Circulation. 1998;97:1746-1754
(Circulation. 1998;97:1746-1754.)
© 1998 American Heart Association, Inc.
Myocardial Architecture and Ventricular Arrhythmogenesis
Nicholas S. Peters, MD, MRCP;
; Andrew L. Wit, PhD
From the Department of Cardiology, St Mary's Hospital and Imperial
College School of Medicine, London, UK (N.S.P.), and Department of
Pharmacology, Columbia University College of Physicians and Surgeons, New
York, NY (N.S.P., A.L.W.).
Correspondence to Nicholas S. Peters, MD, Department of Cardiology, St Mary's Hospital, Praed St, London W2 1NY, UK. E-mail n.peters@ic.ac.uk
Key Words: conduction • arrhythmia • myocardium
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Introduction
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Conduction of the cardiac
impulse is dependent on both the active membrane properties of cardiac
cells (generating the action potential) and the passive properties
determined by architectural features of the myocardium. The
influence of tissue architecture on conduction is determined
principally by the size, shape, and packing of individual myocytes and
by the quantity, three-dimensional distribution, and
physiological behavior of the specialized
intercellular junctions responsible for impulse propagation from cell
to cell, the gap junctions.1 It has long been
recognized that abnormalities in conduction of the cardiac impulse are
an important cause of arrhythmias2 in
that they alter the relationships between conduction velocity, path
length, and recovery of excitability (the determinants of reentrant
excitation). However, it was not until more recently that myocardial
architecture was considered important in determining patterns of
activation and conduction velocity3 4 and was
therefore thought to have a central role in
arrhythmogenesis,5 and some of the evidence for
this forms the basis of this review.
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Electrophysiological Architecture of
Ventricular Myocardium: From Muscle to
Molecule
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Myocardial Syncytium: Anisotropy of Structure and Function
The early observation that conduction properties in
myocardium were different in different
directions,6 with more rapid conduction in the
direction parallel to the myocardial fiber axis than in the transverse
direction (the definition of the anisotropic conduction characteristic
of heart muscle [Figure 1
]), is
attributable principally to the lower resistivity of
myocardium in the longitudinal than the transverse
direction. Gap-junctional channels create continuity between the
cytoplasmic compartments of abutting myocytes but act as resistive
discontinuities to the cytoplasmic current flow between the
intracellular compartments of the cells (the "intracellular"
conduction . . . [Full Text of this Article]
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