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Electrocardiograms (ECG), McFee vectorcardiograms (VCG), and ventricular activation data were collected from 25 anesthetized dogs before, immediately after, and 4 weeks after surgically induced discrete left anterior divisional block. Left anterior divisional block resulted in minor ECG changes: small S waves developed in leads II, III, and aVF and the QRS complex was prolonged 5-15 msec (mean 9 ± 2.7 SD msec). Prominent VCG changes also occurred: maximal and terminal forces were shifted posteriorly, superiorly, and slightly leftward, the duration of the loop was increased 5-15 msec (mean 9.8 ± 2.8 msec), and the terminal portions of the loop were slurred. Epicardial surface mapping revealed a consistent area of 5-20-msec delay (mean 12 ± 5.1 msec) confined to the lateral-basal surface of the left ventricle. Transmural activation studies in this area invariably revealed 6-20-msec (mean 12.8 ± 4.8 msec) delays in Purkinje and 3-25-msec (mean 12.4 ±5.6 msec) delays in endocardial activation. The wave front propagated across the wall with normal velocity. Q waves developed due to a "window effect" in the area of delay. Combining division of the septal fibers with left anterior divisional block resulted in surface delays of greater magnitude with marked axis shifts toward the left. Despite the extensive interconnections of the left ventricular conduction system, discrete proximal left anterior divisional block resulted in a significant alteration in the sequence of ventricular activation, confirming the fascicular nature of the left ventricular conduction system. The septal division appears to be an integral part of this system. The methodology described in this paper can be used to readily differentiate between epicardial delay due to conduction delay and that due to intramural myocardíal delay.
Gallagher et al. (Fri,) studied this question.