Junichi Sugenoya

Diagnosis of right ventricular infarction: Experimental study through the use of body surface isopotential maps

This investigation was designed to diagnose right ventricular infarction, which is difficult to diagnose by the standard twelve-lead ECG, through the use of body surface isopotential maps which have significant diagnostic information. Right ventricular infarction was experimentally caused by ligation of the canine right coronary artery. Each dog had a series of maps recorded before and a week after experimentally-induced myocardial infarction. The common features of maps in right ventricular infarction are: 1. In the early stage of the ventricular depolarization the negative area occupies a comparatively large part of the right anterior chest surface, and in the middle stage, the larger part of the right anterior surface is also occupied by the negative area. 2. A minimum appears on the right anterior chest surface in the early stage. The delayed excitation resulting from intraventricular conduction disturbance caused by infarction, as verified by the epicardial isochronic map, is also well represented by the body surface isopotential map. In conclusion, through the use of body surface isopotential maps, it is much easier to diagnose right ventricular infarction and intraventricular conduction disturbance caused by infarction even in cases in which the standard twelve-lead ECG does not show the abnormalities clearly.

Experimental study of myocardial infarction through the use of body surface isopotential maps: Ligation of the anterior descending branch of the left coronary artery

This investigation was undertaken to diagnose the location and extent of myocardial infarction with the use of maps which give significant information about the ventricular activation process. Myocardial infarction was experimentally caused by ligation of the anterior descending branch of the left coronary artery. All classes were classified into three groups (A,B, and C) according to the location and extent of infarction. The map of each group had its own characteristics, as follows. In Group A no pisitive potentials appeared on the left anterior chest surface all through ventricular depolarization. In Group B, like Group A, the negative area occupied the whole left anterior chest surface in the early stage. But in the later stages there appeared a positive area on the left anterior surface. As to Group C, there was no abnormality in its early stage, but in its middle stage, the negative area was found on the left anterior chest surface. Thus the sequential maps can be helpful in diagnosing the location and extent of myocardial infarction, and will be applied to clinical use much more.

Diagnosis of high posterior infarction: experimental study through the use of body surface isopotential maps.

This investigation was designed to diagnose high posterior infarction easily through the use of body surface isopotential maps. High posterior infarction was experimentally caused by ligation of the branch of the circumflex artery of the canine left coronary artery. Each dog had a series of maps recorded before and four weeks after experimentally induced myocardial infarction. The common features of maps in high posterior infarction are: 1) The positive area expanded into the dorsal surface so slowly that, in the middle stage of the ventricular depolarization, a large area of the dorsal surface was still covered by the negative area. 2) from the middle to the late stage, the absolute value of the minimum significantly decreased and absolute potential of the dorsal surface also significantly decreased. In conclusion, we propose that it is possibile to diagnose high posterior infarction through the use of maps.

Genesis of body surface potential distribution in right bundle branch block

In order to investigate the specific sites of conduction block in the three types (I, II, III) of right bundle branch block (RBBB) classified by body surface isopotential maps, the simulation of ventricular propagation process and mathematically reconstructed maps were used. Four assumptions were introduced from the results of clinical observations and animal experiments. The maps reconstructed from two of these assumptions, in which the conduction block was placed on the main stem of the right bundle branch, showed two different patterns at late stages of excitation, and these two kinds of map resembled Types I and II in clinical maps, respectively. The maps reconstructed from the other two assumptions, in which the site of the conduction block was located mainly in the Purkinje system of the right ventricular free wall, resembled Type I at the late stage of excitation in one of two assumptions and agreed with Type III through all stages of excitation in other case. Based on the above results, it is speculated that the differences of ranges and degrees of conduction block ascribed to abnormal activation in the Purkinje system of the right ventricular free wall are responsible for the genesis of clinical RBBB map patterns.

Experimental Studies on the Antiarrhythmic Action of a Lidocaine Analog

The electrophysiologic properties of a lidocaine analog (Kö 1173) was experimentally studied in 41 mongrel dogs. The threshold for occurrence of repetitive ventricular extrasystoles was significantly raised by the administration of 2, 4, and 8 mg/kg of the drug, while atrioventricular and intraventricular conduction times were not affected. After ligation of the anterior descending branch of the left coronary artery, the threshold for occurrence of repetitive ventricular extrasystoles was significantly lowered before the administration of Kö 1173 but it returned to control values after the administration 1 mg/kg of the drug. The strength-interval curve shifted profressively to the right when the dose was increased from 2 to 4 and 8 mg/kg. These results indicate that Kö 1173 prevents the decrease in threshold for occurrence of repetitive ventricular extrasystoles in acute coronary insufficiency at a dose which does not affect the conduction system.

Body surface potential distributions in posterior ventricular pre-excitation***

Waveform of the QRS complex during ventricular pre-excitation is subject to the influence of both the site of pre-excitation and the time of pre-excitation relative to that of excitation via the normal AV path. This paper reports a case in which lead V1 of the electrocardiogram (ECG) could be altered from an R to an rS pattern by the administration of atropine sulfate. The provable mechanism was that of reduced conduction time in the normal AV path with altered time phase of normal excitation and pre-excitation. This mechanism was simulated in experiments on dogs and yielded similar findings. Body surface mapping in both the patient and the dogs provided evidence that pre-excitation could be recognized by that means with varied time phase of normal excitation and pre-excitation. It was demonstrated that the QRS complex of right sided precordial leads could be altered from an R to an rS pattern by altering the time phase of normal excitation and pre-excitation of the posterior ventricular wall. This alteration was related to the degree to which negative potentials on the anterior chest wall due to right ventricular breakthrough of normal activation developed in relation to the time of pre-excitation.