No abstract

SUMMARYThe conduction systems of eight cases diagnosed clinically as having complete left bundle branch block (LBBB) were serially sectioned. Left axis deviation was present in six and normal axis in two. In all cases there was evidence of ischemia of the myocardium and left bundle branch (LBB) We therefore studied the pathology of the conduction system and the entire heart in eight cases which were diagnosed electrocardiographically as having complete LBBB. Our findings lend credence to the view that most cases of LBBB have an anatomic basis in lesions of the LBB. Association.'4 They are as follows: 1) QRS duration of 0.12 sec or greater; 2) presence of a broad monophasic R wave in lead V6; 3) ST depression and T-wave inversion in V6; and 4) absence of Q waves in V6.Pathologically, the coronary arteries were opened by dissection in the fresh heart. The heart was then opened and examined in a manner previously described,"5 the chambers were packed with cotton, and the heart fixed in 10% formalin (4% formaldehyde).Histologic examination was then carried out as follows:"5 the sinoatrial (SA) and atrioventricular (A-V) nodes and their approaches and the beginning of the penetrating portion of the bundle were serially sectioned and every twentieth section was retained. The remainder of the penetrating and all of the branching portion of the bundle, the main LBB and the first part of the right bundle branch (RBB) were serially sectioned, and all sections were retained. The remainder of the bundle branches up through the level of the moderator band were serially sectioned and every tenth section was retained. The remainder of the heart was cut into blocks and two sections were taken from each block. Alternate sections were stained with hematoxylin-eosin and Weigert-van Gieson stains. The findings in these hearts were evaluated in light of previous studies of aging changes in the conduction system of the normal heart.16 17 In these studies the SA node of seven patients, 41-50 years of age; 14 patients, 51-60; eight patients, 61-70; and three patients, 71-90 had been examined. The A-V node, bundle, and bundle branches of 14 patients, 41-50; 12 patients, 51-60; and five patients, 61-70 had been similarly examined. These patients had no history of heart disease, no evidence of LBBB, and had normal hearts at autopsy. ResultsThe results are given in tables 1, 2, and 3. From the electrocardiographic standpoint (table 1) ( fig. 1), the QRS duration varied from 0.12 to 0.20 sec.

This is a clinicopathologic study of 2 patients who electrocardiographically presented so called "masquerading" bundle-branch block. The conduction systems and the entire hearts of these patients were studied pathologically by methods especially devised by Lev for electrocardiographic correlation. This report is part of a long-term project attempting to ascertain the anatomic substrate of electrocardiographic abnormalities.THE electrocardiographic complex referred to as "masquerading bundlebranch block, " consisting of the pattern of left bundle-branch block (LBBB) in the limb leads and right bundle-branch block (RBBB) in the unipolar precordial leads, has generated considerable speculation and interest relating to possible mechanisms responsible for its production. It has been designated " masquerading" by Richman and Wolff1 because they thought that even though the precordial leads suggested RBBB according to Wilson's criteria (right precordial leads showing late R or R' deflections, regardless of the morphology of the limb leads), this complex was actually the result of LBBB. This discrepancy was believed to be the result of the probable transmission of high septal potentials through the infareted free right ventricular wall. These authors' described 4 such cases in which the veetoreardiograms were interpreted as L1BBB. The Sodi-Pallares and Rodriguez2 in an earlier study on activation of the interventricular septum and the clinical evaluation of septal damage described this same electrocardiographic complex. In an effort to clarify this discrepancy between limb and precordial leads, they studied additional leads taken around the thorax at different levels searchingr for the electrocardiographic evidence of L1BBB in these leads to conform with what the limb leads showed. In some of their cases this was found in leads taken in higher interspaces than the conventional chest leads. However, even here the precordial leads showed delayed intrinsicoid deflections over both the right and left precordial regions. The explanation offered was that the infarct had involved the lower portion of the interventricular septum and invaded the adjacent right and left free ventricular walls. The infarct then would extend in the septum to portions of the septum formed by the right ventricle and would only partially involve the portion formed by the left ventricle. The left intraventricular cavity potential would be that found in the presence of L1BBB with the pattern varying, depending upon the orientation of the precordial elec-