Activation Studies following Experimental Hemiblock in the Dog

Abstract

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, HI, 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 lateralbasal 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 myocardi'al delay. KEY WORDS epicardial mapping left anterior hemiblock vectors myocardial conduction delayPurkinje activation myocardial infarction• Experimental injury to subdivisions of the left bundle branch was first reported in 1910 (1). Subsequent studies over the ensuing 60 years have gradually led to the concept of two functionally distinct subdivisions of the left bundle, i.e., the anterior and posterior divisions (2-24). More recently, in vitro studies by Myerburg et al. (25,26) have suggested that widespread interconnections between the anterior and posterior Purkinje networks of the left ventricle make it unlikely that isolated lesions in proximal subdivisions of the left bundle branch would result in significant changes in ventricular activation. Furthermore, histological examinations of the human conduction system in patients who exhibited electrocardiographic evi- This investigation was supported in part by U. S. Public Health Service Grants HL 05736 and HL 08845 from the National Heart and Lung Institute.Dr. Wallace is the recipient of Research Career Development Award HL 19949 from the National Heart and Lung Institute.This study was presented in part at the 46th Annual Scientific Session of the American Heart Asso...

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