Nonuniform epicardial activation and repolarization properties of in vivo canine pulmonary conus.

Abstract

The relation between nonuniform epicardial activation and ventricular repolarization properties was studied in 14 pentobarbital anesthetized dogs and with a computer model. In 11 dogs, isochrone maps of epicardial activation sequence were constructed from electrograms recorded from the pulmonary conus with 64 electrodes on an 8 X 8 grid with 2-mm electrode separation. The heart was paced from multiple sites on the periphery of the array. Uniformity of epicardial activation was estimated from activation times at test sites and their eight neighboring sites. Acceleration shortened and deceleration prolonged refractory periods. The locations of acceleration and deceleration sites of activation differed during drives from various sites, and differences in uniformity of activation during pairs of drives were correlated to differences in refractory periods (r = 0.76, range 0.59-0.93). In three additional experiments, transmural activation sequence maps were constructed from electrograms recorded from needle-mounted electrodes placed upstream and downstream to epicardial activation delays. Activation proceeded from epicardium to endocardium upstream to the delays and from endocardium to epicardium downstream to the delays. A computer simulation of two-dimensional action potential propagation based on the Beeler-Reuter myocardial membrane model provided insights to the mechanism for the results of the animal experiments. The two-dimensional sheet modeled the transmural anisotropic histology of the canine pulmonary conus and corresponded to previous reports and histology of specimens from five experiments. Simulated activation patterns were similar to those found in the experimental animals. In addition, action potentials were electronically prolonged at sites of deceleration and shortened at sites of acceleration, results comparable to the animal experiments. Our findings demonstrate that the location of areas of nonuniform epicardial activation is dependent on drive site and that nonuniform activation electronically modulates repolarization properties. Therefore it seems likely that the site of origin of ectopic ventricular complexes, especially in ischemic myocardium where activation is nonuniform, could be an important determinant of whether ectopic activity initiates sustained tachyarrhythmias.

Myocardial electrical propagation in patients with idiopathic dilated cardiomyopathy.

“…One of these patients had relatively frequent single PVCs, but this is sometimes seen among healthy subjects. While nonuniform anisotropy is known to occur in normal myocardium (49,56), it has not been previously reported in this region of the heart and we have never observed it in this position of the canine left ventricle (37,42). A relation between nonuniform properties and age has been noted (49).…”

“…The activation path that accounts for the large gradients in activation times cannot be determined with precision. However, based on previous work (56), the presence of near simultaneous activation times distal to the band of dense isochrones (i.e., the lower halves ofthe maps in Fig. 7, A and C) suggest that activation spreads to this area from an intramural route.…”

“…Human left ventricular myocardium tends to be arranged in "onion skin" layers where the fiber orientation of each successive layer is slightly rotated ( 55 ). Thus, myocardial tissue subject to activation via transverse propagation at the surface can be "preexcited" by a wavefront that travels more rapidly in a subepicardial layer which can lead to an overestimation of6 (56 …”

“…Nonuniformity of activation was quantified by using the NAI, which has been described in detail previously (56). In brief, the NAI at an electrode site x (NAIl) is the sum of the second spatial derivatives of activation times in four directions times the electrode spacing.…”

Rate-related electrophysiologic effects of long-term administration of amiodarone on canine ventricular myocardium in vivo.

“…The electrodes were chosen in an area of relatively uniform propagation to avoid acceleration and deceleration effects on repolarization. 20 The repolarization time was defined as the time of maximum first derivative of the potential of the T wave of the local electrogram as previously described.16 This corresponds to the time of maximum rate of change of voltage during phase 3 of the action potential. 17 The temporal correspondence between repolarization time as measured from electrograms and repolarization measured from action potentials has been shown by simultaneous measurements of intracellular and extracellular potentials.17,2' The repolarization interval for an electrode site was defined as the difference between the repolarization time and the activation time obtained at that site.…”