Transmural activations and stimulus potentials in three-dimensional anisotropic canine myocardium.

Abstract

Epicardial and endocardial pacing are widely used, yet little is known about the three-dimensional distribution of potentials generated by the pacing stimulus or the spread of activation from these pacing sites. In six open-chest dogs, simultaneous recordings were made from 120 transmural electrodes in 40 plunge electrodes within a 35 X 20 X 5-mm portion of the right ventricular outflow tract during epicardial and endocardial pacing at a strength of twice diastolic threshold and at 1 mA. The magnitude of extracellular potentials generated by the stimulus and the activation times were compared in regions proximal (less than 10-12 mm) and distal to the pacing site. Local fiber orientation was histologically determined at each recording electrode. For endocardial pacing, endocardial potentials were larger than epicardial potentials only in the proximal region (p less than 0.001); while in the distal region, epicardial potentials were larger (p less than 0.001), and endocardial activation occurred earlier than epicardial activation for both regions (p less than 0.001). For epicardial pacing, epicardial potentials were larger than endocardial potentials in both regions (p less than 0.001), and epicardial activation occurred earlier only in the proximal region (p less than 0.02), while endocardial activation occurred before epicardial activation in the distal region (p less than 0.01). In planes of recording electrodes parallel to the epicardium and endocardium, the initial isochrones were elliptical with the major axes of the ellipses along the mean fiber orientation between the pacing site and recording plane rather than along the local fiber orientation in the recording plane. Thus, the ellipses in each plane rotated with respect to each other so that in three dimensions the activation front was helicoid, yet the twist of the helix was less than that of the corresponding transmural rotation of fibers. For pacing from the right ventricular outflow tract, we conclude that beyond 10-12 mm from endocardial and epicardial pacing sites epicardial stimulus potentials in both cases are larger than endocardial potentials because of resistivity differences inside and outside the heart wall and activation in both cases is primarily endocardial to epicardial because of rapid endocardial conduction, and we conclude that the initial spread of activation is helicoid and determined by transmural fiber direction.

Epicardial and intramural excitation during ventricular pacing: effect of myocardial structure

“…Numerous experimental studies show that, in canine hearts, a family of concentric, quasi-elliptical isochrones appears on the ventricular surface in the vicinity of an epicardial pacing site (2,4,12,22,32). Arisi et al (2) referred to this region as the "primary area".…”

“…propagation patterns; excitation mapping KNOWLEDGE OF THE MECHANISMS that govern the spread of excitation in the heart is a necessary prerequisite for understanding and interpreting abnormal sequences that occur in conduction disturbances, cardiac arrhythmias, localized ischemia, and myocardial infarctions. With the recent advancements in cardiac resynchronization therapy and other pacing strategies (15,35), it is even more relevant to better understand the spread of excitation during paced ventricular beats, as affected by the architecture of myocardial fibers and their anisotropic electrical properties.Experimental data published during the last 20 years show that epicardial and intramural ventricular pacing in canine hearts result in complex patterns of epicardial excitation, with multiple distinct areas of relatively slow and fast propagation (2,4,12,23,30,32). Published computer simulations of the spread of excitation in the ventricles, mostly based on eiconal equations, propose possible electrophysiological mechanisms for many of these complex patterns (8, 9, 13, 33), but some of the suggested mechanisms have not yet received experimental confirmation.…”

“…Experimental data published during the last 20 years show that epicardial and intramural ventricular pacing in canine hearts result in complex patterns of epicardial excitation, with multiple distinct areas of relatively slow and fast propagation (2,4,12,23,30,32). Published computer simulations of the spread of excitation in the ventricles, mostly based on eiconal equations, propose possible electrophysiological mechanisms for many of these complex patterns (8, 9, 13, 33), but some of the suggested mechanisms have not yet received experimental confirmation.…”

Effects of Procainamide on Wave-Front Dynamics During Ventricular Fibrillation in Open-Chest Dogs

“…Furthermore, the conduction velocity calculation may be influenced by the subendocardial spread of activation via the Purkinje fiber network 11 ; therefore, we were not able to calculate the core size, refractory period, or conduction velocity in this dog.…”

Effect of nontransmural necrosis on epicardial potential fields. Correlation with fiber direction.

“…Those investigators5 tentatively interpreted the CCW expansion as being the epicardial projection of a rotating deep positivity, generated by the excitation wavefront as it propagated along deep fibers whose direction rotates CCW from epicardium to endocardium.9,10 CCW rotation of the intramural elliptical isochrones at increasing intramural depths after right ventricular epicardial pacing was shown by Frazier et al. 12 It is reasonable to expect that the associated potential distribution should also exhibit some kind of CCW rotation, although the amount of rotation may be different for fiber direction, isochrone pattern, and potential distribution for reasons explained in Frazier et a112 and in the "Discussion." In the present study, we tested the above interpretation by locally destroying some of the superficial or deep fibers that supposedly participated in generating the rotating epicardial positivity.…”