Why the study?
Although conduction abnormalities have long been recognized as an important cause of arrhythmias, myocardial architecture has more recently been considered important in determining activation patterns and conduction velocity and thus playing a central role in arrhythmogenesis.
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Design
Review
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Informs arrhythmia models; leaves open whether targeting architecture improves clinical outcomes.
C onduction 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 arrhythmias 2 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 velocity 3,4 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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Peters et al. (1998) studied this question.
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