Interaction of fiber orientation and direction of impulse propagation with anatomic barriers in anisotropic canine myocardium.

Abstract

We developed a computer model of the interaction of impulse propagation with anatomic barriers in uniformly anisotropic tissue. Its predictions were confirmed experimentally by using an in vitro cut to create a 6x 1-mm anatomic barrier in 12 canine epicardial strips. The model predicted that long, thin barriers located parallel to the direction of impulse propagation would have little effect in delaying conduction regardless of the arrangement of cardiac fibers. In this situation, the mean experimental ratio of postcut to control conduction times across the barrier was 1.05:1.00 in 10 tissues. When impulses were proceeding perpendicular to an anatomic barrier, significant distal conduction delay was predicted and found to occur only when the conduction from pacing to recording sites was initially longitudinal to fiber orientation (mean experimental ratio, 2.34: 1.00 in five tissues) but not transverse to fiber orientation (ratio, 1.08: 1.00 in five tissues). We conclude that the direction of initial impulse propagation and the orientation of myocardial fibers have large effects on the degree to which anatomic barriers delay activation in cardiac tissue. These findings may have implications for the participation of anatomic barriers in reentrant circuits. (Circulation 1988;78:1478-1494 S low conduction and unidirectional block are requirements for reentrant pathways.1-9 In addition to slow conduction because of a decrease in the rate of rise of the intracellular potential, differences in cell-to-cell coupling and the geometric arrangement of fibers in cardiac tissue may also produce slow conduction. [10][11][12][13][14][15] pathway defined by fixed areas of block could provide a long enough conduction pathway to allow sufficient time for an impulse conducting at a normal velocity to return to fully recovered cardiac tissue. The extent of increased conduction time distal to anatomic barriers in cardiac tissue has not been extensively investigated. In addition, the consequences of the interrelation of fixed anatomic barriers and tissue anisotropy are unknown. Such activation delay distal to a barrier may have important implications for the participation of a barrier in reentrant circuits.Therefore, we developed a computer model of the interaction of fixed anatomic barriers with conduction in anisotropic tissue. Our goals were to verify the hypotheses that the direction of impulse propagation and the orientation of fibers relative to a fixed anatomic area of block were crucial in determining the degree of conduction delay and perturbation of activation patterns produced distal to the block. We then validated the predictions of this computer analysis in a simple model of anatomic barrier in canine epicardium produced by a thin surgical cut in an in vitro preparation. Materials and Methods Model of Conduction and Anisotropic TissueDirectional differences in conduction velocity in canine myocardium related to fiber orientation have

A Conformal, Bio-Interfaced Class of Silicon Electronics for Mapping Cardiac Electrophysiology

“…S14B). These results are consistent with anisotropic conduction properties measured in previous studies using mammalian hearts (17, 18). …”

Ultrasound backscatter tensor imaging (BTI): analysis of the spatial coherence of ultrasonic speckle in anisotropic soft tissues

“…The orientation of the myofibers varies smoothly and continuously through the wall thickness [1]. This specific fiber architecture is related to mechanical [2][3][4] and electrical [5][6][7][8] properties of the myocardium. Therefore, imaging the fiber architecture in vivo is of major interest in the understanding of cardiac function and in the progression of myocardial diseases.…”

Nondestructive optical determination of fiber organization in intact myocardial wall

“…It has been well documented that propagation velocities are several times faster along fibers than in the transverse direction (Panfilov and Keener, 1993; Taccardi et al, 1997), making fiber organization the most important determinant of the activation sequence (Punske et al, 2005). In addition, fiber organization is thought to play an essential role in arrhythmogenesis (Fenton and Karma, 1998; Kadish et al, 1988); and fibers are known to be altered in some diseased states, including ischemic heart disease (Wickline et al, 1992) and ventricular hypertrophy (Koide et al, 1982; Roberts and Ferrans, 1975; Tezuka et al, 1990). Fiber organization also plays an important role in the generation of myocardial stress and strain (Omens et al, 1991; Waldman et al, 1988) and in the structural adaptation of the myocardium (Arts et al, 1994).…”