlated with
transmural differences in fiber orientation. A tachyarrhythmia induced in
the presence of acetylcholine, which demonstrated a focal activation
pattern, was shown to have a reentrant loop that used free- running muscle
bundles connecting the epicardial and endocardial surfaces, resulting in a
three-dimensional pathway. CONCLUSIONS. The findings of this study
demonstrate that epicardial and endocardial activation can be discordant in
specific regions and that discordance increases with abnormal activation
sequences. Many of the differences in the epicardial and endocardial
activation can be correlated with the heterogeneity of the anatomic
architecture of the right atrium. The study also demonstrates that reentry
can occur in a three-dimensional plane using the epicardial and endocardial
surfaces connected by transmural muscle fibers.
ARTICLES
Simultaneous epicardial and endocardial activation sequence mapping in the isolated canine right atrium
Division of Cardiothoracic Surgery, Washington University School of Medicine, Barnes Hospital, St Louis, Mo.
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