Gustavo A. Medrano

Electrocardiographic diagnosis of myocardial infarction in the presence of bundle branch block (right and left), ventricular premature beats and wolff-parkinson-white syndrome

Summary The diagnostic difficulties in the recognition of myocardial infarction in the presence of bundle branch block and the Wolff-Parkinson-White syndrome are discussed. However, through a “deductive” approach in the analysis of the electrocardiogram, such difficulties may be eliminated to a great extent. The knowledge of the sequence of cardiac activation in normal and abnormal circumstances as in bundle branch block, “pre-excitation syndrome”, and extrasystolia, is fundamental. To sum up, the “deductive” approach to clinical electrocardiography not only facilitates the general diagnosis but also indicates the limitations in arriving at a precise diagnosis of infarction.

The activation of the free left ventricular wall in the dog's heart; in normal conditions and in left bundle branch block.

Abstract In this study a critical attempt was made to review some of the more recent experimental studies on ventricular activation. A study of the activation of the normal free ventricular wall using the cathode-ray tube confirmed our previous observations. The spread of activation in the subendocardial muscle mass and at least one-half of the thickness of the adjacent free ventricular wall, reaches values of 2,000 or more mm. per sec. In these regions QS complexes are recorded as described by Prinzmetal and collaborators. An attempt to explain this morphology is presented. In left bundle branch block the sequence, sense, and speed of activation in the free left ventricular wall are unchanged as compared to the normal control. The alterations in morphology are mainly due to changes in direction of activation and delay of conduction in the interventricular septum.

VENTRICULAR PREMATURE BEATS IN THE DIAGNOSIS OF MYOCARDIAL INFARCTION.

The importance of ventricular premature beats (VPB) in the clinical diagnosis of myocardial infarctions has been pointed out by several authors. Dressler (1943) reported a case in which the electrocardiographic signs of infarction were present in such beats (deep and slurred Q waves in lead III) and absent in the sinus beats. Simonson et al. (1945), Bellet (1953), Scherf and Schott (1953), Katz et al. (1958), Silverman and Salomon (1959), and Anttonen et al. (1959) recognized that myocardial infarctions can be diagnosed from VPB and, at times, even earlier from these cycles than from the sinus beats. The similarity of ventricular activation in VPB and in right bundle-branch block (RBBB) and left bundle-branch block (LBBB) has long been accepted. Consequently, VPB with unipolar patterns of LBBB are right VPB, and VPB with patterns of RBBB are left VPB. The same considerations apply also for supraventricular premature beats (SVPB) with aberrant conduction, since the aberration is due to some degree of either RBBB or LBBB (Bisteni et al., 1960). Thus, right VPB and SVPB with aberration similar to that in LBBB are analysed in the same manner as sinus beats with LBBB. In fact, in these three situations the process of ventricular activation follows a similar sequence: the right ventricle is activated before the left. This type of reasoning applies also for left VPB, RBBB, and SVPB with RBBB: in these three instances the left ventricle is activated before the right. A better knowledge of the ventricular activation process in normal conditions and in bundlebranch block has served for a new approach to the diagnosis and localization of myocardial infarctions. Sodi-Pallares et al. (1957, 1960) have shown that tracings with electrical signs of infarction are better understood when analysed in the light of recent studies concerning the ventricular activation process (Sodi-Pallares et al., 1955; Medrano et al., 1956, 1957, and 1958). It has been demonstrated also that septal infarctions may be more easily recognized in the presence of bundle-branch blocks (Sodi-Pallares, 1956), in contrast with the view generally held. On the basis of these considerations the significance of experimental and clinical VPB in the diagnosis of myocardial infarction is studied in this paper.

Clinical electrocardiographic and vectorcardiographic diagnosis of the left anterior subdivision block isolated or associated with RBBB

Abstract Experimental findings previously observed in dogs demonstrated that block of the posterior subdivision of the left bundle branch of His (LPSB) delays the activation of the posterior portion of the free left ventricular wall and of the posterior portion of the interventricular septum, and gives rise to characteristic ECG and VCG changes. These observations permit the recognition of LPSB in clinical tracings. In this paper a study of 17 clinical ECG and VCG records is presented. The main ECG characteristics of LPSB are: qR or QR complexes in Leads III and aV F , with slurring and/or a notch in the downstroke of the R; sometimes a slurring in the initial portion is also observed. Also there is a delayed onset of the intrinsicoid deflection of the R wave in aV F (45 msec.). In vertical hearts the above features are also observed in Leads V 5 and V 6 . ÂQRS is generally situated in the fourth quadrant (between +90 degrees and 0 degrees), although it may be deviated to the right. Frequently the S I -Q III pattern is present. The most important VCG data are: clockwise rotation of the VCG frontal plane ( F ), counterclockwise rotation of the VCG horizontal plane ( H ), and slurrings of the initial and terminal portions of the curve in the three planes. LPSB can diminish or mask the ECG and VCG signs of a posteroinferior myocardial infarction. Based on experimental observations, it was concluded that in a postero-inferior infarction, the presence of terminal and slurred R waves with a delayed intrinsicoid deflection in Leads III and aV F , even with QRS complexes of less than 0.12 second, is due predominantly to an associated LPSB rather than to peri-infarction block. LPSB may diminish the manifestations of right bundle branch block in aV R . Nevertheless the rsR complexes persist in Lead V 1 , while the signs of LPSB are recognizable in Leads III, aV F , and V 6 .

A new approach for the recognition of ventricular premature beats

Abstract Experimental work is presented to prove that many extrasystoles, classically diagnosed as ventricular premature beats, are not. Most of them correspond to atrial or nodal extrasystoles with some degree of aberrancy. On the other hand, there are ventricular premature beats with normal QRS duration and supraventricular beats with QRS duration greater than 0.12 second. The differentiation of ventricular and supraventricular premature beats must be established by considering the morphology of the extrasystolic complex as well as the time in the cardiac cycle when the premature beat is recorded. Definitions of ventricular extrasystoles from several recent textbooks are reviewed. A new definition is proposed based on experimental work performed in the dogs heart.

The electrograms of the conductive tissue in the normal dog's heart

Abstract Simultaneous recording of electrograms of the A-V node, bundle of His, right and left branches and the Purkinje tissue was successfully achieved and is herein presented. The speed of the activation wave in some segments of this specific tissue is calculated. A few considerations for future research are also made.

Importance of the unipolar leads in the diagnosis of dextrocardias, levocardias, dextropositions, and dextrorotations.

Abstract The electrocardiogram provides definite aid in the diagnosis of dextrocardias, dextrorotations, and dextropositions, either complicated or not by other congenital heart disease. An electrocardiographic interpretation must necessarily be understood in all of its aspects before it can be considered as a complete study. “Deductive electrocardiography” would perhaps be the correct name for this type of electrocardiographic interpretation. The sequence of the activation of the heart which explains the electrocardiographic morphologies is indispensable to an understanding of the tracing. Using the aforementioned method we are able to determine the position of the auricles and ventricles within the chest. In this paper we present several examples, one of which will serve to define clearly our point of view. An electrocardiogram was interpreted by us as indicating a transposition of the ventricles. Clinicians and radiologists refused to admit our diagnosis and demurred. We took the stand that unless there was ventricular transposition, we simply did not understand the tracing. The angiocardiographic study proved the transposition of the chambers.

The ventricular activation and the vectorcardiographic curve

Abstract The vectorcardiogram gives valuable information on the sequence of ventricular activation.

The mean manifest electrical axis of the ventricular activation process (ÂQRS) in congenital heart disease: A new approach in electrocardiographic diagnosis

Abstract A new approach in the electrocardiographic diagnosis of congenital heart disease is studied. The combination of the determination of ÂQRS in the frontal plane with the knowledge of the electrocardiographic pattern of each congenital heart malformation permits the main diagnosis of the anomaly in a great number of cases.

Vectorcardiographic study and anatomic observations in 21 cases of Ebstein's malformation of the tricuspid valve

Abstract Twenty-one cases of Ebsteins malformation of the tricuspid valve were studied vectorcardiographically; in 6 cases vectorcardiographicanatomic correlations were made. The anomaly is viewed as part of a generalized disturbance in the development of the right and, in some cases, the left ventricle. Autopsy sections obtained from the septum and free wall of the right and left ventricle showed areas in which muscle fibers were replaced by connective tissue. The fibrosis in the medial posterior and superior portions of the ventricular septum (first published anatomic observation) explains the reduction and abnormal direction of the initial QRS forces and the appearance and correlation with the vectorcardiogram (absent or very diminished slurred Q loop or, in the absence of the Q loop, an initial slurred R loop) and the electrocardiographic configuration (QR in leads V1, V2 and, at times, V3) in some cases of Ebsteins anomaly. Fibrotic areas of this kind may produce similar configurations in other types of cardiomyopathy. A clue to the differential diagnosis between right atrial enlargement due to Ebsteins anomaly and that due to other causes is the slurring in the QH loop or in the initial RH loop when the QH loop is absent. The diminished muscle areas or the pouch of the right ventricular free wall, or both, give rise, in the presence of the right bundle branch block, to the abnormal slurring of the SH loop in the patients without type B Wolff-Parkinson-White syndrome. This is the equivalent of the electrocardiographic qR, qrR′ or qRR′ configuration in leads III and aVF. Left ventricular enlargement was diagnosed in almost 50 percent of cases. The diagnosis was validated by the anatomic enlargement of the left ventricle in 4 autopsy cases, thereby giving anatomic support to this Vectorcardiographic finding in Ebsteins anomaly.