[A case of intrahepatic cholesterol stone].
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Biomedical subjects
Publications and source records attributed to Y Nimura.
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Mitral valve lesions accompanying secundum atrial septal defect were examined in 120 successive patients from May 1978 to December 1980 using real time two dimensional echocardiography. The conclusions were as follows: (1) The characteristic feature of the mitral lesion accompanying secundum atrial septal defect is a dislocation of the mitral leaflet toward the left atrial side in the area of coaptation. (2) The mitral lesion is seen in about half the patients with secundum atrial septal defect. (3) It is usually seen only in the anterior leaflet, and is found near the posteromedial commissure. Lesions in other sites on the leaflet all accompany those near the posteromedial commissure. (4) The incidence, extent, and degree of the mitral valve lesion increase with age. (5) It is assumed that the mitral valve lesion in secundum atrial septal defect starts near the posteromedial commissure in the anterior leaflet, gradually deteriorates, and extends toward the anterolateral commissure. (6) It is probable that the mitral lesion results in mitral regurgitation. (7) The mitral valve lesion is similar in appearance to mitral valve prolapse caused by the floppy mitral valve, though their causative factors may be different. It is probably the reason why the mitral valve abnormality has been described as mitral valve prolapse in previous reports. In the present study the mitral lesion was evaluated on the distance of the dislocation between both leaflets at the area of coaptation. These criteria proved useful. Because of the similarity in appearance, it may be helpful in the assessment of primary mitral valve prolapse.
The mechanism of systolic anterior motion of the mitral valve and the localisation of the intraventricular pressure gradient were determined in 15 cases of hypertrophic obstructive cardiomyopathy by the combined use of real time two dimensional echocardiography and intracardiac manometry. We arrived at the following conclusions. The systolic anterior motion of the mitral echo in the M-mode echocardiogram can be classified into two types, I and II, based on two dimensional echocardiographic findings. In type I, the echo sources of systolic anterior motion are the anteriorly shifted mitral chordae and, in part, the papillary muscles. The intraventricular pressure gradient occurs at the level of the tip of the papillary muscle. The suprapapillary part of the outflow tract and the inflow part show a low pressure, while the apical cavity shows a high pressure. In type II, the echo sources of systolic anterior motion are the anterior and posterior mitral leaflets which are oriented in such a way as to obstruct the outflow tract. The pressure gradient occurs at the level of the anterior and posterior mitral leaflets. The inflow tract and the outflow tract just below the mitral leaflets show a high pressure, in contrast to type I systolic anterior motion. The inappropriate and maloriented papillary muscles play an essential role in causing both types of systolic anterior motion and outflow obstruction. The direction of the axis of the papillary muscle is changed in late systole, moving its tip away from the interventricular septum, resulting in a simultaneous reduction in systolic anterior motion.
Mitral regurgitation and its haemodynamic features were investigated non-invasively in cases of hypertrophic cardiomyopathy by means of two dimensional Doppler echocardiography. There were 28 patients, 14 of whom showed systolic anterior motion (SAM) of the mitral echo; the other 14 did not. The following results were obtained. (1) Mitral regurgitation was detected by the Doppler technique in all cases with systolic anterior motion of the mitral echo and in half of those without it. (2) Doppler signals of mitral regurgitation started immediately after the first heart sound. (3) Mitral regurgitant flow was often distributed from the entire mitral orifice over the entire or the posterior half of the left atrium in the cases with systolic anterior motion. In the cases without systolic anterior motion the regurgitation was usually localised near the mitral orifice. These features differ from those of regurgitation usually seen in rheumatic mitral valve disease and idiopathic mitral valve prolapse. (4) The Doppler technique and left ventriculography were equally efficient in detecting mitral regurgitation. (5) The early systolic component of the murmur of hypertrophic myopathy is considered to result in the main from concomitant mitral regurgitation, but not from turbulent blood flow in the left ventricular outflow tract, so that in cases with mitral regurgitation as a complication, mitral regurgitation may also contribute to the development of the midsystolic portion of the systolic murmur, while the main origin of this portion of the murmur is the left ventricular outflow obstruction.
The aim of the present study is to perform a detailed analysis of the spot echoes which show chaotic motion of the left ventricular cavity of patients with ruptured chordae tendineae. The subjects were 12 patients with surgically documented ruptured chordae tendineae. They were carefully examined preoperatively by real-time two-dimensional echocardiography with a commercially available wide-angle phased array system (Toshiba SSH-11A). An abnormal moving spot echo was often seen instantaneously in the left ventricle. Its motion was chaotic, and it moved both longitudinally and laterally. Lateral movements were seen in 10 of the 12 subjects and were not found in any of 10 controls. The site of this echo in the left ventricle was identical with the site of the rupture of the mitral chordae confirmed during surgery. Therefore, it was concluded that the spot echo with chaotic motion represents a direct visualization of ruptured chordae. This chaotic motion is considered to be a useful clue in diagnosis. The lateral component (left to right) of the movement is especially important. However, one must carefully examine the left ventricular cavity with moving pictures over a period of many heart beats in order to detect these chaotic movements of spot echoes.
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Blood flow of the portal vein was non-invasively studied in healthy and diseased humans with the combined use of the ultrasonic pulsed Doppler technique and real-time two-dimensional echography. In addition, the influence of food intake to the portal flow was assessed.
A 73-year-old man visited our hospital complaining of chest distress in September 1979. A chest X-ray film showed a tumor shadow in the left lung and left inferior lobectomy was performed. The tumor measured 50 X 40 X 30 mm; it was diagnosed as large cell carcinoma. In November 1980 the patient suddenly noticed macroscopic hematuria although there had been no microscopic hematuria at his first visit. Ultrasound-guided percutaneous pyelography confirmed complete obstruction of the left ureter and he underwent left ureteronephrectomy. The papillary tumor, measuring 23 cm, was diagnosed as transitional cell carcinoma.
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Perineural invasion of carcinoma is of considerable interest especially in the pancreas, because this organ is adjacent to the main autonomic plexuses of the abdomen. The present study was based upon 14 cases of primary carcinoma of the pancreas head in which total pancreatectomy with extensive dissection of the regional lymph nodes and autonomic plexuses was performed. Information concerning perineural invasion was obtained from histological specimens of the pancreas, lymph nodes and autonomic plexuses. Carcinomatous involvement of nerves was observed in all 14 cases within parenchyma of the pancreas head, but never found in the body and tail. Perineural extension of carcinoma to the regional autonomic plexuses was observed in 9 cases, which included the pancreatic capital plexus in 8 patients, superior mesenteric plexus in 3, celiac plexus in 2 and plexus on the common bile duct in 2 patients. This manner of invasion had no relationship with behaviour of lymph node metastasis. Thus, invasion and extension along the autonomic nerves by carcinoma of the pancreas were more common than usually recognized. Extensive dissection of the regional autonomic plexuses should be performed to increase the possibilities of a curative procedure.
Inflow pattern at the tricuspid orifice was examined using two-dimensional Doppler echocardiography. The cases examined consisted of 24 cases of hypertrophic cardiomyopathy (HCM), 10 cases of left ventricular hypertrophy (LVH) due to hypertension or aortic valvular stenosis and 23 healthy subjects. The right ventricular inflow pattern in HCM was characterized by a slow deceleration of a rapid filling wave, an increase in the duration of an inflow due to atrial contraction and an increased ratio of the peak velocity in atrial contraction phase to that in rapid filling phase (A/R). No definite difference was noted in the right ventricular inflow pattern between HCM with and without left ventricular obstruction. The abnormalities in the right ventricular inflow pattern in LVH were similar to those in HCM. The abnormal inflow patterns in HCM and LVH suggested a reduced distensibility of the right ventricle in early diastole and the compensatory augmentation of right atrial contraction. The changes in the deceleration of the rapid filling wave and A/R ratio were significantly correlated with interventricular septal thickness (base and papillary muscle levels) in cases with LVH. This result seemed to indicate that the changes in the right ventricular inflow are mainly resulted from the influence of hypertrophy of the interventricular septum on right ventricular function. There was hypertrophy of the interventricular septum in all cases of HCM and, in addition, that of the right ventricular anterior wall in some of them. The changes in the inflow pattern in HCM are also considered to be resulted from hypertrophy of the right ventricular anterior wall and the influence of hypertrophy of the interventricular septum on right ventricular function. However, in the cases of HCM, the extent of the changes showed no significant correlation with right ventricular anterior wall thickness and interventricular septal thickness. In HCM, hypertrophy of the interventricular septum and right ventricular free wall may coexist, and ventricular hypertrophy is often nonuniform and may exhibit disarrangement in myocardial architecture. Therefore, influential factors on the right ventricular inflow are considered to be more complicated in HCM than in LVH, resulting in the absence of significant correlation to the abnormal inflow mentioned above.
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In 35 of 70 patients with rheumatic mitral valve disease, two dimensional echocardiography revealed the posterobasal wall of the left ventricle to be entrapped between the left ventricular and atrial cavities and bent inward. The motion of the bending segment was paradoxical. This abnormality was assumed to be induced by the left atrial dilatation extending inferiorly behind the left ventricle, because the length of the bending segment correlation with the left atrial dimension. There was no correlation between the degree of abnormal bending and left atrial pressure, mitral valve pressure gradient or left ventricular dimension. The systolic excursion of the posterobasal wall of the left ventricle was reduced according to the length of the bending segment. This abnormal feature was also observed in five postmortem heart specimens with an extremely dilated left atrium. The macroscopic and microscopic findings in the myocardium of the bending segment were not different from those of the remaining segment of the left ventricle. Therefore, the asynergic motion of the bending segment is assumed to be caused by the abnormal spatial orientation of the left ventricle and the left atrium. It should be considered that the giant left atrium not only oppresses the surrounding organs but also affects the left ventricle.
Evidence is present that plasma contains non-specific factors which interfere with the 30K glucagon assays. A correction can be made for these interference factors because the factors can be quantitated following absorption of glucagon with charcoal-dextran. Using a correction factor the range of fasting plasma immunoreactive glucagon (IRG) in 12 totally pancreatectomized patients was below detectable limit. Fasting levels of IRG were determined on the plasma from 25 liver cirrhotics complicated by abnormal GTT, 13 pancreatic diabetics with chronic calcified pancreatitis (CCP), 25 adult-onset primary diabetics and 25 healthy subjects. When all samples were measured using no correction factor, the mean levels of IRG were 358 +/- 24 (mean +/- SE), 170 +/- 26, 178 +/- 16 and 178 +/- 7 pg/ml, respectively. Using a correction factor the mean level of IRG were 177 +/- 26, 16 +/- 4, 39 +/- 9 and 20 +/- 4 pg/ml, respectively. The mean values of the interference factor were not significantly different among all five groups. During an arginine infusion the interference factor remained unchanged despite an increase in IRG. It is available but not always necessary to apply a correction factor for 30K glucagon radioimmunoassay.
Regurgitant flow was analysed in 40 cases of mitral regurgitation, using combined ultrasonic pulsed Doppler technique and two dimensional echocardiography. Abnormal Doppler signals indicative of mitral regurgitant flow were detected in reference to the two dimensional image of the long axis view of the heart and the short axis view at the level of the mitral orifice. The overall direction of regurgitant flow into the left atrium was clearly seen in 28 of 40 cases, and the localisation of regurgitant flow in the mitral orifice in 38 cases. In cases with mitral valve prolapse of the anterior leaflet or posterior leaflet the regurgitant flow was directed posteriorly or anteriorly, respectively. The prolapse occurred at the anterolateral commissure or posteromedial commissure and resulted in regurgitant flow located near the anterolateral commissure or posteromedial commissure of the mitral orifice, respectively. In cases with rheumatic mitral regurgitation the regurgitant flow is usually towards the central portion of the left atrium and is sited in the mid-part of the orifice. The Doppler findings were consistent with left ventriculography and surgical findings. The ultrasonic pulsed Doppler technique combined with two dimensional echocardiography is useful for non-invasive analysis and preoperative assessment of mitral regurgitation.
Sixty patients with pulmonary regurgitation were studied by the pulsed Doppler technique combined with two-dimensional and M-mode echocardiography. Patients with pulmonary regurgitation had abnormal Doppler signals just below the pulmonic valve in the right ventricular outflow tract in diastole on the two-dimensional image. These signals were considered to indicate the regurgitant flow. There are two patterns of pulmonary regurgitant Doppler signals. In pulmonary hypertension, the maximal component of instantaneous flow velocity is sustained at about the same signal strength throughout diastole, but when the pulmonary arterial pressure is normal, the velocity slows down gradually from early diastole to end-diastole. Pulmonary regurgitation was detected by phonocardiography in about half the patients. In the remaining half, pulmonary regurgitant murmur could not be differentiated from aortic regurgitant murmur or was masked by coexistent aortic regurgitation or patent ductus arteriosus, whereas the Doppler technique indicated pulmonary regurgitation.