Biomedical subjects
Publications and source records attributed to T Niki.
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A 16-year-old high school boy showed various types of aberrant QRS complexes during supraventricular premature beats. The aberrant beats showed right bundle branch block pattern associated with varying degrees of left axis deviation. Rosenbaum et al explained it by slowing in conduction through the anterior fascicle in a bifascicular nature of human left bundle system. The alternative explanation might be possible if we consider a fan-like left bundle as proposed by Massing et al: namely incomplete or slight left axis deviation results from block of a small group of anterior parts of the fan-like left bundle, whereas marked left axis deviation results from block of a large number of fibers. The initial QRS force also changed to various degrees according to changes of the QRS axis. This case suggested the existence of an incomplete type of left anterior hemiblock, which produced not only an incomplete QRS axis change but also an incomplete change of the initial QRS forces.
Changes of the activation sequence and vectorcardiogram (VCG) resulting from experimental block of specific sites of the left bundle branch were studied to determine the functional significance of the septal Purkinje network. Discrete block of the septal Purkinje network (11 dogs) resulted in slight delay of epicardial activation in the apical area. In lead Z of McFee system of VCG, the antero-posterior ratio was increased from 1.4 to 2.6, and the QRS loop tended to be displaced anteriorly. Discrete block of the left posterior division (9 dogs) resulted in slight delay of activation in the posterior basal area. Block of the left posterior division plus the septal Purkinje network (11 dogs) resulted in marked delay in activation of a wider area extending from the posterior basal area to the apical area. In lead X, the S wave became evident and the direction of the maximum QRS vector in the frontal plane showed significant right axis deviation. Discrete block of the left posterior division did not change the epicardial activation sequence or the direction of the maximum QRS vector, because there is extensive interconnection of the left ventricular conduction system. These results suggest that block of the septal Purkinje network itself may produce an electrocardiographic change and that this network may also be important in left anterior and posterior hemiblocks producing axis changes in the frontal plane of VCG.
Fibrinolytic activity and plasmin inhibitor activity were determined by Blue Dextran-fibrin method in patients with acute myocardial infarction. The normal values of fibrinolytic activity and plasmin inhibitor activity were 3.34 +/- 0.74 units and 10.10 +/- 2.39 units (mean +/- SD), respectively. The fibrinolytic activity in normal women (3.63 +/- 0.99 units) was slightly higher than that in normal men (3.17 +/- 0.79 units), but the plasmin inhibitor was not significantly different in the two sexes statistically. Neither activity varied significantly with age. The blood fibrinolytic activity was depressed in the first week after acute myocardial infarction, the decrease being maximal 3 to 4 days after the event (1.73 +/- 0.31 units). The mean plasmin inhibitor activity remained normal after acute myocardial infarction, but it was increased in 3, and decreased in 4 of 7 patients in whom it was measured 3 to 4 days after the event.
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To clarify the genesis of the aortic thudding sound (AK), phono-, mechano- and pulsed Doppler echocardiography were performed in 16 patients with pure aortic insufficiency (AI), 3 with AI associated with mild aortic stenosis (AIs) and 5 with AI associated with mitral insufficiency (AI + MI). The results obtained were as follows: 1) AK was composed of two components, that is, one (AK1) occurred in early systole and the other (AK2) near the end point of an ejection systolic murmur. Patients studied were divided into 4 groups following the appearance of AK1 and/or AK2: group with only AK1 (4 cases), group with only AK2 (7 cases), group with both AK1 and AK2 (5 cases) and group without AK (8 cases). 2) AK1 was a low frequency sound and was well recorded from the cardiac base to the right supraclavicular region. AK1 was not observed in cases with mild to moderate AI and with AI associated with mild AS. In atrial fibrillation, when the preceding R-R intervals were long, AK1 was loud and appeared in early systole, and when short, small and in mid-systole. Marked augmentation of AK1 was observed in the first beat after premature ventricular contraction with a compensatory pause. 3) AK2 was also low in frequency and was most intensively recorded near the apex. Although the intensity of AK2 tended to increase in the severe cases of AI, AK2 could be observed in mild to moderate cases. Intensity of AK2 also showed the post-extrasystolic potentiation similar to that of AK1. 4) The carotid pulse showed pulsus bisferiens in all cases with AK2 (group with only AK2 and group with both AK1 and AK2). On the other hand, in cases without AK2 (group without AK and group with only AK1), carotid pulse showed a monophasic systolic wave except 3 cases. These results suggested that there was a close relationship between AK2 and pulsus bisferiens in the carotid pulse. (5) In the apex cardiogram (ACG), systolic notches coincident with AK1 and/or AK2 were observed in 10 of 12 cases with AK2 and in 4 of 9 cases with AK1. In cases without AK, however, no notch was seen in ACG. Therefore, these notches might be resulted from the shock of the anterior chest wall produced simultaneously with the occurrence of AK. 6) Flow patterns at the left ventricular outflow tract (aortic flow patterns) were recorded in 13 cases, including 3 with only AK1, 2 with only AK2, 3 with both AK1 and AK2 and 5 without AK. In 5 of 13 cases the flow patterns were recorded simultaneously with phonocardiograms. Systolic aortic flow showed biphasic patterns in all cases with AK2, and monophasic patterns in cases without AK2. AK1 occurred coincidentally with the first peak of the biphasic flow patterns, and AK2 with the second peak. These results suggested that AK1 might be produced by rapid ejection of massive amount of blood containing a regurgitant flow into the aorta with the ordinarily distensiblwe aortic wall, and AK2 by the clash between the second ejected flow and the reflected flow returning from the peripheral artery against the first ejected flow.
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The conduction system of bovine heart was studied to clarify the characteristics of its energy metabolism. Results showed that its mitochondrial oxygen uptake was much lower than that of ordinary heart muscle with succinate as substrate but similar to that of ordinary heart muscle with glutamate + malate as substrate. The activity of succinate dehydrogenase was lower than that in ordinary heart muscle. The total activity of isozymes of lactate dehydrogenase was lower in the specialized heart muscle than in ordinary heart muscle. The main isozyme of lactate dehydrogenase in the specialized heart muscle was LDH 1 (H4). The cytoplasmic NAD+/NADH ratio as much higher in the specialized heart muscle than in ordinary heart muscle. These results suggest that in the specialized heart muscle energy is mainly derived from aerobic metabolism.
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