Epicardial Breakthrough Research Articles

The limitations of epicardial mapping as a guide to the surgical therapy of ventricular tachycardia.

The adequacy of intraoperative epicardial mapping as a guide to surgical procedures performed to terminate ventricular arrhythmias was investigated. Ligation of the anterior septal or left anterior descending coronary artery in 28 dogs produced ventricular arrhythmias that were studied 24-36 hours following occlusion. The sites of origin of 26 tachycardias were determined to be in the subendocardium by using extensive epicardial, endocardial and intramural mapping techniques and were verified by demonstrating unaltered activation sequences during pacing from these earliest sites. Epicardial breakthrough followed earliest directly recordable ventricular activity by as little as 7 msec. Without endocardial mapping many of these tachycardias would have been incorrectly identified as originating in the fascicles or epicardium. The sites of epicardial breakthrough were anatomically distant from the sites of origin by a markedly varying extent (5mm to 6cm). Two rhythms might be close in their sites of earliest epicardial appearance yet distant on the endocardium or vice versa. We conclude that epicardial mapping may not be sufficient to identify or predict the origins of many ventricular tachycardias and that the success of surgery to abolish these arrhythmias may be enhanced by preoperative and intraoperative endocardial mapping.

Spread of the epicardial excitation in right bundle branch block pattern.

Electrophysiologic mapping was performed on 29 dogs and 35 patients to investigate the ventricular excitation sequence of normal hearts and various cardiac lesions exhibiting the electrocardiographic pattern of right bundle branch block (RBBB). The activation times of epicardial surface were referenced to the onset of left ventricular cavity potential or QRS wave of lead II ECG. Epicardial activation sequence was represented by isochrones. 1. In normal hearts, the earliest epicardial breakthrough occurred at the mid-anterior paraseptal area in the right ventricle and the activation spread in a circular fashion. In the left ventricle, the epicardial activation occurred at three areas and then spread to the posterobasal area. The epicardial activation sequence was a good representation of the ventricular excitation. 2. In RBBB due to trauma to the main right bundle branch, the right ventricular activation showed marked delay and the characteristic V-shaped pattern. 3. Following vertical ventriculotomy, the right ventricular epicardial activation showed marked delay at sites distal to the incision but no significant delay proximal to it. Regarding postoperative RBBB, central right bundle branch injury was able to be differentiated from distal Purkinje injury due to right ventriculotomy by means of epicardial mapping. 4. In left ventricular pacing, the activation spread in a circular fashion with the prolonged right ventricular activation. 5. In ostium secundum defect, the right ventricular epicardial activation sequence showed various patterns of activation delay resulting from right ventricular hypertrophy. In ostium primum defect, the earliest epicardial activation was found in the left posterior paraseptal area, and the right ventricular activation showed a normal pattern with some delay. Epicardial mapping has been the precise representation of ventricular excitation by direct measurement of cardiac potentials. Cardiac lesions exhibiting the electrocardiographic RBBB pattern provided various patterns of the right ventricular activation delay according to the geneses of RBBB.

The origin of ventricular arrhythmias 24 hours following experimental anterior septal coronary artery occlusion.

The anterior septal coronary artery was acutely ligated in 16 open-chest anesthetized dogs to produce an infarct of the septal myocardium. Twenty-four hours following occlusion complete epicardial mapping and extensive plunge electrode recording techniques were used to localize the sites of origin and patterns of activation of the ventricular tachyarrhythmias that developed during recovery. The earliest electrical activity for 13 individual rhythms was recorded from surviving septal subendocardial Purkinje fibers at the margins of the infarct, in the right or left ventricle, directly underlying the sites of earliest epicardial breakthrough. The sites of origin were verified by demonstrating unchanged activation sequences during pacing through the electrode sites which recorded the earliest activity. None of the arrhythmias arose from the His bundle or bundle branches despite the fact that these tissues course directly through the necrotic septum. The data presented supports the hypothesis that ventricular arrhythmias occuring in the 24-36 hour post acute infarction period may originate in the surviving subendocardial Purkinje system. Our experimental model shows that in cases in which a malignant rhythm arises from a focus, whether it is due to enhanced automaticity or local re-entry, epicardial mapping alone may not identify the source of the arrhythmias. Extensive endocardial mapping may provide a more rational basis for surgical interventions designed to abolish these arrhythmias.

Developing cardiac rupture as initial sign of acute myocardial infarction.

Pathological data are given of 4 patients in whom the development of cardiac rupture was the initial sign of myocardial infarction. The term 'concealed cardiac rupture' is proposed for this condition. In each instance the clinical diagnosis was 'onset of infarction', whereas the necropsy suggested that the acute onset of symptoms was caused by the start of rupture. The arguments for classifying the cases as 'concealed rupture' are (1) the lack of correlation between histological and clinical dating of the infarct, (2) the observation that the tear may take considerable time before actual epicardial breakthrough occurs, and (3) the fact that a high percentage of infarcts may pass clinically unnoticed.

Initial forces of ventricular depolarization in the Wolff-Parkinson-White Syndrome. Analysis based upon localization of the accessory pathway by epicardial mapping.

The epicardial activation sequence of 34 patients with the Wolff-Parkinson-White syndrome was determined. Epicardial pre-excitation occurred at a spectrum of sites over either the free wall of the left or right ventricle or in a paraseptal region, always adjacent to the atrioventricular rings. The site of pre-excitation was related to the spatial position of the 10 msec vector of the vectorcardiogram (VCG) in 15 patients and the 20 msec vector of the electrocardiogram (ECG) in 29 patients with a single accessory pathway. All patients whose 20 msec vector (ECG) was directed to the right had accessory pathways which caused epicardial breakthrough over the free wall of the left ventricle. When the 20 msec vector (ECG) was to the left and inferior, epicardial pre-excitation was over either the right ventricular free wall or in the region of the pulmonary outflow tract. Superior location of the initial forces, especially the 10 msec vector (VCG), strongly suggested the presence of a septal bypass tract. The polarity of the delta wave and maximum QRS forces in precordial lead V1 were discordant in a significant number of patients, pointing to probable shortcomings of a classification based upon the latter.

Ventricular intramural and epicardial potential distributions during ventricular activation and repolarization in the intact dog.

Ventricular intramural and epicardial potential distributions were measured during normal excitation and repolarization in intact dogs. Potential distributions were chosen because they can be unambiguously measured, are useful in understanding the shapes of wave forms at many specific sites, and provide a direct measure of repolarization. Unipolar wave forms were recorded from intramural and epicardial electrodes and converted into potential distributions. Well-known shapes of wave forms recorded at the inner and outer layers of the ventricles as well as peak-to-peak voltages were shown by the potential distributions to be determined primarily by superposition effects of distant excitation waves. These effects were most prominent before epicardial breakthrough and then receded during the last half of the QRS complex. However, the potential distributions became more complex as excitation waves merged, collided, and terminated. During terminal depolarization, there were scattered positive repolarization potentials intramurally. Normal repolarization was characterized by positive potentials over the ventricular epicardium while there were changes intramurally and on the atrium. Throughout the T wave, there was a predominant transmural unidirectional gradient with the inner wall being more negative than the outer wall. This finding confirms that the sequence of repolarization is from the epicardium to the endocardium with the middle layers having an intermediate time.

Sequential change in the different of potential distribution between a normal subject and simulated torso model.

Isopotential map was obtained every 3 msec after the onset of ventricular activation from 85 unipolar lead ECGs of a normal subject (Measured map) and similar map at the corresponding instant (Simulated map) was also obtained by means of mathematical calculation under the assumption that the cardiac electromotive force can be represented by a single electric dipole fixed at the heart center. These 2 maps were quantitatively compared and difference was delineated on a map (Difference map). Although, in major aspect, there was a fairly good agreement between Measured and Simulated maps during early stages of ventricular activation, a remarkable difference of potential distribution began to appear between them around the time of occurrence of epicardial breakthrough of the ventricular activation front. From that t me on, it became impossible to represent the cardiac electromotive force into 2 or more electric dipoles in Difference map. Difference maps around the instant of epicardial breakthrough of the ventricular activation were supposed to be helpful for the estimation of the spread of ventricular activation.

Activation of the human fetal heart

Epicardial activation of atrial and ventricles, endocardial activation of the ventricles, and intramural activation of the interventricular septum, were studied in 11 isolated, revived, and perfused human fetal hearts. No evidence was found for specialized pathways in the atria. Earliest epicardial breakthrough in the ventricles occurred in the area pretrabecularis of the right ventricle; sometimes an early area was found on the posterior aspect of the right ventricle. Latest activated areas were the diaphragmatic and basal aspects of the right ventricle; on occasion, the latest region was the posterolateral part of the left ventricle. On the endocardial surface three regions of early activity were found; the central part of the middle third of the left part of the septum, an area located near the base of the left anterior free wall, and a region near the middle lower part of the left posterior paraseptal region. Septal activation occurred in a left-to-right direction only; nowhere was a right-to-left spread of excitation found. The intramural spread of excitation was perpendicular to the endocardial surface in the central part of the interventricular septum and in the free wall of the left ventricle. In the basal and apical parts of the interventricular septum and in the free wall of the right ventricle, excitation spreads in a tangential fashion.

Interpretation of isopotential surface maps in patients with Ostium Primum and Secundum atrial defects.

The purpose of this study was to determine if there were consistent differentiating patterns in body surface potential maps in children with normal hearts and in those with ostium primum versus ostium secundum atrial septal defects. A second purpose was to interpret the isopotential surface maps in terms of the position of intracardiac electrical wave fronts. Body surface activity throughout QRS demonstrated three major intervals: developing, transitional, and declining potentials. Patients with both types of atrial septal defects demonstrated complex distributions (multiple maxima) during the transitional interval which were not encountered in normal subjects. In the primum group, the distribution of positive and negative potentials sequentially changed in an inverted pattern as compared to the pattern in those patients with secundum defects. Furthermore, during the transitional interval the potential distribution was considerably more complex in the primum group. In two additional patients, body surface maps were helpful in clarifying misleading and atypical conventional electrocardiograms. The presence of simultaneous multiple maxima could only be accounted for by the existence of multiple wave fronts simultaneously present within the heart. In particular the emergence of two widely separated anterior chest maxima in patients with secundum atrial defect indicated the simultaneous presence of prominent left and right ventricular wave fronts. Also, the marked differences in the relative positions of the major body surface maximum and minimum could be accounted for only by considerable differences in the position and extent of intracardiac wave fronts. For example, the target distribution, consisting of an isolated minimum surrounded by multiple maxima and positive potentials over the upper body, in the ostium primum patients, indicated epicardial breakthrough in a wave front positioned in the anterosuperior portion of the heart. In contrast, normal subjects and patients with secundum defect had distributions indicating antero-inferior wave front position at the time of right ventricular epicardial breakthrough.

Activation of the normal and hypertrophied human right ventricle

From the above observations, we have concluded that the sequence of activation of the normal human right ventricle is similar to that which has been studied in considerably more detail in the normal dog. In patients with right ventricular hypertrophy there is a delay of epicardial breakthrough over the entire free wall of the right ventricle. The degree of epicardial delay can be accounted for by an increase in right ventricular thickness without postulating altered spread in the underlying Purkinje network. The sequence of right ventricular epicardial activation, in the presence of right ventricular hypertrophy, appears to be influenced importantly by whether the hypertrophy is symmetric or asymmetric. With increasing degrees of right ventricular hypertrophy, activity in the right ventricular free wall contributes to the late or terminal portions of the QRS complex. The region of the right ventricle which contributes activity to the terminal portions of the QRS complex was different in the three forms of hypertrophy which were examined in this study.

Body surface isopotential maps in normal children, ages 4 to 14 years

A method is presented for the production of isopotential surface maps in children. After recording from 150 to 250 points over the body, the data were processed for analysis by a digital computer with the output of an instantaneous surface map for approximately every millisecond. The presence of dipolar and nondipolar distribution of body surface potentials varied throughout QRS; however, the children demonstrated considerably more of a nondipolar distribution than found by Taccardi in adults. Direct evidence was obtained relating the development of a central minimum over the sternum to epicardial breakthrough of wave fronts in the right ventricular free wall. These studies add emphasis to the need for the further accumulation of data in patients with normal and abnormal hearts to define the time course and location of electrical events on the body surface, since important information is available in areas not sampled by conventional electrocardiographic lead systems.