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Biomedical subjects

K Harumi

Publications and source records attributed to K Harumi.

At least 91 records · Page 5Linked to original sources
PubMed1982

Moving multiple dipole model for cardiac activity.

A single-dipole model and a two-dipole model have been examined to approximate the electrical activity of heart; positions as well as vector components of these dipoles were estimated from the body surface potential distribution that was measured with 64 electrodes arranged on the chest. The "residue" has been defined as a measure for how much potential component is left that cannot be attributed to the equivalent dipoles. A locus of the vector end of an equivalent dipole in the single-dipole model is very much like ordinary vectorcardiogram (VCG). The residue has a peak in the last half of QRS; this means that the single-dipole approximation is not valid there. Then another dipole is introduced, which is the two-dipole approximation. The residue has been greatly reduced and the peak disappears; the resultant two dipoles move around in the right and left parts of the heart with nearly opposite directions. The moving-two-dipole model for normal subjects describes the cardiac activity in QRS much better than with the moving-single-dipole model.

Electrocardiography↗
PubMed1981

The processed map of the body surface potential.

As the processed maps, the variance map and the residue which was the ratio of the nondipolar cardiac field were introduced. The variance map was made from the root mean square of the distance from the mean value of QRS, T or QRST. The variance map may be useful to find the area of the peak variation of QRS, T or QRST on the body surface. The residue is the expression how much was the nondipolar component included in the body surface potentials. This may be relevant to detect the abnormal cardiac potentials included in the body surface potentials.

Electrocardiography↗
PubMed1980

Detailed activation sequence in the region of electrically induced ventricular fibrillation in dogs.

We determined the details of ventricular activation sequence during the onset of ventricular fibrillation in 6 dogs. Unipolar electrograms were simultaneously recorded from 192 ventricular epicardial sites evenly spaced in a 3 by 3 cm square area surrounding 2 central sites to which stimuli for inducing fibrillation were delivered. In 5 dogs, 2 to 10 msec duration pulses with amplitudes of 150 to 220 v were used to induce fibrillation, and in 1 dog, 3 successive permature stimuli of 3 v intensity were used to induce fibrillation. In 2 dogs the pattern of activation at the onset of fibrillation was compatible with local reentrant paths near the stimulus site. Fibrillation was induced with a single high intensity pulse in both of these dogs. In the other 4 dogs, the pattern of activation at the onset of fibrillation was highly suggestive of reentrant paths distant from the stimulating electrodes. In 3 of these dogs fibrillation was induced by a single high intensity pulse and in the other it was induced by 3 repetitive stimuli. Activation patterns resembling supraventricular activation occurred prior to fibrillation in the latter animal. The data demonstrate 2 distinct modes of onset of electrically induced ventricular fibrillation. The findings support local reentry in the region of the stimulus site as the mode of onset of fibrillation in some animals and possible reentry at sites distant from the stimulus site with participation of the specialized conduction system in other animals. The differences in mode of onset of electrically induced fibrillation may be responsible for instability of fibrillation threshold measurements in some animals. In addition the role of the specialized conduction system in the onset of fibrillation may be responsible for the effects of sympathetic and vagal stimulation on fibrillation threshold.

Animals↗
PubMed1980

Nocturnal angina pectoris. Comparison between angina with ST segment elevation and depression documented by continuous orthogonal ECG recording.

In 30 patients with nocturnal angina, the night-time ECGs were continuously recorded, and the time and duration of attack, cyclic character of attacks, the relation of chest pain to ischemic ECG changes and arrhythmias during attack were compared between 18 cases with ST elevation and 12 cases with ST depression during attack. In cases with ST elevation, 1) attacks occurred between 2:00 and 8:00 a.m., being most frequent between 4:00 and 5:00 a.m. 2) the duration of attack measured from the duration of ischemic ECG changes was less than 5 min in 88% of the attacks, 3) the attack often recurred with intervals less than 30 min and ECG changes were often unaccompanied bt chest pain, 4) the attack was complicated with various kinds of arrhythmias. These features were in marked contrast to the cases with ST depression, in which attacks were evenly distributed over the night-time, of longer duration, sporadic in occurrence and far less complicated with arrhythmias. These data suggest that the difference of mechanisms causing attacks between both groups.

Adult↗
PubMed1978

The magnitude of the electromotive force of canine ventricular myocardium.

The isolated and perfused dog heart was placed in a cubic container filled with Tyrode's solution. Ventricular ectopic beats were produced by electrical stimulation of the left ventricular wall, and initial QRS vectors of these beats were determined with orthogonal leads from the surface of the container. At the same instants, the activated area on the epicardial surface was measured by means of a large number of contiguous bipolar leads from the epicardial surface. The QRS vector and the activated epicardial area were found to be nearly porportional. By use of these results and a calibration system with artificial dipoles, the double layer moment of the ventricular activation wave was calculated as 0.13 mA.cm per unit area. This value corresponds to 60% of the maximal possible strength of the tissue electromotive force. Lowering the conductivity of the surrounding solution increased the QRS voltage but not as much as the potential caused by a constant-current dipole within the solution. The relationship between the QRS voltage and the conductivity of the medium was analyzed by a simplified model of the system and was found to correspond approximately to that of a constant-current source within a spherical heart with a resistivity 2 to 3 times that of Tyrode's solution.

Animals↗
PubMed1978

Changes in ventricular recovery properties during and after temporary coronary artery occlusion.

The sequence of localized changes in ventricular repolarization time during and after temporary coronary artery occlusion was studied in 10 open chest dogs. Immediately after the onset of coronary occlusion functional refractory periods (FRPs) prolonged slightly in the ischemic area, then shortened with continued occlusion. Within the first minute following release of occlusion, FRPs underwent a further brief decrease in duration. By varying the period of occlusion from 1 1/2 to 6 1/2 min, evidence was obtained that the post-release shortening of RFPs was temporally related to release of the clamp and not to the onset of occlusion. Ventricular fibrillation occurred in 2 dogs, in each instance soon after release of the coronary artery occlusion. The possible relationship of these experimental FRP changes to waveform abnormalities and arrhythmias in ischemic heart disease is discussed.

Animals↗
PubMed1977

Prolongation of ventricular action potential due to sympathetic stimulation.

The changes of monophasic action potential durations due to stellate stimulation for the period of 3 sec were studied in dogs with suction electrodes from the anterior surface of the right ventricle and the posterior surface of the left ventricle. Prolongation of monophasic action potential duration was observed from the period of 2 to 3 sec during stimulation to that of 10 to 20 sec after the termination of stimulation. Prolongation of monophasic action potential duration due to right stellate stimulation was predominant in the right ventricle and that due to left stellate stimulation was predominant in the left ventricle. The transient T wave change in the surface electrocardiogram occurring immediately after the beginning of stellate stimulation could be explained by this local difference in prolongation of ventricle repolarization. Since the onset of prolongation of monophasic action potential duration preceded increase in blood pressure following stellate stimulation, this prolongation of monophasic action potential duration did not result from the hemodynamic changes and could be a primary effect of the sympathetic nerve stimulation.

Action Potentials↗