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Biomedical subjects

F Ohmori

Publications and source records attributed to F Ohmori.

At least 37 records · Page 2Linked to original sources
PubMed1994

Myocardial involvement in patients with sarcoidosis. An analysis of 75 patients.

The authors studied 75 nonselected patients (30 men and 45 women; mean age 48 years) with sarcoidosis retrospectively to assess the applicability of nuclear examinations for detecting myocardial involvement. All patients were studied with Tl-201 myocardial perfusion scan (TMPS), Ga-67 myocardial scan (GMS), and left ventricular ejection fraction (LVEF) using ECG-gated radionuclide ventriculography. The positive GMS group had a significantly higher occurrence of abnormality on TMPS (100%) than the negative GMS group (41%). Patients with TMPS abnormality and positive GMS showed significantly lower LVEF (36.3%) than those of normal perfusion or negative GMS. When LVEF decreased, occurrences of TMPS abnormality and positive GMS increased. The authors demonstrate that in patients with sarcoidosis LVEF was closely related to TMPS and GMS, and LVEF reflected the progression of sarcoid heart disease and can be considered a reliable indicator of cardiac function. Patients with sarcoidosis with TMPS abnormality and positive GMS should be thought to have myocardial sarcoidosis and their cardiac functions can be assessed by ECG-gated radionuclide ventriculography, while the remaining patients should be examined with TMPS and GMS periodically for detection of myocardial involvement.

Adult↗
PubMed1994

[Usefulness of various echographic examinations in the study of extrapulmonary lesions of sarcoidosis].

Echocardiographic study performed by Ohmori and others revealed a statistically significant difference between sarcoidosis patients with and without left ventricular perfusion defects in regards to LVDd, LVDs, LVEF, %FS, WT and EPSS. Echocardiography is a useful noninvasive tool in addition to Thallium-201 myocardial scintigraphy, in detection of myocardial involvement of sarcoidosis. Marked swelling of abdominal lymph node and splenomegaly was found by abdominal echography, in the sarcoid patients at onset as well as in the chronic stage. Both abdominal echography and CT revealed a hepatic sarcoid mass lesion in patients with and without hepatic dysfunction. Improvement of these abdominal echographic abnormalities correlated well with clinical improvement of sarcoid lesion. In addition, muscular echographic abnormalities were found in muscular sarcoid lesion. It can be said that echography is useful in the detection and follow up of extrapulmonary lesions of sarcoidosis.

Cardiomyopathies↗
PubMed1994

[Corticosteroid therapy in cardiac sarcoidosis].

Corticosteroid treatment of cardiac sarcoidosis is not conclusive, although sarcoid granulomas in the heart may be more responsive to steroid therapy than in other organs. Healing of sarcoidosis lesions in the heart results in fibrosis and sinning of the myocardium, which may lead to aneurysm formation causing congestive heart failure or sudden death. Congestive heart failure is the leading cause of death in patients with cardiac sarcoidosis in Japan. It is reasonable to initiate steroid therapy as soon as the diagnosis of cardiac sarcoidosis is established in order to prevent fibrosis. Early initiation of steroid therapy with conventional treatment for specific cardiac manifestations (antiarrhythmic therapy, pacemaker implantation and heart failure medication) should bring improvement in the left ventricular systolic and diastolic function with prevention from malignant arrhythmias. Systemic disorder represents a contraindication to organ transplantation, but heart transplantation is now a feasible treatment for patients with end-stage cardiac sarcoidosis with congestive heart failure.

Adrenal Cortex Hormones↗
PubMed1993

Rapidity of progression of aortic stenosis in patients with congenital bicuspid aortic valves.

The rapidity of progression of aortic stenosis in patients with congenital bicuspid aortic valves, and its relation to aging and valve anatomy are not well known. To elucidate these aspects, 75 patients aged 15 to 76 years were examined by echocardiography. Aortic valve sclerosis began from the second decade, the sclerotic index progressing with age (r = 0.72; p < 0.0001). Aortic valve calcium was noted from the fourth decade. Aortic valve pressure gradient increased approximately 18 mm Hg each decade, concomitant with progression of valve sclerosis (r = 0.78; p < 0.0001). Progression of cusp sclerosis was faster in patients with anteroposteriorly located cusps than in those with right-left-located cusps (p < 0.005), and was faster in those with eccentric cusps (width ratio of major and minor cusps > or = 1.2) than in those with symmetric cusps (p < 0.05). In patients with eccentric and anteroposteriorly located cusps, aortic valve pressure gradient increased 27 mm Hg per decade. In patients with congenital bicuspid aortic valves, the progression of aortic stenosis is rapid, and the rapidity depends to some extent on the position and eccentricity of the cusps.

Adolescent↗
PubMed1993

Involvement of cyclo-oxygenase-generated vasodilating eicosanoid(s) in addition to nitric oxide in endothelin-1-induced endothelium-dependent vasorelaxation in guinea pig aorta.

This study investigates the vasodilatory effects of endothelin-1 (ET-1) in isolated guinea pig aortic rings in vitro. Cumulative dose-response curves to ET-1 were constructed and ET-1 actions on prostaglandin F2 alpha (PGF2 alpha)-precontraction were studied in both endothelium-intact and endothelium-denuded preparations, in the presence or absence of a cyclooxygenase inhibitor (indomethacin) and/or nitric oxide inhibitors (NG-nitro-L-arginine methyl ester and hemoglobin). In endothelium-intact preparations, pretreatment with indomethacin (10(-5) M, 30 min), alone or in combination with NG-nitro-L-arginine methyl ester (L-NAME, 10(-4) M), significantly augmented the constrictive responses to ET-1, whereas indomethacin, L-NAME, and hemoglobin (10(-5) M) had no significant effects in the endothelium-denuded preparations. Furthermore, in PGF2 alpha-precontracted, endothelium-intact preparations, ET-1, at a dose of 10(-9) M, induced initial relaxation followed by subsequent contraction, while it only contracted the endothelium-denuded preparations. The initial relaxation was abolished by indomethacin, but not by L-NAME or hemoglobin. In addition, this relaxation was not inhibited by a specific ETA receptor antagonist, BQ-123 (6 x 10(-6) M). In addition to the involvement of nitric oxide, these results show the involvement of cyclo-oxygenase-generated vasodilating eicosanoid(s) derived from endothelium in ET-1-induced vasorelaxation in guinea pig aorta in vitro. The results also indicate that this vasorelaxation is mediated by ETB receptor activation.

Animals↗
PubMed1993

Different modes of endothelin-1 action in pressor response in vivo and pulmonary parenchymal contraction in vitro in the guinea pig.

Intravenously administered endothelin-1 (ET-1) (2 x 10(-11)-6 x 10(-10) mol/kg) induced dose-dependent pressor responses in anesthetized guinea pigs. Pretreatment with indomethacin (5 mg/kg, i.v.) or with a thromboxane A2/prostaglandin endoperoxide receptor antagonist, ONO-3708 (0.5 and 1.0 mg/kg, i.v.) significantly attenuated the pressor responses. ET-1 (10(-11)-10(-7) M) dose-dependently contracted guinea pig pulmonary parenchymal strips in vitro. However, neither pretreatment with indomethacin (10(-5) M) nor one with ONO-3708 (10(-6) M and 10(-5) M) significantly affected the ET-1-induced guinea pig pulmonary parenchymal contraction in vitro. Moreover, pretreatment with a platelet activating factor receptor antagonist, CV-3988 (2 x 10(-5) M) did not significantly affect the contraction. Thus, in guinea pigs, the mechanism of ET-1-induced pressor response in vivo mediated via cyclooxygenase-generated-eicosanoid(s), possibly, thromboxane A2 is not identical to that of ET-1-induced contraction of pulmonary parenchymal strips in vitro.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1991

Acute reduction of mitral valve area after percutaneous balloon mitral valvuloplasty: assessment with Doppler continuity equation method.

Mitral valve areas before and after balloon mitral valvuloplasty were serially determined by the Doppler continuity equation method in 16 patients. Ultrasound examinations were performed before and immediately after balloon inflation and 24 hours, 1 week, and 1 month after valvuloplasty. Mitral valve area determined by the Doppler continuity equation method correlated well with that determined at catheterization by the Gorlin formula, not only before but also immediately after balloon inflation (y = 0.87 x + 0.05, standard error of estimate = 0.22 cm2, r = 0.90). Serial calculation of mitral valve area by the Doppler continuity equation method showed a slight but significant decrease in the valve area at 24 hours after balloon mitral valvuloplasty but no change after that. We conclude that the Doppler continuity equation method provides an accurate estimation of mitral valve area before and even after balloon valvuloplasty. Mitral valve area dilated by balloon inflation is decreased slightly within 24 hours after the procedure, which corroborates valve stretch as one mechanism for increasing mitral valve area with balloon valvuloplasty. Estimation of mitral valve area immediately after balloon mitral valvuloplasty may overestimate the long-term efficacy of the procedure.

Cardiac Catheterization↗
PubMed1990

[A study of proteinuria. (12) The incidence of the patients with proteinuria, microscopic hematuria and glycosuria in Fukuoka Dental College students in 1987 and 1988].

An investigation was made on the incidence of patients with proteinuria, microscopic hematuria and glycosuria in 757 (in 1987) and in 681 (in 1988) students of Fukuoka Dental College; and the results were as follows. 1) The incidence of patients with proteinuria was 6.3% (48/757) in 1987, and 6.9% (47/681) in 1988. 2) The incidence of patients with microscopic hematuria was 4.0% (30/757) in 1987, and 5.0% (34/681) in 1988. 3) The incidence of patients with glycosuria was 0.5% (4/757) in 1987, and 0.1% (1/681) in 1988. 4) Further medical examinations were made on 33 students in 1987, and 37 students in 1988. a) 27 students in 1987 and 34 students in 1988 were diagnosed as normal respectively. b) In three cases, clinical diagnoses could not be established without long-term observation and two cases were diagnosed as urinary tract infection and a case was diagnosed as possible chronic glomerulonephritis in 1987. c) In 1988, a case was diagnosed as urinary tract infection, a case was urethritis and a case should be needed a longterm observation.

Adult↗
PubMed1990

[A case of psittacosis].

A 67-year-old Japanese housewife, who had been attended the out patient department of medicine, Fukuoka Dental College (FDC) Hospital for paroxysmal atrial fibrillation, was admitted to FDC Hospital because of high fever, exhaustion, anorexia, myalgia and mild stupor. Her ECG finding revealed atrial fibrillation and roentgenologic examination of the chest showed diffuse opacities in the left lung field (S10) without pleural effusion. As she had told her physician that her pet parakeet had been dead recently, she was diagnosed immediately as psittacosis. She was instantly treated with minocycline orally and deslanoside intravenously. Laboratory findings on admission disclosed the following results: Complement-fixing antibodies against Chlamydia psittaci were 1:64, and liver dysfunction (GOT 253, GPT 86, LDH 846) was shown. The white blood cell count was 4,700 associated with shift to the left, C-reactive protein was 6 plus and the erythrocyte sedimentation rate was 109 mm in 1 hour. The course in the hospital was satisfactory and after 38 hospital days she was discharged with complete recovery from the psittacosis. It is emphasized the importance of that the question about the history of contact with psittacine birds or other avian species is essential to diagnose psittacosis.

Aged↗
PubMed1990

[Progression of idiopathic mitral valve prolapse estimated by echocardiography].

To evaluate the progression of idiopathic mitral valve prolapse (MVP), a long time follow-up study (mean 7.1 years) was performed using echocardiography in 27 cases (11 males, 16 females, mean age: 50.4 years). Morphological changes, the degree of prolapse of the mitral valve, left atrial dimension (LAD) and left ventricular end-diastolic dimension (LVDd) were estimated at the first and last examinations. The degree of prolapse was assessed by measuring the distance of the dislocation between the anterior and posterior leaflets at the area of coaptation (degree I:5 mm or less, degree II: 6 to 10 mm, degree III: 11 mm or greater). The results were as follows: 1. The degree of prolapse did not progress in all 27 cases. 2. LAD increased with an advance of age. A remarkable increase of LAD was recorded in cases older than 45 years with atrial fibrillation or prolapse of degree II and III or with ruptured chordae tendineae. 3. The mitral ring was enlarged over 5 mm in six of 15 cases with prolapse of degree II and III. 4. Mitral regurgitation evaluated by Doppler echocardiography in patients with posterior leaflet prolapse was more severe than that in patients with anterior leaflet prolapse in the last examination. 5. LVDd increased gradually. In the present study, LAD was increased in most cases of MVP and it seemed to depend on complications (atrial fibrillation and ruptured chordae tendineae) or severity of regurgitation rather than the degree of prolapse.

Adult↗
PubMed1989

Rapid reduction of plasma atrial natriuretic peptide levels during percutaneous transvenous mitral commissurotomy in patients with mitral stenosis.

To clarify the direct contribution of the left atrial pressure to secretion of human atrial natriuretic peptide (hANP), we have attempted to study the relations between plasma hANP levels, neurohumoral factors, and hemodynamic changes in 13 patients with mitral stenosis undergoing percutaneous transvenous mitral commissurotomy (PTMC). After PTMC, the left atrial pressure fell from 14.7 +/- 1.9 (mean +/- SEM) to 6.5 +/- 0.7 mm Hg in all patients studied (p less than 0.0005), whereas there were no remarkable changes in either the right atrial pressure, mean arterial pressure, or heart rate. Plasma immunoreactive hANP levels obtained from the pulmonary artery decreased from 278 +/- 51 to 137 +/- 31 pg/ml after PTMC (p less than 0.0005). There was a significant correlation between the decrement of hANP levels and that of left atrial pressure (r = 0.72, p less than 0.005). Neither plasma renin activity nor norepinephrine levels changed. In contrast, plasma aldosterone concentrations significantly increased from 11.3 +/- 1.5 to 16.4 +/- 2.7 pg/ml after PTMC (p less than 0.01), although there was no casual relation between plasma concentrations of aldosterone and hANP. The present result with PTMC-induced rapid fall of the left atrial pressure with a concomitant reduction in hANP secretion strongly suggests the importance of the left atrial pressure on hANP secretion in humans.

Adult↗
PubMed1988

[Anterolateral papillary muscle motion before and after septal myotomy in hypertrophic obstructive cardiomyopathy].

The left ventricular outflow pressure gradient in hypertrophic cardiomyopathy results from systolic anterior motion of the mitral valve (SAM). This abnormal orientation of the valve was previously proposed to be caused by inappropriately hypertrophied papillary muscles which protrude to the interventricular septum (IVS). Septal myotomy can alter the orientation of the papillary muscles and resolve the pressure gradient, without myectomy. Recently, we have experienced two instructive cases to prove our previously advocated hypothesis. Case 1: This 54-year-old man complained of effort dyspnea, and his echocardiogram disclosed marked SAM, and a thickened IVS (28 mm) and left ventricular posterior wall (16 mm). The intraventricular pressure gradient was 134 mmHg, and there was mitral regurgitation of grade 2/4. A longitudinal incision via the aorta on the anterior portion of the IVS, toward the base of the anterolateral papillary muscle, resolved the pressure gradient and mitral regurgitation, and two-dimensional echocardiography demonstrated that the SAM resolved at the lateral aspect of the valve, but it remained on the medial side. Case 2: This 57-year-old man complained of dyspnea during effort. He had marked SAM. The intraventricular pressure gradient was 65 mmHg, and there was grade 3/4 mitral regurgitation. Longitudinal incisions on the anterior, medial and posterior parts of the IVS abolished the SAM and reduced mitral regurgitation to grade 1/4. In both cases, during systole, the anterolateral papillary muscle protruded into the left ventricular ontflow tract, causing SAM. After surgery, the direction of the muscle axis moved toward the mitral orifice during systole, resulting in alleviation of SAM on the same side of the location of septotomy. This further confirmed our concept that disoriented papillary muscles play essential roles in causing SAM. If the Venturi forces previously stressed by other investigators cause SAM, the latter should resolve on both the medial and lateral aspects, even by septotomy. Thus, the Venturi theory seems untenable.

Cardiomyopathy, Hypertrophic↗
PubMed1987

[The physiological role of the pericardium: studies based on right heart inflow dynamics in cases of left-sided pericardial defect].

Using pulsed Doppler echocardiography, the effects of postural change on the blood flow pattern in the superior vena cava and in the right ventricular inflow tract were investigated to evaluate the physiological role of the pericardium. Eight cases of left-sided pericardial defect and eight healthy subjects were examined. 1. Suppressed inflow into the right atrium during systole in left-sided pericardial defect was manifested as a reduction of the systolic wave (S) in the superior caval vein and impairment of the systolic shift of the tricuspid annulus. This suppression suggested unsatisfactory volume expansion in the right atrium due to the absence of negative intrapericardial pressure. 2. In left-sided pericardial defect, the right ventricular inflow pattern differed from the normal, most distinctly in the right lateral recumbent position, though the cardiac motion was nearly identical with that of the normal in this position. In this position, the ratio of the peak velocity of presystolic filling to that of rapid filling was increased, and the deceleration half time of rapid filling was prolonged. These findings indicated that the right ventricular rapid filling was retarded, and was compensated by the filling due to atrial contraction. It is assumed that right ventricular filling is influenced by hydrostatic pressure due to changes in posture in the absence of restriction by the pericardium. 3. It is concluded that the pericardium maintains negative intrapericardial pressure, so that each cardiac chamber is uniformly expanded for its filling, and that this function minimizes the influence of posture on cardiac hemodynamics.

Adult↗