Left ventricular hemiblock patterns in ventricular pre-excitation.

In a study of 32 cases of ventricular pre-excitation, I2 of i8 cases of type B and 2 of I4 cases of type A were found to have left axis deviation.In 6 (i type A and 5 type B) of the ii (4 type A and 7 type B) who had intermittent pre-excitation, a striking shift to the left occurred in the frontal-plane axis with the transition from normal conduction to pre-excitation; that is 5 of 7 type B and only I of 4 type A. Grant's hypothesis that the frequency of left axis deviation may be explained by premature excitation of either division of the main left bundle-branch is therefore not compatible with the currently held belief that type A represents left, and type B right, ventricular pre-excitation.We have been interested in the association of ven- tricular pre-excitation and complete bundle-branch block (Robertson et al., I963) and the clues pro- vided by this association in determining which ven- tricle is excited early.We now consider that pre- excitation combined with ventricular conduction defects oflesser degree deserve closer attention.Their study is best made either on patients with intermit- tent ventricular pre-excitation or on those whose pre- excitation is constant except during attacks of supra- ventricular tachycardia in which the delta wave is no longer evident.Others (Grant, Tomlinson, and Van Buren, I958; Bleifer et al., i959) have com- mented on the striking difference between the scalar and vector electrocardiograms during normal ventricular conduction and pre-excitation in such patients.The dissimilarity is difficult to ascribe to the addition of a delta vector to the normal vector- cardiogram, and Bleifer et al. (i959) concluded that pre-excitation altered the entire course of the spread of excitation in both ventricles.Grant et al. (I958) found that in about half of their cases, when the delta vector is ignored, the change from normal con- duction to pre-excitation was accompanied by a striking change of the frontal-plane axis without prolongation of QRS.They attributed this to a left ventricular conduction defect based upon the bi- divisional structure of the left ventricular conduction pathways; in other words, what would now be called left ventricular hemiblock (Rosenbaum, Elizari, and Lazzari, I967).With this aspect in mind