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Biomedical subjects

K Harumi

Publications and source records attributed to K Harumi.

18 recordsLinked to original sources
PubMed1991

Study on the genesis of giant negative T wave in apical hypertrophic cardiomyopathy using a three-dimensional computer model.

Apical hypertrophic cardiomyopathy is characterized by a spade-like left ventricular cavity and by both giant negative T waves and tall R waves in the electrocardiogram. However, the mechanisms of these ECG abnormalities have not been satisfactorily clarified. We have recently developed a three-dimensional computer model of ventricular depolarization and repolarization processes. This model has successfully simulated normal QRST waves and changes characterizing some abnormal conditions. A model of apical hypertrophic cardiomyopathy was constructed by adding model units to the endocardium of the left ventricular apex. The surface ECG was then calculated by assuming different gradients of action potential durations and different proportions of the hypertrophic cells in the apical segment. A negative T wave of -1.45 mV in lead V4, similar to the clinically reported ECG, was obtained by assuming: (1) diffusely distributed hypertrophic cells at the apex and (2) uniform, long action potential durations of hypertrophic cells. It is suggested that these properties may account for the distinctive ECG abnormalities in apical hypertrophic cardiomyopathy.

Cardiomyopathy, Hypertrophic↗
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↗
PubMed1976

The significance of T-loop change in Frank's lead exercise electrocardiography.

Thirty-one patients with angina pectoris and 15 patients with myocardial infarction who performed exercise test by Master's double two-step test have been longitudinally followed up for 4-10 years. Exercise electrocardiogram was taken by Frank's lead and T loop was constructed in frontal and horizontal planes from 3 scalar tracings recorded at a paper speed of 100 mm/sec. ST vector was determined at 100 msec from the beginning of Q wave and the line connecting 2 ST vectors before exercise and at the point of the maximal ST change after exercise was determined as ST exercise vector. To indicate width of the T loop, the length to width ratio (L/W) was used and the change of width of the T loop induced by exercise was expressed by a ratio of L/W between before exercise and at the maximal change in frontal and horizontal planes. In cases having ST exercise vector of 0.1 mV or more the magnitude or the direction of the ST exercise vector alone has little prognostic value and widening of the T loop in addition to the ST exercise vector of 0.1 mV or more occurring after exercise was a predictive sign of poor prognosis and no widening of the T loop was a predictive sign of good prognosis.

Aged↗