(Circulation. 1996;93:603-613.)
© 1996 American Heart Association, Inc.
Articles |
From the Departments of Medicine and Biomedical Engineering and the Cardiac Bioelectricity Research and Training Center, Case Western Reserve University, Cleveland, Ohio.
Correspondence to David S. Rosenbaum, MD, Case Western Reserve University, Department of Biomedical Engineering, Wickenden Bldg, Room 504, Cleveland, OH 44106-7207. E-mail dsr@pace.cwru.edu.
Background Although the relationship between cardiac
wavelength (
) and path length importantly determines the stability
of reentrant arrhythmias, the physiological
determinants of
are poorly understood. To investigate the cellular
mechanisms that control
during reentry, we developed an
experimental system for continuously monitoring
within a reentrant
circuit with the use of voltage-sensitive dyes and a new guinea pig
model of ventricular tachycardia (VT).
Methods and Results Action potentials were recorded
simultaneously from 128 ventricular sites in
Langendorff-perfused hearts (n=15) in which propagation was
confined to a two-dimensional rim of epicardium by an endocardial
cryoablating procedure. The reentrant path was precisely controlled by
creating an epicardial obstacle (2x10 mm) with an argon laser. To
control for fiber orientation and rate-dependent membrane
properties,
during reentry was compared with
during plane wave
propagation transverse and longitudinal to cardiac fibers at a stimulus
cycle length (CL) comparable to the VT CL. Reentrant VT
(CL=97.0±6.2
ms) was reproducibly induced by programmed stimulation in 93% of
preparations.
varied considerably within the reentrant circuit
(range, 10.6 to 22.5 mm), because of heterogeneities of conduction
rather than action potential duration.
was significantly shorter
during reentrant propagation (ie, with pivoting) parallel to fibers
(10.6±4.2 mm) compared with plane wave propagation (ie, without
pivoting) parallel to fibers (32.8±6.5 mm, P<.02),
indicating that wave-front pivoting was primarily responsible for
shortening of
during reentry. The mechanism of
shortening was
conduction slowing from increased current load experienced by the
pivoting wave front.
Conclusions We provide direct experimental evidence that
multiple wavelengths are present even within a relatively simple
reentrant circuit. Abrupt changes in loading during wave-front
pivoting, rather than membrane ionic properties or fiber structure,
were a major determinant of
and, therefore, may play an important
role in the stability of reentry.
Key Words: reentry tachycardia mapping action potentials electrophysiology
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