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Biomedical subjects

R Okada

Publications and source records attributed to R Okada.

At least 55 records · Page 3Linked to original sources

Morphological study of vagal innervation in human semilunar valves using a histochemical method.

To determine the innervation of human semilunar valves, we examined the pulmonary and aortic valves of the normal autopsied hearts of 3 men (53 to 71 years old). Whole valve tissues with the aorta or pulmonary trunk were stained for acetylcholinesterase by a histochemical method. Acetylcholinesterase-positive nerve fibers with a diameter of 2 to 20 mm were located on the ventricular side of the semilunar valves. Innervation of the semilunar valves was extremely sparse compared with that of the atrioventricular valves and that of the aortic or pulmonary arterial wall. The nerves originated from the subendocardium of the ventricles and the adventitia of the arterial walls. The nerves were more distributed in the basal site than in the marginal site of the semilunar valve. The nerve fibers formed a network in basal two-thirds of the leaflet. Thick nerves ramified in the thin nerve plexus. The thick nerves had a varicose-like structure. Thin nerves had a dot- and brush-like ending. The nerves in human semilunar valves may play a role in valve motion.

Aged↗

Marked arteriosclerosis of the descending aorta in a teenager with interruption of the aorta.

Marked arteriosclerosis localized to the descending thoracic and abdominal aorta was observed in a 19-year-old girl with interruption of the aorta (type A) and a ventricular septal defect. She died from rupture of saccular aneurysm of the pulmonary trunk. The descending thoracic and abdominal aorta showed marked thrombogenic, lamellar thickening of the intima. In contrast, no significant arteriosclerosis was detected in the ascending aorta. Several factors including diffuse sludging of blood, mural thrombosis and hemodynamic changes, in close association with polycythemia, are hypothesized to be causative factors in the development of this lesion.

Adult↗

[Late coronary artery aneurysm formation following directional coronary atherectomy].

The most important factor to reduce late restenosis following directional coronary atherectomy is the technical provision of the largest luminal diameter as possible. However, the safety of deep arterial resection and the resulting arterial perforation or late aneurysm formation is questionable. This study examined the frequency of coronary artery aneurysm formation in patients treated by directional coronary atherectomy. Ninety-eight patients with 123 lesions were analyzed by quantitative angiographic and histologic data. Coronary aneurysms (ratio of dilated vessel segment to the adjacent reference segment > 1.2:1) occurred in seven patients (seven lesions: 5.7%). Specimens were categorized by the deepest layer retrieved. Forty lesions (32.5%) were treated by resection of the intima alone, 65 (52.8%) by resection of the medial tissues and 18 (14.6%) received resections of the adventitial tissues including fatty tissues in three lesions. Late coronary aneurysms occurred often in lesions with resection of adventitial tissue (38.9%) and occurred in all three lesions with resections of fatty tissues. Six coronary aneurysms occurred in the left anterior descending artery (six in segs. 6, 7), and one aneurysm in the left circumflex artery. Among the target lesions in which coronary artery aneurysms were formed, six lesions were primary lesions and one lesion was a restenotic lesion after percutaneous transluminal coronary angioplasty. Statistically, patients with coronary artery aneurysms frequently have associated hypertension (p = 0.02) but rarely diabetes mellitus (p = 0.05). Lesions with late aneurysms had significantly high specimen weight (p = 0.01) and a trend to lower postprocedure % diameter (p = 0.20). There was no significant preprocedural angiographic predictor of aneurysms such as minimal lumen diameter or reference vessel diameter.

Adult↗

[Lev's disease].

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Aged↗

[Clinicopathological analysis of rheumatic heart disease].

Autopsy cases of rheumatic heart disease which took natural courses without surgery were clinicopathologically analyzed. The patients had pancarditis (2 patients), mitral stenosis (MS; 12), mitral regurgitation (MR; 8), aortic stenosis and regurgitation (ASR; 5) and combined valvular disease (CVD; 30). The patients with pancarditis (mean age 15 years) showed high rheumatic activity, short clinical course, enlargement of the heart, edematous swelling and inflammation of the valves, myocardium and pericardium with multiple Aschoff nodules. Patients with MS (mean age 42 years) showed low rheumatic activity, enlarged left atrium and right ventricle, thickening and calcification of the valve edge which was categorized into oval shape and slit shape ostial narrowing, and fibromuscular thickening of the small coronary artery wall. Patients with MR (mean age 32 years) showed moderate rheumatic activity, enlarged left ventricle, left atrium and right ventricle, diffuse thickening of the valve, contraction of the posterior leaflet and healing Aschoff nodules. Patients with ASR (mean age 36 years) showed moderate rheumatic activity, elongated enlargement of the left ventricle, adhesion of the commissures, thickening with contraction and calcification of the cusps, hypertrophy and fibrosis of the myocardium. Patients with CVD were divided into the left-sided double stenosis group (CVD-S; 16 patients) and double regurgitation or triple valve disease group (CVD-R; 14). The CVD-S group (mean age 51 years) showed low rheumatic activity, female predominance and similar morphology to MS. The CVD-R group (mean age 32 years) showed moderate rheumatic activity, relatively short clinical course, male predominance and similar pathology to pancarditis and/or MR. The valvular pathology in rheumatic fever was modified by connective tissue matrix of the valves, especially of acid-mucopolysaccharides.

Adolescent↗

[Surgical pathology of infective endocarditis].

Underlying pathologic disorders of infected valves were analyzed in 36 consecutive patients with infective endocarditis (from April 1987 to May 1995) of 18 aortic, 11 mitral and 8 prosthetic valves. Among 29 cases of native valve endocarditis, 27 had known organic changes [aortic valve prolapse 8, bicuspid aortic valve 4, annuloaortic ectasia 1, mitral valve prolapse 9 (including 2 cases associated with hypertrophic cardiomyopathy), looping chordae 1, rheumatic heart disease 4]. However, the remaining two cases had unknown etiology. Histological examination of these two aortic valves revealed proliferation of small vessels and remnants of vascular smooth muscle cells, suggesting postinflammatory valve prolapse. Five cases with definite pathology had no clinical signs of infection. The preponderance of surgically resected valves with infective endocarditis in Japan is non-rheumatic in origin.

Adult↗