Improvement of bioavailability of poorly intestinally absorbed drugs from medium-chain glyceride base. Enhancement of the rectal absorption of cefmetazole sodium in rabbits.
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Biomedical subjects
Publications and source records attributed to R Okada.
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Although nonspecific pericarditis, myocarditis, valvulitis, and coronary arteritis are known as cardiac lesions that accompany rheumatoid arthritis (RA), there have been few reports of the occurrence of clinically severe valvular disease. We report here the case of 69-year-old man with a 25-year history of RA who died of acute left-sided heart failure complicating to aortic steno-insufficiency and angina pectoris. Autopsy findings revealed the coincidence of a congenital bicuspid aortic valve with chronic inflammation, fibrosis and calcification; eccentric hypertrophy and myocardial fibrosis of the left ventricle; 75% luminal narrowing of the proximal portion of the coronary artery due to atherosclerosis, and narrowing of the small arteries of the cardiac muscle due to angitis. It is deduced that the coronary artery lesions, aortic valve lesions and myocardial lesions were aggravated by the bicuspid aortic valve, changes with ageing and corticosteroid therapy.
In order to define quantitatively the histological characteristics of the hypertrophied myocardium of the right ventricular outflow tract in patients with congenital heart disease, a light-microscopic study of biopsy specimens obtained from 20 cases with tetralogy of Fallot (TOF) and 14 cases with muscular obstruction of the right ventricular outflow tract ( RVOTO ) was performed using a semi-automatic sampling counter. As the controls, the crista supraventricularis of 11 autopsied cases without cardiac disease were used. The TOF patients were divided into two groups: those with (9 cases) or without (11) a history of hypoxic spells. The myocyte diameter was calculated according to Chalkley 's and Arai 's method. The areas of myocardial fibrosis and myocyte disarray were determined quantitatively by the point count method. Myocardial fibrosis was classified into five types: focal, mild perimysial, severe perimysial, perivascular and plexiform. In the control group, the myocyte diameter and area of fibrosis and disarray tended to increase with age. In the obstructive groups, the myocyte diameter and area of disarray were greater than those of the control in any age group. Myocyte diameter tended to increase with age in all groups, except for the TOF cases with a history of hypoxic spells. The latter also had the largest area of myocardial disarray (25.3%) (p less than 0.01), and a largest area of fibrosis (20.5%) than the TOF cases without spell (14.4%), but severe perimysial fibrosis was observed in only five out of the nine patients with spells. The lack of a relation between the pressure and the presence of an increased area of the myocardial disarray in TOF with spells implies that this myocardial change is brought about by myocardial abnormality accompanied by cardiac malformation.
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We successfully removed a fibroma of the left ventricle in a 13-year-old boy. The tumor had caused recurrent ventricular tachycardia, which was resistant to antiarrhythmic drugs. Preoperative and intraoperative electrophysiological studies led to a diagnosis of reentrant ventricular tachycardia. After surgical excision of the tumor, the ventricular tachycardia stopped completely and until now, 1 year after the operation, no antiarrhythmic drugs have been required.
The location and course of the atrioventricular (AV) conduction system were studied histopathologically in 6 hearts by sectioning serially, 4 having common AV orifice (CAVO) with complete or partial transposition of the great arteries (TGA) and 2 having ventricular septal defect of the persistent common AV canal type (VSD-C) with complete TGA. Two cases of CAVO with TGA and asplenia syndrome (Cases 1 and 2) had 2 discrete AV conduction systems, being posterior and anterior to the site of the defect, respectively. In these 2 cases posterior AV conduction system well developed, whereas the anterior one was hypoplastic. In another case of CAVO with TGA and asplenia syndrome (Case 3), only the anterior AV conduction system existed near the base of the great arteries. In the other case of CAVO with TGA and polysplenia syndrome (Case 4), the posterior AV conduction system was found to have a congenital interruption of the AV bundle of His. Two cases of VSD-C with TGA but with no splenic anomaly (Cases 5 and 6) showed the posterior AV conduction system with communication-free accessory bundles. The posterior AV node, bundle of His and left bundle branch inevitably shifted postero-inferiorly, except in Case 3. The bundle branches were always distributed appropriately to their morphologically matched ventricles. The superiorly oriented vector in the mean frontal QRS axis in Cases 1, 5 and 6 seemed to be related to the postero-inferior displacement of the posterior AV conduction system, whereas those of the left-inferior oriented vector in Cases 2 and 3 were thought to be responsible for the excessively unbalanced size of ventricles. The complete AV block in Case 4 was correlated with the interruption of the bundle of His. The morphogenesis of the anterior AV conduction system was discussed in relation to the asplenia syndrome.
A 2-month-old female infant with pancarditis was reported. The patient died after a 26-day clinical course. The autopsy showed pancarditis, including inflammation in all 4 valves and chordae, fibrinoid vasculitis, pharyngolaryngitis and atrophy of the lymph nodes. Microscopic examination revealed proliferative inflammation in the endocardium, valve, myocardium, epicardium and coronary vessels. The histological findings suggested the etiology to be a rheumatic-type reaction at an extremely young age.
Serial sections of the atrioventricular (AV) conduction system were microscopically studied in 12 autopsied hearts: four with complete type common AV orifice (CAVO), two with atrial septal defect of the ostium primum type (ASD-I), two with ventricular septal defect of the persistent common AV canal type (VSD-C) and four without heart disease. The anatomic findings were semiquantitatively compared with the normal control using Feldt's method and correlated to the mean frontal QRS axis on ECG. The cases of CAVO or VSD-C with left axis devation invariably showed similar patterns regarding the location and course of the AV conduction system: (1) posterior displacement of the AV node, (2) relatively short distance between the AV node and the beginning of the left bundle branch (LBB), and (3) postero-inferior displacement of the bundle of His and the LBB. The postero-inferior displacement of the LBB seemed to be responsible for left axis deviation. The cases of ASD-I showed some additional findings: (1) impaired contiguity between the AV node and the bundle of His might have caused the occasional advanced AV block in one case, and (2) the posterior radiation of the LBB traversed down through the branch-free muscle bundle, which was assumed to be related to the right axis deviation in the other case. These findings suggest that the disposition of the AV conduction system in CAVO and in its related anomalies were basically the same whatever the type of defect, and this was considered to be correlated to the established ECG pattern.
In order to clarify the importance of the conduction system involvement in cases of sudden cardiac death, 35 autopsied hearts, obtained from the patients who died within one hour after the onset of a critical attack, were examined histopathologically and compared with 27 both age- and disease-matched and 30 only age-matched control hearts from individuals who had not died suddenly. The conduction system was serially sectioned using Lev's method and observed under a light microscope. Purkinje cell lesions, which made a structural maze compatible to the electrophysiological re-entry mechanism, abnormalities of the AV node artery and hypertrophy of the AV node and the bundle of His were more prominent in the sudden-death group with long QT syndrome, isolated ventricular fibrillation and AV and bundle branch blocks due to both ischemic heart and myocardial diseases. Sinus node fibrosis with minor anomalies of the sinus node artery was specifically seen in the sudden death of apparently healthy young males (Pokkuri disease). The same lesion, but with sclerosis of the sinus node artery, was seen in the cases of sudden death with hypertensive heart disease.
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The effect of aging on histological changes of the conduction system was studied by serially sectioning 55 autopsied hearts weighing less than 300 Gm. None of the hearts showed evidence of cardiovascular disease nor were there any abnormalities in the clinical findings and ECG taken during the last 3 months of life. A reduction in the number of muscle cells and an increase in the number of collagen fibers were apparent in hearts taken from patients over 70 years of age. These findings were most evident in the S-A node and less so in A-V node, bundle of His, and left and right bundle branches. Deposition of amyloid substances was not observed in any portion of the conduction system.
Thirty-six patients with the angiographic diagnosis of left ventricular mural thrombus were reviewed. All had a history of myocardial infarction. In 9 of these patients (25%), coronary neovascularity was related to a left ventricular mural thrombus. Although no relationship was found between either the size of the mural thrombus or the duration of illness and the neovascularity, the incidence of neovascularity was low in a group taking anticoagulants. Arteriographic characteristics of the neovascularity in the present cases are: 1) In all cases, the neovascularity arose from the left anterior descending coronary artery. 2) The neovascularity consisted of a hypervascular region in the same location as the mural thrombus. It was observed as a dense mass of small vessels penetrating the left ventricle in a form resembling a toothbrush. 3) The neovascular region had no veins and it extended through the narrow gap of the thrombus to communicate with the left ventricle. Histological studies were consistent with coronary arteriography. The demonstration of neovascularity by coronary arteriography suggests either that the thrombus is relatively new or that a new thrombus is further organized on the old thrombus. This seems to be useful information from a therapeutic viewpoint.
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The purpose of this study was to determine whether two-dimensional echocardiography (2DE) can differentiate ischemic myocardial disease (IMD) from dilated cardiomyopathy (DCM). The subjects consisted of six cases of IMD which showed left ventricular dilatation (LVDd greater than or equal to 60 mm) and diffuse abnormality of wall motion, but did not show obvious localized myocardial infarction or left ventricular aneurysm on 2DE, and 16 cases of DCM. Two cases of IMD had previous myocardial infarction, and five cases of DCM had cardiomegaly following myocarditis. A short-axis image of the left ventricle was recorded at the chordal and the papillary muscle levels. Each image was divided into 4 segments, which were comprised of the septum, anterior wall, lateral (posterolateral) wall, and posterior (posteromedial) wall. Regional wall motion abnormality with reference to systolic thickening was analyzed qualitatively in each segment. The results were as follows: In ECG findings in IMD group, only one case showed abnormal Q waves and five cases showed left ventricular hypertrophy (LVH) similar to intraventricular conduction defect. On the other hand, in DCM group seven cases showed abnormal Q waves and five cases showed LVH. Two cases of IMD had two-vessel disease and four three-vessel disease, respectively. Left ventricular ejection fraction by cine-angiography ranged from 0.10 to 0.39 (mean 0.24) in IMD group and from 0.22 to 0.42 (mean 0.36) in DCM group. Mean LVDd showed no significant difference between these two groups. Five cases of DCM showed marked left ventricular dilatation (LVDd greater than or equal to 75 mm), but there were no such cases in IMD group. B-B' step was recognized in only one case of IMD, though it was present in eight cases in DCM. In regional wall motion, incidence of asynergy such as akinesis or dyskinesis was higher in IMD group than in DCM group. Left ventricular asynergy was more serious in the posteromedial wall than the posterolateral wall at the same image in five cases of IMD. However, in 12 cases of DCM, the degree of asynergy was equal at the both walls. In conclusion, it is recommended to examine echocardiographically the extent of severe asynergy in the posteromedial and posterolateral walls in order to differentiate IMD from DCM.
Two experiments investigated the effect of performance feedback when testing recognition memory for short prememorized lists. Subjects were provided with either response-accuracy or response-latency feedback on a trial-by-trial basis. Payoff in both conditions depended solely upon accuracy performance. Subjects familiarized with their latencies responded faster than subjects given only accuracy feedback. There was no speed-accuracy trade-off. These results are discussed with reference to similar data from the choice reaction-time task. It is concluded that failure to provide subjects with adequate feedback on all aspects of this task is a serious oversight. This oversight is particularly surprising in those designs focusing upon speed.
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