Manifestaciones eléctricas de alteraciones miocárdicas asociadas a preexcitación ventricular / On the electrical manifestations of some heart diseases associated with ventricular preexcitation

Electro-Vectorcardiographic curves, corresponding some heart diseases, must be analyzed in the light of the ventricular depolarization sequence, as well as on the heart's position and rotation. A more than 30-msec interval between the end of the initial slurring (delta) and the vertex of the R wave in the left unipolar leads or the main axis of the vectorcardiographic ventricular curves, allows us to infer the coexistence of left ventricular hypertrophy. On the other hand, segmental irregularities or distorsions of the electric curves suggest the presence of a limited myocardial zone unable to be activated. Extensive or multiple deformations of these curves are more suggestive of a diffuse myocardial damage. Sometimes signs of preexcitation, due to a pharmacological action, can also appear.

[Usefulness of vector analysis of the electrocardiogram]. / Utilidad del análisis vectorial del electrocardiograma.

An electrocardiogram corresponding to an obese, hypertensive woman 52 years old, is presented. It shows a left bundle branch block of advanced degree and the AQRSF at 70 degrees. In this case, the key of the electrocardiographic diagnosis is that the second vector originated by depolarization of the lower left septal mass is oriented downward, which is unusual in the presence of left bundle branch block. This fact may be due to a marked clockwise rotation. Therefore, it is possible that right ventricle pathologic conditions be associated to those involving the left ventricle. Cardiopulmonary tests determined the existence of a chronic pulmonary emphysema. Furthermore the study of this case shows the usefulness of vectorcardiographic exploration in clinical practice.

The rational approach to the electrical exploration of the heart.

A rational approach is inevitable in any scientific activity. Such an approach is opposed not only to irrationality, at all inadmissible in scientific thinking, but also to empiric reasoning. Many years ago, Sodi Pallares introduced the rational method in the electrical exploration of the heart based on experimental findings obtained in his laboratory. This method has progressively been accepted and used with good results for diagnoses and has led to logical therapeutic inferences. To confirm the results from the logical interpretation of electrical tracings, we present some examples of its application in three fields: arrhythmias, myocardial infarction, and left ventricular hypertrophy. In the studied cases--two with tachycardia, one with a posterior infarct, and two with left ventricular hypertrophy--a very satisfactory correlation has been observed between the electrical exploration findings and those obtained through direct examination of the heart. It is desirable, and even profitable, to analyze in this way the electrical tracings to get as close as possible to reality, rejecting the stereotyped aspects of a simple routine exploration, which often induce errors and lead to some fallacious asseverations.

[Rational electrovectorcardiography]. / En torno a la electrovectocardiografía racional.

The mental process of electrocardiographists to adjust the electrocardiogram's or vectorcardiogram's interpretation with the sequence of myocardial depolarization and repolarization can be accomplished in two ways. The first one is through vectorial analysis and the second concerns the analysis of unipolar morphologies. The most suitable is to follow both ways. The first procedure constitutes the classic method accepted since Einthoven's time and refers to the vectorial representation of the electrical charges of the heart. This representation approaches the electrical moment of a unique dipole, when cardiac exploration is performed at the smallest adequate distance. This allows to establish the spatial position of the instantaneous vectors, or of the mean vector, by using different leads. The study of unipolar morphologies permits to know the distribution of the mentioned charges in the conducting medium. The adjustment of the electrical charges depends on the location of the wave fronts. These charges produce potential variations in the physical sense--Gaussian type--at the epicardial surface and also at any point of the conducting medium surrounding the heart as far as the skin. This procedure requires the use of Poisson's integral, based on the principle of Helmholtz' electromotive surface. Thereafter, it is mandatory to perform another adjustment for the results of both procedures and to scrutinize the inner cellular metabolic process, which can explain the behavior of the observed electrical phenomena and suggest the adequate treatment.

On the electrocardiographic diagnosis of biventricular infarctions.

To diagnose posterior and anterior biventricular infarctions it is necessary to record from right and left thoracic and high abdominal unipolar leads. These supplementary leads are dependable, can be repeated as many times as needed and show the evolution from signs of myocardial injury to those of dead tissue (Q waves of 0.04 sec or more). This electrocardiographic evolution increases the diagnostic value of the electrical exploration, since the injury current can be observed also in other conditions. The diagnosis of right ventricular infarction can be established even in the presence of RBBB. Signs of a dead zone in the free right ventricular wall are more frequently observed in posterior biventricular infarctions than in anterior ones. In these cases, the signs of subepicardial injury are more accentuated in the right thoracic unipolar leads than in V3, indicating anterior right ventricular involvement. These signs are also observed in experimental studies made in animals. This electrocardiographic exploration opens a wide field for the diagnosis of myocardial infarction, particularly in biventricular involvement, including old myocardial scars, and in discarding signs of pericarditis manifested only by the upward displacement of the ST segment. A review of the medical literature concerning diagnosis of biventricular infarctions is presented.

[Is the concept of "jumping wave" still valid?]. / Es aún válido el concepto de "salto de onda"?

UNLABELLED: The concept of the "jumping wave" phenomenon, i.e. of the slow and difficult passage of activation fronts from one septal mass to the other through an "intraseptal barrier", is derived from experimental studies of the Mexican School of Electrovectorcardiography. OBJECTIVE: To confirm the existence of histologically bipartite interventricular septum and of the electric independence of both septal masses. METHODOLOGY: We examined the histological characteristics of both septal masses in rat, canine, and human hearts. We also analyzed the morphological and chronological data of intracavitary records in the presence of different degree proximal blocks, comparing these findings with those obtained when peripheral blocks existed. RESULTS: We found a medial, longitudinal band between the two septal masses in animal as well as in human hearts. The analysis of intracavitary electric records confirmed a slow and difficult transmission of the activation fronts from one septal mass to the other, in the presence of proximal blocks and ventricular arrhythmias. Morphological and chronological changes of intraventricular complexes could not be explained if the septal activation process were of syncytial type. CONCLUSIONS: Results of this study firmly support the validity of our approach to the septal activation process in the presence of ventricular conduction disorders and arrhythmias. This approach helps to detect the possible coexistence of dead septal tissue.

Effects of verapamil in ventricular tachycardias. An experimental and clinical study.

To determine the effect of verapamil in ventricular tachycardias, we performed an experimental and clinical study. Experimental ventricular tachycardias (VT) were produced in dog hearts with minute aconitine crystals introduced into the periphery of a left ventricular area, damaged by intramural injection of 1.0-1.5 ml phenol. The response of these tachycardias to 0.2 mg/kg verapamil was analyzed. Verapamil was infused into the superior vena cava over 15-20 min. Leads II, aVL, intraventricular right and left unipolar records, as well as one of the superior vena cava, were registered under control conditions, in the presence of VT, and after application of verapamil. Recordings were obtained at constant intervals, waiting for the recovery of sinus rhythm (SR) and the posterior reappearance of tachycardia. Experiments were performed for 6 to 8 h under continuous infusion of Hartmann's solution. Throughout these periods, variations in systemic systolic pressure were recorded. From 75 animals submitted to this treatment, 30 (40%) recovered transiently the SR, whereas the drug exerted no antiarrhythmic effect in 19 (25%), and arterial systolic pressure fell importantly in 10 (13%) animals. In two more groups, of 15 dogs each, the VT response to verapamil was compared with the response to lidocaine and flecainide. Endovenous verapamil (5-10 mg) was administered to 10 patients, coursing with VT and having a structurally normal heart, after this arrhythmia was induced by electrical stimulation. The response to verapamil was satisfactory in nine patients (90%), in which VT originated in the septal and apical regions of the left ventricle. Verapamil seems to be effective in experimental and clinical ventricular tachycardias related to calcium-dependent potentials, in which the sustaining mechanism could either be triggered activity or reentry.

[Effect of intravenous verapamil in experimental ventricular arrhythmia]. / Acción del verapamil intravenoso en arritmias ventriculares experimentales.

Experimental ventricular tachycardias (VT) were provoked in dog hearts with minute crystals of aconitine introduced into the periphery of an infarcted area, produced by intramural injection of 1-1.5 ml of phenol. The response of these tachycardias to verapamil was studied. Leads II, aVL, intraventricular right and left unipolar records, as well as one on the superior vena cava were registered under control conditions, with VT and after the injection of the antiarrhythmic agent. This injection was infused into superior vena cava over 15-20 minutes. Records were obtained with constant intervals, waiting for the recovery of sinus rhythm (SR) and the posterior reappearance of ventricular tachycardia. The experiments were performed 6 to 8 hs with continuous infusion of Hartmann's solutions. Throughout these periods, the variations of systemic systolic pressure were registered. Of the 75 dogs treated with 0.2 mg/kg of verapamil, SR was recovered transiently in 30 (40%), while it exerted no antiarrhytmic effect in 19 (25%). Arterial systolic pressure fell importantly in 10 animals (13%). In 3 other groups, of 15 dogs each, comparative administration of verapamil vs lidocaine (I), vs mexiletine (II) and vs propafenone (III), was tried. In Group I, verapamil reestablished transient SR in 73% and lidocaine in only 7%; in II, SR resulted from verapamil in 33% and from mexiletine in 7%; in III, SR reappeared in 21% with verapamil and in 28% with propafenone. The repeated positive effect of verapamil was found in 33% of 15 experiments. This drug is effective in certain experimental ventricular tachycardias, probably related to calcium-dependent potentials.

[The action of intravenous flecainide in experimental ventricular arrhythmias]. / Acción de la flecainida intravenosa en arritmias ventriculares experimentales.

Experimental ventricular tachycardias were provoked in dog hearts with minute crystals of aconitine introduced into the periphery of an infarcted area, produced by intramural injection of 1-1.5 ml of phenol near the apex of left ventricle. The response of these tachycardias (VT) to flecainide was studied. Leads II, aVL, intraventricular right and left unipolar records, as well as one on the superior vena cava (SVC) were registered under control conditions, with VT and after the injection of this antiarrhythmic agent. This injection was infused into SVC over 15-20 minutes. Records were obtained with constant intervals, waiting for the recovery of sinus rhythm (SR) and the posterior reappearance of ventricular tachycardia. The experiments were performed 6 to 8 hs with continuous infusion of Hartmann' solutions. Throughout these periods, the variations of systemic systolic pressure were registered. Of the 22 dogs receiving 4 mg/kg of flecainide, transient SR was observed in 12 (55%), while in 4 (18%) this medication had no effect. Heart block presented in 2 animals and a fall of arterial pressure in 4. Of another 25 dogs receiving 2.5 mg/kg of flecainide, similar to clinical doses, transient SR appeared in 11 (44%), while in 3 (12%) SR was not observed. In other 2 groups, each of 15 dogs, the repeated antiarrhythmic action of flecainide was present in 33% with 4 mg/kg and in 20% with 2.5 mg/kg. This medication had no effect in 20% of the former and in 40% of the latter. However the low dose did not produce undesirable effects. Furthermore these differences were no significant statistically. Flecainide is effective in certain experimental ventricular tachycardias probably related to sodium-dependent potentials.

Electrocardiographic features in experimental subendocardial infarctions in canine hearts.

Chemical necrosis was produced with the infiltration of 96 degrees alcohol on the middle anterosuperior segment 5 (nomenclature of the International Society for Computerized Electrocardiology) of the free left ventricular (LV) wall in 45 dogs and on the apical segment 10 and middle posterolateral segment 11 in 30 others. In five animals from each group, a 10 bipolar arrow assembly was used to obtain Purkinje fiber potentials and to determine the degree to which QS complexes are recorded from the inner portions of the free LV wall. When transmural necrosis was present, QS complexes were generally obtained in both the epicardial and thoracic leads. Subendocardial necrosis was manifested by qrS complexes on the epicardium, as well as in the peripheral leads. When the posterolateral middle third of the LV wall was damaged, Rs or qRs complexes were recorded in leads II, III, and aVF, and an increase in the voltage of the R wave in leads V1 and V2 was observed. Intramural myocardial necrosis diminished the voltage of the R wave in the corresponding leads. Left peripheral blocks obscured the manifestation of myocardial necrosis.

[Response of experimental ventricular tachycardia to class I anti-arrhythmia agents]. / Respuesta de taquicardias ventriculares experimentales a antiarritmicos de la clase I.

Active ventricular arrhythmias were provoked in damaged dog myocardium to study their response to some antiarrhythmic agents of Vaughan-Williams' class I. Dogs anesthetized with intravenous sodium pentobarbital (30 mg/Kg) were intubated and submitted to artificial ventilation using a Palmer pump. An infarction was produced near the apex of the left ventricle by intramural injection of 1-1.5 ml of phenol, and 30 to 60 min later, minute crystals of aconitine were introduced into the periphery of the infarcted area. Once ventricular tachycardia appeared and became stable, corresponding records were obtained and the antiarrhythmic agent to be studied was administered through the superior vena cava over a period of 5 to 15 min. Electrocardiographic tracings were registered at constant intervals in order to detect the recovery and duration of sinus rhythm. The reappearance of arrhythmia was always required in order to consider the action of the medication administered positive. High doses of lidocaine (6 mg/Kg) reestablished transient sinus rhythm in 23% of 35 treated dogs. Fifteen mg/Kg of mexiletine reestablished it in 45% of 22 animals and 2.5 mg/Kg of propafenone restored it in 39% of 18 animals receiving this drug. The positive effect of these antiarrhythmic agents of groups I B and I C consisted essentially in controlling no-rapid tachycardias with the "wave jumping" phenomenon and fusion beats, which may be due to activity of ectopic foci. Very rapid ventricular tachycardia with "wave jumping" generally did not respond to the antiarrhythmic agents tested. These tachycardias may be maintained by reentry or by the intervention of calcium-dependent potentials. Rapid ventricular tachycardias without extensive "wave jumping" also occurred. These were never controlled by the group I B antiarrhythmic agents, although they were sometimes suppressed with propafenone. These tachycardias probably originated near the intraseptal barrier. In few animals, amiodarone of class III was employed with a marked hypotensive effect.

[Experimental subendocardial postero-inferior infarctions]. / Infartos experimentales subendocardicos posteroinferiores.

In 30 mongrel dog hearts, epicardial and thoracic unipolar records were obtained after myocardial damage was produced by infiltration of 96% alcohol in the postero-inferior free left ventricular wall. Necrosis was transmural in 5 cases, subendocardial in 11 and intramural in 10. In 4 dogs, intramural unipolar and bipolar leads were recorded in order to determine the electrical subendocardium and its relation to potentials of Purkinje's fibres. At the end of each experiment, left posterior subdivision block (LPSB) was provoked. In 90% of the cases, direct epicardial records were QS in transmural infarction, qrS or less frequently QRS in subendocardial ones, and rS or qRS in the presence of intramural necrosis. In several cases myocardial necrosis was located in the middle third instead of the inferior third, but the direct registries were similar. Nevertheless the surface leads (II, III and aVF) did not show abnormal Q waves or greater voltage of Q and S, but there were RS complexes in V1 and V2. In 80% of the cases, transmural necrosis of inferior third was manifested by QS complexes and subendocardial necrosis by rS or qRS complexes with increased Q and S waves and reduced R waves. LPSB masked the signs of necrosis. There is no justification for speaking of myocardial infarction with or without abnormal Q waves, because it does not add more precision. Moreover these expressions can create confusion in cases of middle or high posterior myocardial necrosis, revealed by RS complexes in V1 and V2.

[Vectorcardiographic manifestations of atrial enlargements]. / Manifestaciones vectocardiográficas de los crecimientos auriculares.

Rational interpretation of changes of the P loop due to atrial enlargements must to rely on the magnitude and spatial orientation of main resultant vectors of the activation sequence of the atria. Under normal conditions, these vectors give rise to a mean vector oriented to the left downward and discretely forward with respect to their point of origin. In the presence of right atrial enlargement, the manifestation of the first vector of atrial depolarization, oriented downward and forward, is increased. This one moves in the same direction as the mean vector of atrial depolarization, originating an elongated P loop of more than 100 mcv in the three planes. Nevertheless, in the horizontal plane, increase of the P loop voltage predominates when hypertrophy exists, while augmentation of its area predominates when dilatation exists. In left atrial enlargement, the manifestation of the second vector of atrial depolarization, oriented to the left and backward, is augmented, and it moves in the same direction as the mean vector of atrial depolarization. For this, the PF loop acquires a characteristic aspect of a boxing glove, an the PH loop becomes diphasic, with its posterior area more or less prominent, or with a typical figure-eight conformation. If a biatrial enlargement is present, the manifestation of both the main resultant vectors of atrial depolarization is accentuated. Therefore the voltage of the diphasic P loop increases. Moreover the Ps loop has a triangular configuration, with its base of 30 msc or more, located below its point of origin. Generally disturbances of interatrial and intraatrial conduction coexist owing to myocardial damage.