Abstract

IntroductionIn this study, the mechanisms for onset and maintenance of mid-myocardial (intramural) reentrant circuits are considered, based upon anatomical structure. MethodA model of electrical activation wavefront curvature in the mid-myocardial postinfarction border zone is developed. Two arrhythmogenic structures are considered: 1. a constrained slab of viable tissue, and 2. a strand of surviving myocardial fibers with distal expansion. Equations are formulated to estimate activation coupling intervals, and ranges in taper and circuit dimensions, that will support functional conduction block during premature stimulation and reentrant ventricular tachycardia. ResultsFor onset and maintenance of reentry, the arrhythmogenic regions forming both slab and strand circuits are in the range of 50–600µm at their thinnest dimension. For constrained slabs, unidirectional block leading to reentry forms in the thin-to-thick direction during premature stimulation, and functional block at lateral boundaries enable formation of a double-loop circuit. The activation wavefront proceeds around the impediment and then curves in the opposite direction through the slab, reentering the previously excited tissue. For strands, unidirectional block forms at a distal expansion in response to premature stimulation. The strand reentrant circuit is bounded by infarcted tissue causing anatomical block, and can be single-loop or coaxial. For all architectures, circuit dimensions ranging from 1.6×1.6mm to 3.5×3.5mm support functional block when premature stimulus coupling intervals are 117–150ms and ventricular tachycardia cycle lengths are 160–350ms. ConclusionsFor slab and strand mid-myocardial arrhythmogenic structures, taper and circuit dimensions govern ranges in premature excitation coupling intervals and tachycardia cycle lengths necessary to support functional block.

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