Analysis of Ventricular Activation and Repolarization from Intramural and Epicardial Potential Distributions for Ectopic Beats in the Intact Dog

Ventricular activation and repolarization were examined by measuring intramural and epicardial potential distributions during ectopic sequences in intact dogs. Potential distributions were used because they provided a direct measure of all of repolarization. Ectopic sequences produced almost unidirectional excitation across the heart along with repolarization events that were different from normal. During ectopic repolarization, positive potentials occurred over a broad area surrounding the ectopic focus, and negative potentials occurred over a large area on the opposite side of the heart where excitation terminated. The potentials in the walls of both ventricles were more positive in the outer layers and more negative in the inner layers, a gradient similar to normal. A maximum initially was at the ectopic site with a magnitude greater than that of the minimum, but the maximum subsequently decreased in magnitude and shifted toward the minimum while the minimum increased in magnitude. The steepest gradients were initially around the maximum, and they then shifted toward the minimum. The results show that ventricular repolarization potential distributions during ectopic beats are predominantly influenced by gradients from one side of the heart to the other (transventricular gradients) in contrast to normal repolarization distributions which are predominantly influenced by gradients across the wall (transmural gradients). • In this investigation, we studied ventricular repolarization by using potential distributions to directly measure ventricular repolarization throughout the heart both intramurally and epicardially (1). Schaefer (2) noted in 1957 that there was little hope of gaining a perfect and lasting theory of the order of repolarization processes with the knowledge available then. Subsequently, in 1964 van Dam and Durrer (3) pointed out that most current knowledge about the T wave was based on theoretical considerations and indirect evidence, and Christian and Scher (4) stated in 1967 that no adequate data indicated how the T wave originated. A primary objective of experiments related to the T wave has been to determine the distribution of currents throughout the heart, as considered initially for a single cardiac fiber by MacLeod (5). In contrast, however, most of the studies related to the genesis of the T wave have been oriented toward body surface electrocardiograms as measured with a small number of leads and have been designed, in one way or another, around the idea of From the Departments of Pediatrics, Physiology, and Biomedical Engineering, Duke University School of Medicine, Durham, North Carolina 27710. This investigation was supported by U. S. Public Health Service Grants HL 11307, HL 5372, and HL 5716 from the National Heart and Lung Institute. Received May 22, 1975. Accepted for publication September 23, 1975. the ventricular gradient as originally put forth by Wilson et al. (6). The ventricular gradient concept considers only the average T-wave effects (2, 7), not moment-by-moment events, and is limited in other ways as noted by Schmitt (8) and Simonson et al. (9). The concept has been expanded from the original frontal plane analysis (6) to the vectorcardiographic three-dimensional analysis by Harumi et al. (10) and further extended by Abildskov et al. (11). However, all of these studies have been directed toward QRS-complex and T-wave deflections on the body surface for either standard electrocardiographic or vectorcardiographic wave forms, and, consequently, have not provided direct information about the heart. Indirect measurements of repolarization made from the heart have consisted of the determination of refractory periods at different sites in the ventricles (12-15). In such experiments, Burgess et al. (15) have shown that transmurally the order of recovery of ventricular excitability is from epicardium to endocardium and from base to apex. Such findings pertain only to a limited time interval near the peak of the T wave and provide no basis for explaining the major portion of the entire ST-T wave, a phenomenon occurring over a much longer period of time, van Dam and Durrer (14) have concluded that such indirect measurements do not provide information to explain the epicardial T 830 Circulation Research, Vol. 37, December 1975 by gest on N ovem er 2, 2017 http://circhajournals.org/ D ow nladed from HEART POTENTIAL DISTRIBUTIONS FOR ECTOPIC BEATS 831 waves recorded in their experiments. Direct measurements of repolarization in the heart have focused on its time course as measured intracellularly (16, 17), limited to only a few sites in vitro with emphasis on the papillary muscle (18) and on epicardial monophasic action potentials (19, 20). In the present report, the results show that repolarization in normal hearts is controlled by two predominant influences: (1) the time difference between the earliest and the latest area of ventricular activation and (2) the characteristic tendency of the epicardium to repolarize before the endocardium, with unidirectional change in repolarization progress across the wall. Although the left and right ventricular ectopic excitation sequences presented are principally used to produce varied repolarization events, they are noteworthy in themselves, since no total ventricular excitation sequences for ectopic beats have previously been reported. These excitation sequences are presented as potential distributions as well as isochrones, since the overlapping of depolarization and repolarization events, which occurs over a long interval, is only apparent from the potential distributions.