Contributions of the specialized conduction system to the
activation sequence in the canine pulmonary conus.
Pollard, Andrew E., Kenneth W. Spitzer[grave]a, and Mary Jo
Burgess[grave]a.
Department of Biomedical Engineering, University of Alabama
Birmingham, Birmingham, Alabama USA and Nora Eccles Harrison
Cardiovascular Research and Training Institute[grave]a, The
University of Utah, Salt Lake City, Utah, USA
APStracts 3:0511H, 1996.
This study was designed to characterize the relative contributions of
the specialized conduction system and the myocardial architecture to
the ventricular activation sequence. In animal experiments, the
activation sequence within a 14 mm by 14 mm region on each surface of
the pulmonary conus from isolated canine hearts was determined from
electrograms recorded during ventricular drives applied at the
periphery of the measurement region. Recordings were obtained
simultaneously from electrode arrays mounted on the endocardium and
epicardium. Activation sequences were determined before and after
bathing the right ventricular cavity with a dilute Lugol/Normal
Tyrode's (LNT) solution that selectively inhibited excitation of
Purkinje cells. Simulations of action potential propagation in three
-dimensional models (14.4 mm long by 7.2 mm wide by 3.6 mm thick) that
included the major features of the mid-wall architecture were
performed to aid in the interpretation of the experimental findings.
During endocardial pacing (7 animals, 43 total drives), LNT
application markedly prolonged the endocardial (13.7+/-1.3 msec) and
epicardial (5.7+/-1.0 msec) activation sequences. However, epicardial
isochrone maps constructed using electrograms recorded before LNT
application showed no signs of multiple breakthrough sites, and with
the exception of overall timing, closely resembled isochrone maps
constructed using electrograms recorded after LNT application. During
epicardial pacing (9 animal, 55 total drives), LNT application
prolonged the endocardial (3.7+/-0.6 msec) and epicardial (1.9+/-0.6
msec) activation sequences much less dramatically than during
endocardial pacing, suggesting a primary contribution of myocardial
architecture. However, in those instances where nonuniform anisotropy
slowed epicardial expansion of the depolarization wavefront, the
specialized conduction system contributed to the activation sequence
to a greater extent.
Received 25 October 1995; accepted in final form 1 November 1996.
APS Manuscript Number H995-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996