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

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... iorly, 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 delay Purkinje activation myocardial infarction 752 dence of left anterior divisional block have demonstrated extensive pathological changes in the left ventricular conduction system that are not confined to the anterior division (27-30). The present investigation was undertaken to determine the effects of discrete superficial left septal lesions on the vectorcardiogram (VCG), the electrocardiogram (ECG), and the sequence of ventricular activation in the intact dog. An attempt was also made to develop a method to differentiate conduction disturbances associated with endocardial activation delays from those secondary to intramural factors. Methods Epicardial, intramural, and endocardial studies were carried out in 25 adult mongrel dogs of both sexes weighing 15-20 kg. Each dog was anesthetized with sodium pentobarbital (25 mg/kg, iv), intubated, and placed on a respirator in the supine position. Standard ECGs were obtained as well as VCGs using the McFee orthogonal system (31); care was taken to use identical foreleg positioning (32). The surface landmarks for the vector leads were marked with permanent sutures in the chest wall. The heart was exposed through a sternotomy and positioned in a pericardial cradle. A reference electrode was sewn on the anterior right ventricle. A purse-string suture was placed in the subepicardial Canine left ventricular endocardium stained with LugoFs solution. Note the discrete raised lesion transecting the anterior division of the left bundle branch and the intact state of the septal branches and the posterior division.