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Biomedical subjects

K Harumi

Publications and source records attributed to K Harumi.

At least 19 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↗
PubMed1990

Computer simulation of supraventricular tachycardia with the Wolff-Parkinson-White syndrome using three-dimensional heart models.

Supraventricular tachycardias with the Wolff-Parkinson-White (WPW) syndrome have been successfully simulated using a newly developed simulation system. The heart model, including atria and ventricles, was constructed of about 50,000 discrete elements (model cells) in three dimensions with 1.5-mm spatial resolution. The model cells covered all of the types of cells in the actual heart, including the normal myocardium, special conduction system and abnormal cells, such as the bundle of Kent (accessory pathway) and ectopic pacemaker (premature beat). Different model cells were specified by their electrophysiologic parameters, such as action potential, refractory period, and conduction velocity. The WPW syndrome was simulated by setting an accessory pathway between the right atrium and ventricle. Based on this model a premature atrial beat was introduced, which initialized the tachycardia. By adjusting the parameters, three types of reciprocal supraventricular tachycardia were simulated with the reentry circuits (1) formed anterogradely by the A-V node and retrogradely by the accessory pathway, (2) formed anterogradely by the accessory pathway and retrogradely by the A-V node, and (3) confined within the A-V node. Time relations for initializing and maintaining the tachycardias were evaluated. The simulated ECGs were in good agreement with the clinical findings.

Computer Simulation↗
PubMed1990

Determination of the site of the accessory pathway in WPW syndrome by an electrocardiographic inverse solution.

The initial portion of the QRS complex in WPW syndrome might be represented by a single dipole, since the delta wave corresponds to the localized ventricular activation propagated over the accessory atrioventricular pathway. In order to examine whether the site of the accessory pathway in WPW syndrome could be localized by an equivalent dipole method, the dipole positions during the delta wave were determined in 30 patients using a three dimensional model of the torso and were then compared with the sites of accessory pathways localized by body surface maps. The single dipole approximation during the delta wave appeared to be appropriate since the index of the nondipolarity of the potentials was as low as 28% on average. The dipole positions determined on the atrioventricular ring during the delta wave were compatible with the sites of accessory pathways localized by body surface maps in 22 of the 30 patients. The dipole positions were adjacent to the sites of accessory pathways in 7 of the remaining 8 patients. Thus the equivalent dipole method might be an additional noninvasive tool to determine the site of the accessory pathway in WPW syndrome.

Adult↗
PubMed1990

Reduction of the number of electrodes in the measurement of body surface potential distribution.

The number of electrodes required to reproduce a body surface potential map (BSPM) can be reduced by making use of the correlations among potentials measured at different sites on the body surface, as pointed out by Lux et al. in 1978. In the present paper, we have introduced two distinct methods which can be used to improve the accuracy of the potential estimation. In the first method, the BSPMs are divided into several classes according to the direction of the vectorcardiogram, while the temporal as well as the spatial correlations are taken into account in the second method. They are called the 'partition method' and the 'spatiotemporal correlation method', respectively. By means of the partition method using 40 electrodes, the estimation error becomes 75% of that estimated with the Lux method, which is equivalent to the Lux method with 47 electrodes. In other words, the partition method saves seven electrodes. When the electrodes are restricted on the chest, our methods are more effective. In particular, the partition method saves no less than 20 electrodes.

Electrocardiography↗
PubMed1990

[Quantification of the extent of myocardial infarction by thallium-201 single photon emission computed tomography: comparisons with post-mortem findings].

A circumferential profile analysis with a two-dimensional polar representation of thallium(Tl)-201 myocardial single photon emission computed tomograms (SPECT) is an objective and quantitative method to evaluate myocardial infarction (MI). However, the diagnostic capability depends on the normal range of thallium distribution. Therefore, the quantitative analysis of Tl-201 myocardial SPECT was correlated with the pathological findings of the heart in 50 autopsy cases (28 with MI; 22 without MI) to determine the lower normal limits at which we can precisely determine the extent of MI on a quantitative basis. For correctly detecting the extent of MI, the lower normal limits were 2.5 standard deviations below the mean values calculated using profiles normalized to the maximum pixel count observed in each profile. Using this lower normal limit, the sensitivity was 63.8%; specificity was 87.4%; and accuracy was 80.7% for determining the extents of ischemic lesions, though these values were lower than those obtained by visual analysis. However, for detecting MI, the sensitivity by quantitative analysis was 97% which was higher than that by visual analysis. A medium sized (2.5 cm) non-transmural infarction, undetectable by visual analysis, was detectable by two-dimensional polar representations. However, the specificity of detecting MI was low (59%), and most of the false positive studies were observed in cases of valvular disease, coronary artery disease or other cardiac complications. The detectability of the extent of MI varied according to the location of the lesion. False negative lesions were most frequently observed in the septal region; false positive lesions were most frequently observed at the posterolateral regions of the dilated hypertrophic hearts. The septal region located at the peripheral portion of the MI and septal hypertrophy in cases of hypertension, were the likely negative cases, thus, these pathological characteristics may explain the high incidence of false negative results in the septal region quantitatively as well as by visual analysis. In cases with dilated hearts, the radioactivity of the thallium at the posterolateral region was more reduced by absorption compared with that in the non-dilated hearts. This reduction in counts was empirically regarded as abnormal lesions by visual analysis, however, the same situation can objectively and automatically be recognized as false positive by quantitative analysis. We concluded that quantitative analysis by Tl-201 myocardial SPECT is useful for evaluating myocardial infarction automatically, but care must be exercised concerning possible false positive diagnosis in cases with dilated hypertrophic hearts.

Aged↗
PubMed1989

Classification of antiarrhythmic drugs based on ventricular fibrillation threshold.

The antifibrillatory action of antiarrhythmic drugs, classified on the basis of their effects on ventricular fibrillation threshold (VFT), was investigated. The relation between drug action and cardiac excitability, orthodromic/antidromic conduction through Purkinje fibers and ventricular muscle and the restitution of premature action potential duration was studied. Drug classifications were: group A, VFT markedly increased; group B, VFT moderately increased; and group C, no significant change. Group A was subdivided according to presence or absence of the dip phenomenon and supernormal period in the anodal strength-interval curve. Drugs in group A significantly reduced the difference between effective refractory period of orthodromic and antidromic conduction and the range over which the premature action potential duration reappeared. In groups B and C, the effective refractory period in orthodromic conduction was longer than that in controls, and the range of the restitution of premature action potential duration for Purkinje fibers was reduced only slightly.

Action Potentials↗
PubMed1989

Identification of susceptibility to ventricular tachycardia after myocardial infarction by nondipolarity of QRST area maps.

The QRST area map has been related to susceptibility to ventricular tachyarrhythmias because it reflects the disparity of ventricular recovery properties. However, the clinical value of the nondipolarity of the QRST area map, a marker of nonuniform ventricular repolarization, has not been fully studied in myocardial infarction. The nondipolarity of the QRST area map (residue), the ratio of minimized deviation by an optimal dipole to the total measured potentials, was quantitatively studied in relation to susceptibility to ventricular tachycardia after myocardial infarction. The residue of the QRST area map was higher in 59 patients with myocardial infarction than in 44 normal subjects (25.0 +/- 9.0 versus 17.8 +/- 3.3%, p less than 0.01). Seventeen patients with ventricular tachycardia in the chronic phase (greater than 10 days) of myocardial infarction showed higher residue in their QRST area map (34.5 +/- 10.3%) than that in 29 patients without ventricular tachycardia throughout the study (22.7 +/- 6.7%) or that in 13 patients with ventricular tachycardia only in the acute phase (21.2 +/- 7.5%). QRST area maps with a residue greater than or equal to 25% (mean + 2 SD of normal subjects) identified patients with ventricular tachycardia in the chronic phase of myocardial infarction with a sensitivity of 82% and a specificity of 71%. These results suggest that quantitative assessment of the nondipolarity of the QRST area map is clinically useful for identifying susceptibility to ventricular tachycardia in the chronic phase of myocardial infarction.

Adult↗
PubMed1989

Clinical application of electrocardiographic computer model.

A three-dimensional computer model was developed to stimulate the ventricular depolarization and repolarization in a clinical setting. The ventricle is composed of approximately 50,000 units arranged in a cubic close-packed structure and the specialized conduction system is distributed so as to obtain the excitation sequence resembling normal ventricular depolarization. The normal distribution of action potential waveforms with the longest duration on the endocardium and the shortest on the epicardium is used in the model. The heart model is mounted in a homogeneous torso model, and the body surface potential distribution generated by the electric dipoles is calculated using the boundary element method. The QRST waveforms corresponding to the normal and some abnormal heart conditions, such as bundle branch block, myocardial infarction, apical hypertrophic cardiomyopathy, and Wolff-Parkinson-White syndrome, is obtained by assuming the abnormal area with altered electrical properties. Thus the three-dimensional computer model may provide further insight into the genesis of the clinical electrocardiogram.

Bundle-Branch Block↗
PubMed1988

Effect of antiarrhythmic drugs on the ventricular fibrillation induced by low intensity train pulses.

We evaluated the effects of antiarrhythmic drugs on ventricular fibrillation threshold (VFT) by analysing the electrophysiologic parameters obtained from strength-interval curves. The VFT determined by low intensity train pulses was significantly increased from the control value under the administration of clinical dosage of procainamide, lidocaine, propranolol, bepridil and prenylamine, although not verapamil. The elevation of VFT could be explained by changes in the strength-interval curve induced by the drugs, including disappearance of dip phenomenon, supernormal period, prolongation of effective refractory period (ERP) and elevation of end diastolic threshold (EDT).

Animals↗
PubMed1988

Effects of exogenous ubidecarenone on cardiac action potential and activation time in hypoxic, glucose-free solution. Possible antiarrhythmic action of ubidecarenone.

Effects of ubidecarenone (coenzyme Q10, CoQ10, E-0216) on the cardiac action potential depressed by the superfusion with hypoxic, glucose-free solution (modified Tyrode solution) and on the activation time (ACT) altered by the same means were investigated. In the control specimens, the action potential duration (APD) was markedly shortened and action potential amplitude (AMP) reduced. The maximum rate of rise of phase zero Vmax) and the resting membrane potential (RMP) were slightly affected. Superfusion with exogenous CoQ10 significantly reversed the depressed APD and AMP, and tended to increase RMP and Vmax. Moreover, the ACT which, in the control, was slightly shortened until after the 10th min of superfusion became progressively longer. It was slightly prolonged during the first 10 min, and from the 12th to the 15th min was slightly shortened by treatment with CoQ10. These results suggest that CoQ10 could evoke an antiarrhythmic action in cardiac cells in depressed metabolic conditions.

Action Potentials↗