Nobuo Niimi

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.

Computational Reconstruction of Body Surface Isopotential Maps in Myocardial Infarction: Comparison between Nontransmural and Transmural Infarction

The relationship between the lack of electromotive force in myocardial infarction and body surface potential distribution was investigated on maps reconstructed from a simulated heart model and transfer impedance vectors of human torso model. The heart model, a cluster of 3-mm cubic blocks, was stored in the memory of a computer. Transfer impedance vectors between 81 lead points on the human torso model and 392 positions covering ventricular areas in the torso were measure. Body surface potential values were calculated mathematically by summing up scalar products between the electromotive force of the heart model and the measured transfer impedance vectors. Thus, reconstructed maps changed in their patterns with the alternation in lacation and/or extent of infarcted region in the heart model. In particular, the appearance of the abnormal potential minimum, which projects the infarcted region in the heart model onto the torso surface, was characteristic in both transmural and subendocardial infarction. In addition, delayed activation in the intact layer of the epicardium overlying the infarcted region produced a potential maximum on the same place as the abnormal potential minimum appeared previously.