[Computer diagnosis of electrocardiograms and vectorcardiograms].
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Biomedical subjects
Publications and source records attributed to T Hiroki.
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A quantitative analysis of adventitial inflammation of the coronary artery with intimal lesions is described in 12 patients who suffered coronary death and had had unstable angina (crescendo angina) at rest (group 1). After autopsy in these patients we examined epon-embedded cross sections by light and electron microscopy, paying particular attention to the adventitia, and compared these results with those in six patients who had had angina but died of noncardiac causes (group 2) and those in 22 patients who did not have angina (group 3). Of the 132 segments from group 1 patients, 39 (30%) were narrowed 76% to 100% by atherosclerotic plaque (group 2, 27%; group 3, 1%), and 23 (17%) had occlusive thrombi. Of the 264 sections (two from each segment) from group 1 that were examined, 98 (37%) (group 2, 15%; group 3, 9%) revealed clustered infiltration of inflammatory cells in the adventitia, half of which were associated with vascular nerve involvement. These findings in the adventitia may be related to the vasospastic component of unstable angina.
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Two cases were reported in which malignant cardiac tumors attached to the mitral valve were diagnosed during their lifetimes using two-dimensional echocardiography. Case 1 was a 29-year-old man with speech disturbance and left hemiparesis. Histological examination of the specimen excised from the cardiac tumor during the operation revealed mesenchymal chondrosarcoma, which is extremely rare etiologically and has never been reported so far. Case 2 was a 62-year-old woman complaining of paroxysmal nocturnal dyspnea and chest pain. The diagnosis of malignant histiocytosis was made from the pathological examination of biopsy specimen taken from the rib metastasis. Using two-dimensional echocardiography, characteristic findings for the cardiac tumor were obtained. The tumor echo in Case 1 showed, unlike to that reported for myxoma, two different echogenic layers; the outer dense and the inner light in the echo density. On surgery, tumor echo was revealed to reflect the cystic lesion. In Case 2, two-dimensional echocardiography on admission revealed two separate tumor echoes which attached to the mitral valve and left atrial wall region, respectively. Within two months, they grew rapidly and finally fused into one mass resulting in so-called ball valve syndrome. Phonocardiographically, the tumor plop in Case 1 was high-pitched in quality, and was extinguished completely after the tumor was resected. The tumor plop in Case 2 was not audible on admission, but became evident after fusion of the tumor echoes and was associated with a presystolic murmur.
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Platelet aggregation was studied in patients with angina pectoris in whom coronary sclerosis was found by arteriography. The subjects consisted of 20 patients with stable angina pectoris, 12 with unstable angina pectoris and 4 with variant form of angina pectoris. Fifteen healthy subjects served as controls. ADP- and collagen-induced platelet aggregations were estimated during resting conditions before and immediately after an exercise test. In patients with unstable angina pectoris, ADP-induced as well as collagen-induced platelet aggregations during resting conditions were significantly less than those in normal subjects. After exercise, however, they significantly increased. In stable angina pectoris, they did not differ from those in the control group and their responses to exercise were also not significant. In general, platelet aggregation during resting conditions was accelerated in relation to an increase in the number of coronary arteries involved. The results demonstrate that examination of platelet aggregation during resting conditions and following exercise aids in a more accurate evaluation of the types and the stages of patients with angina pectoris.
The electrocardiographic effects of mental arithmetic stress were studied in 19 young, healthy male subjects. Blood pressure was measured by the cuff method before and during mental stress and electrocardiogram (V5) was monitored and recorded continuously throughout the study using a computerized ECG monitoring system. Heart rate increased from 65.8 +/- 7.0 (mean +/- standard deviation) to 76.7 +/- 9.9 beats/min (p less than 0.001). Systolic blood pressure rose from 122.7 +/- 9.6 to 129.1 +/- 11.7 mmHg (p less than 0.05), diastolic blood pressure from 76.2 +/- 8.8 to 83.0 +/0 11.0 mmHg (p less than 0.001), and mean blood pressure from 91.7 +/- 7.9 to 98.5 +/- 10.1 mmHg (p less than 0.001). These changes were all statistically significant. R wave amplitude decreased significantly from 18.6 +/- 6.9 to 17.0 +/- 6.5 mm for the group (p less than 0.001). No changes in the ST segment were observed; ST depression decreased from 0.56 +/- 0.47 to 0.54 +/- 0.43 mm (N.S.) and ST slope from 0.87 +/- 0.59 to 0.77 +/- 0.63 mm/sec (N.S.). Thus it is apparent that mental stress reduced R wave amplitude without causing ST segment changes in young, healthy subjects. The mechanism and clinical implications are discussed.
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Angina pectoris patients were divided into two groups of unstable angina and stable angina, platelet aggregation was measured at rest and after treadmill exercise tolerance, and then the effects before and after the administration of nifedipine (Adalat) were examined. As a result, no significant difference in platelet aggregation at rest was seen in either group between before and after the administration of nifedipine, but the acceleration of platelet aggregation response to exercise was significantly inhibited by nifedipine. Moreover, the extent of inhibition was more notable in unstable angina group. It was discussed that such an inhibitory effect of nifedipine on platelet aggregation response to exercise could be related to vasospasm and in its turn possibly takes part in the development of myocardial ischemia.
Triphasic dove-coo murmur in a patient with aortic regurgitation was studied as to the mechanism of its generation using simultaneous recording phonocardiography and dual echocardiography. The murmur arose coincident with the coarse regular fluttering of aortic posterior wall during the opening of mitral valve and decreased coincident with the protrusion of mitral valve anterior leaflet into the left ventricular outflow tract. Thus the murmur might occur, provided that normal mitral valve opening and closure was maintained. It may well explain why the murmur hardly occurs in aortic regurgitation of rheumatic origin in which rheumatic lesion often is thought to involve mitral valve, restricting mitral opening during diastole and thereby inhibits aortic root vibrations.
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The authors present four cases of neonatal giant cell hepatitis who died suddenly and unexpectedly from intracranial hemorrhage, autopsied recently at the Tokyo-to Medical Examiner Office. This series consisted of one male and 3 female infants ranging from 37 to 52 days of age. The cause of death of all cases was thought to be massive intracranial hemorrhage. Referring to the connection between intracranial hemorrhage and neonatal giant cell hepatitis, it was assumed that the former must have occurred due to the hemorrhagic tendencies of the latter, superimposing to the hemorrhage at birth trauma of the head. As to the formation of multinucleated giant cell, it is considered to be of degenerative nature of hepatocytes, i.e. the giant cell is formed by fusion of hepatocytes as a result of the disappearance of bile canaliculi, although the etiology of this hepatitis is still unknown.
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A case of accelerated hypertension, which was unique in a resistance to an angiotensin antagonist, and a lack of the elevation of plasma renin activity (PRA) is reported. Non-elevated PRA was coincided with non-malignant nephrosclerosis in renal histology. The acceleration was attributed to the neurological cause i.e., cerebral hemorrhage in the right hypothalamus which extended to the ventricle and subarachnoid space. The case therefore clinically seemed malignant-like, but it was not malignant hypertension in the sense of Volhard's classical definition. This does not conflict with the usefulness of the determination of PRA in the diagnosis of malignant hypertension with nephrosclerosis.
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