Francis F. Rosenbaum

ANOMALOUS ATRIOVENTRICULAR EXCITATION: PANEL DISCUSSION

H. H. HECHT (University of Utah, Salt Lake City, Utah) : Although we are not primarily concerned with the clinical and physiological aspects of abnormal ventricular excitation, it would seem beneficial to follow the searching analysis of the normal propagation of depolarization presented on the preceding pages with an account of a peculiar syndrome that may occur in otherwise normal individuals-a syndrome characterized by an unusual deformation of the early portion of the QRS complex. Detailed electrocardiographic analyses have led to certain inevitable conclusions that presented the anatomist and the histologist with pointed questions. FIGURE 1 illustrates the general configuration of the entity, a short PR interval with a wide QRS complex in a subject who a t other times displayed an entirely normal atrioventricular (AV) and intraventricular conduction, and who, in the sequence from which the illustration was taken, alternated between normal and abnormal complexes. When the two types of complexes are superimposed (FIGURE 2) it is clear that a relationship exists between the normal and the abnormal complex: the QRS deformation involves only the early portion of QRS, and ventricular depolarization obviously begins earlier in the abnormal complex, encroaching upon the normal PR interval. PR is, therefore, short, while PS and the interval from the beginning of P to the summit of R are identical with those of the normal complexes. Because of its shape, the abnormal early portion of QRS has been termed the “delta wave.”’ If the disorder is due to some unusual spread of excitation over ventricular musculature, the spread of recovery will be altered correspondingly and, therefore, T will change in size and direction (FIGURES 1 and 2). The basic myocardial function will remain unchanged and the total area of QRS and T, the ventricular gradient, will therefore remain unaltered. Some frontal plane measurements for normal and abnormal complexes are listed in TABLE 1. I t is generally referred to as the Wolff-Parkinson-White (WPW) syndrome according to the authors of the first definite account: although isolated cases were reported before, the first by Wilson in 1915.3 The more descriptive term “anomalous atrioventricular excitation,” coined in 194S14 implies no more than the existence of an unusual excitatory sequence, the presence of which cannot be denied. We have made this term the title for the panel. Prinzmetal has demonstrated that experimental procedures involving the atrioventricular junction may result in similar electrocardiographic complexes, and he has proposed the concept of “accelerated conduction.llS Others have demonstrated that complexes of this type may occur as a consequence of damage to certain portions of the ventricular musculature, including the septum.6

Persistent displacement of the RS-T segment in a case of metastatic tumor of the heart

Abstract A case of carcinoma of the esophagus with massive metastases to the heart is reported. Serial electrocardiograms displayed persistent upward displacement of the RS-T segment in Leads II, III, and Lead V F , and in a number of the unipolar precordial leads. It was probably caused by almost continuous acute myocardial injury as the neoplastic tissue infiltrated the cardiac musculature.

The precordial electrocardiogram in high lateral myocardial infarction.

Abstract Six cases of suspected infarction of the basal parts of the lateral wall of the left ventricle are reported. The usual unipolar limb leads and the six standard precordial leads failed to furnish unequivocal evidence of myocardial infarction in these cases. Unipolar leads from points on the anterolateral, lateral, and posterolateral aspects of the upper left thorax supplied electrocardiographic data of greater diagnostic value. The types of lesions differentiated have been classified as high anterolateral, high lateral, and high posterolateral infarcts on the basis of the vertical lines in which the most significant electrocardiographic changes were recorded. The opinion is expressed that in these instances the electrocardiographic changes typical of infarction were most pronounced in leads from the upper left thorax because the infarcted region was more basal and more lateral than is usually the case. It is, however, admitted that rotation of the heart or some other change in the relations of its surfaces to the usual leads may have been responsible for some of the electrocardiographic peculiarities encountered. It is recommended that unipolar leads from the higher levels of the left thorax be taken when the clinical history and Lead I, or Lead V L , both suggest that myocardial infarction has occurred and the standard leads from the left side of the precordium fail to display changes of the kind and magnitude expected.

The effects of anterior infarction complicated by bundle branch block upon the form of the QRS complex of the canine electrocardiogram

Abstract In dogs, myocardial infarcts induced by ligating the anterior descending coronary artery in its middle third do not usually modify the QRS complexes of the standard limb leads in a characteristic manner when bundle branch block is present. When such infarcts are complicated by right bundle branch block, the QRS complexes of unipolar leads from the right side of the precordium display a large, initial Q deflection, followed by an R wave which attains its summit late in the long QRS interval. The first component is due to potential variations transmitted from the epicardial surface of the infarcted region, and the second to potential variations transmitted from the epicardial surface of the free wall of the right ventricle. Leads from that part of the precordium overlying the infarct present large, broad QS deflections, often conspicuously slurred or notched. When left branch block is present, infarction of the kind in question does not give rise to characteristic changes in the QRS complexes of the precordial leads because the potential of the left ventricular cavity and, therefore, of the epicardial surface of the infarcted region is positive during the earliest part of the QRS interval. In direct leads from the epicardial surface of the infarct the QRS complex consists of an initial R deflection of variable size, followed by an S component of like or greater voltage. In the case of very large lesions, QRS complexes of this kind probably occur in leads from precordial points overlying the part of the left ventricular wall which is affected, but cannot be considered reliable evidence of infarction.

Variations in A-V and V-A conduction dependent upon the time relations of auricular and ventricular systole: The supernormal phase

Abstract Two cases of transient complete heart block are reported in which there was a supernormal phase in the conductivity of the depressed region. In the first case, penetration of the depressed zone by an impulse arising in the ventricle produced a supernormal phase during which A-V conduction occurred. The conducted impulse in turn gave rise to a supernormal phase which permitted the next impulse to pass, so that normal sinus rhythm was established. It was maintained until auricular slowing caused the auricular impulse to fall outside of the period of supernormal conductivity. In the second case, impulses arising in the auricle produced in the depressed zone a supernormal phase which permitted retrograde conduction.

Changes in the precordial electrocardiogram produced by extension of anteroseptal myocardial infarction

Abstract Electrocardiographic studies are reported on two patients, each of whom had anteroseptal infarction, followed in a few days by lateral extension of the initial lesion. The worth of multiple precordial leads in the diagnosis of extension of such infarcts is illustrated. Evidence is again presented that infarcts which are anteroseptal in location, as shown by diagnostic changes in leads from the right precordial area, often fail to produce equally significant changes in the limb leads. It is suggested that, in cases of coronary arterial disease, some of the attacks of pain which have usually been considered prodromal symptoms of myocardial infarction, actually represent the development of a small, anteroseptal infarct, and that the more characteristic symptoms of acute coronary thrombosis which often occur later are due to an extension of this initial lesion. The true situation must be recognized, if such patients are to be properly treated. We do not wish to convey the impression that we are convinced that all attacks of so-called prodromal pain represent actual myocardial infarction. The data, at present available, bearing on this problem are inadequate to justify this conclusion. Some attacks of this character appear to be due to acute processes developing in the coronary arteries or to transient myocardial ischemia associated with such processes.