[How far can heterologous transplantation progress?].
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Biomedical subjects
Publications and source records attributed to M Kawauchi.
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A 28-year-old woman presented with Marfan syndrome combined with severe mitral regurgitation and annuloaortic ectasia. The ascending aorta was dilated to 48 mm in diameter without aortic regurgitation. Considering the increased operative risk due to complication with aortic dissection, simultaneous replacement of the mitral valve and aortic root were performed. Her postoperative course was uneventful. Several options of the surgical treatment for Marfan syndrome are discussed.
A 51-year-old woman presented with mild stenosis of the mitral valve which had become thickened and rigid due to infective endocarditis, manifesting as persistent fever of up to 40 degrees C and general fatigue of a few days' duration. A harsh systolic murmur was heard. Multiple blood cultures revealed alpha-streptococcus. Echocardiography disclosed asymmetric septal hypertrophy (interventricular septal thickness/posterior wall thickness, 19/14 mm) and systolic anterior wall motion of the mitral valve. Continuous wave Doppler ultrasonography showed a peak left ventricular outflow tract pressure gradient of 170 mmHg. Transesophageal echocardiography revealed vegetations on the anterior mitral leaflet, aortic valve and interventricular septum along the left ventricular outflow tract. In particular, the anterior mitral leaflet was thickened and moved poorly. The calculated mitral valve areas was 1.5 cm2 and peak diastolic left atrium-left ventricle pressure gradient was 7 mmHg. A specimen of the mitral valve did not reveal commissural adhesion, but the anterior mitral leaflet showed marked fibrous thickening caused by scarred vegetation. Based on these findings, the diagnosis was hypertrophic obstructive cardiomyopathy complicated by infective endocarditis and "mitral stenosis". Valvular regurgitation is a common complication of active and healed infective endocarditis. In contrast, infective endocarditis rarely causes valvular stenosis except for stenosis caused by large fungus vegetation.
Lesions in the frontal base and clival area have conventionally been approached using the transbasal approach described by Derome and Guiot. However, this approach necessitates removal of the crista galli and sectioning of the olfactory rootlets with the associated risk of anosmia and cerebrospinal fluid leak and, in addition, complex reconstruction of the frontal base is required. We describe a new approach to deeply situated tumors in the frontal base, parasellar and clival area which is a modification of Spetzler's craniofacial approach with preservation of olfaction. In this approach, circumferential osteotomy cuts are made around the cribriform plate to permit en block removal with its attachment to both the dura and underlying mucosa. Opening of the dura is avoided and the cribriform bone is used to reconstruct the frontal base. Three patients underwent surgery using this approach for treatment of recurrent pituitary adenoma in two cases and for clivus chordoma in one. In one patient, olfactory function was not preserved because resection of nasal mucosa was small. In the other two patients, however, olfaction was preserved by creating a cribriform plate complex with a sufficient area of resection of nasal mucosa and tumors were completely removed. Olfaction can be preserved, CSF leakage can be prevented, and facial skin incision and complex frontal base reconstruction can be avoided when this technique for maintaining normal olfactory-cribriform anatomy is used in frontal transbasal approaches.
A 30-year-old female with Marfan's syndrome underwent aortic root replacement for annuloaortic ectasia and mitral valve replacement for mitral regurgitation. She remained well until 16 months postoperatively when she had sudden onset of pain. Preoperative angiogram showed Stanford B aortic dissection. Thoracoabdominal aortic replacement was performed successfully under deep hypothermic bypass.
BACKGROUND: Diagnosis of acute rejection and graft arteriosclerosis (chronic rejection) is critical to the success of cardiac transplantation, but accurate diagnosis is often difficult. We have reported that there are three types of vascular myosin heavy chain (MHC) isoforms: SM1, SM2, and SMemb. SM2 is specifically expressed in differentiated smooth muscle cells (SMCs). SMemb is a nonmuscle-type MHC abundantly expressed in SMCs of fetal aorta. METHODS AND RESULTS: To evaluate the usefulness of MHC expression for diagnosis and analysis of acute and chronic rejection, heterotopic cardiac transplantation was performed in rats and monkeys. Immunohistochemistry, electron microscopy, and Northern blot assay were performed to evaluate MHC expression. SMemb was expressed in spindle-shaped cells located in acutely rejected myocardium in the rats and monkeys. These cells were also observed in areas lacking cellular infiltration. These SMemb-positive cells were activated fibroblasts or myofibroblasts. SMemb mRNA was enhanced parallel to the progression of acute rejection. In the coronary arteries of chronically rejected allografts, enhanced SMemb and reduced SM2 expression was observed in both thickened intima and media. The reduced medial SM2 expression was observed before the intimal thickening occurred. These cells were phenotypically modulated SMCs. CONCLUSIONS: Altered expression of MHC isoforms is a sensitive indicator in the diagnosis of acute and chronic cardiac rejection. The pathophysiology of this alteration in MHC isoform expression should be studied further to elucidate the pathogenesis of cardiac rejection.
Using an animal model of forebrain ischemia in spontaneously hypertensive rats (SHR) by 3-h bilateral carotid occlusion, and various indices of the cerebral cholinergic system were assessed for periods up to 24 weeks. The lesions observed histologically in the hippocampus of SHR 2 weeks after ischemia were less severe than those in the frontal cortex. Marked elevation of acetylcholine concentration was transiently observed in the frontal cortex, hippocampus and thalamus + midbrain at 2 weeks, and in the striatum at 1-4 weeks after ischemia. Choline acetyltransferase activity remained unchanged in all regions throughout the experimental period except for a minimal decrease in the frontal cortex at 4 weeks. Choline esterase (ChE) activity was slightly decreased in the frontal cortex at 2-4 weeks after ischemia but recovered by 8 weeks. A decrease in the hippocampus was seen at 8 weeks. The B(max) for the M1-receptor was significantly reduced by 2 weeks in the frontal cortex and by 4 weeks in the hippocampus. Low B(max) values in both regions persisted through week 24. These delayed hippocampal changes in the ChE activity and M1-receptor in SHR were similar to those of the very much delayed changes in M1-receptor previously reported in the gerbil model for transient ischemia. In contrast, Wistar-Kyoto rats (WKY), used as normotensive controls, exhibited no histological or biochemical changes for up to 24 weeks. The difference between SHR and WKY may depend on the more severe cerebral blood flow depletion during carotid ligation in the former. The chronic state of SHR after the transient ischemia may be a useful pathophysiological model for human cerebral infarctions with hypertension.
Renal cell carcinoma occasionally invades the inferior vena cava and rarely extends to the right atrium. However, despite the frequency of venous extension, it is unusual to recognize patients with massive pulmonary tumor embolus clinically. We describe a 60-year-old man who underwent pulmonary tumor embolectomy using cardiopulmonary bypass combined with profound hypothermia and intermittent low-flow perfusion. The patient is currently alive and well without implantation metastasis 6 months after the operation.
During operations on patients with extracardiac conduits, sternal reapproximation occasionally results in critical compression of the conduit and serious deterioration in hemodynamic function. Permanent splinting of the sternum with a methyl methacrylate resinous plate provides an adequate substernal space for the extracardiac conduit.
Percutaneous transvenous mitral commissurotomy is widely performed as the first choice of the non-pharmacological treatments for mitral stenosis. Five patients have been identified who required mitral valve replacement after percutaneous transvenous mitral commissurotomy. The causes leading to mitral valve replacement were mitral regurgitation in three cases and insufficient commissurotomy in two. Massive mitral regurgitation is one of the most serious complications of percutaneous transvenous mitral commissurotomy. This report aims to elucidate the mechanism of massive mitral regurgitation occurring during percutaneous transvenous mitral commissurotomy. In every such case, there was a large tear in the posterior leaflet without any split in the commissures. The Japanese literature reports that 16 patients have undergone mitral valve replacement for massive regurgitation after percutaneous transvenous mitral commissurotomy: 14 of these cases had a tear in one of the leaflets and no evidence of splitting of the posterior commissure. These facts indicate that relative fragility of the leaflets as compared with rigidity of commissural fusion, especially in the posterior commissure, is an important factor of massive mitral regurgitation during percutaneous transvenous mitral commissurotomy.
The purpose of this study was to develop and to test a pressure-distribution sensor (PDS) for evaluating lip functions. The PDS is fabricated as a disposable cartridge and is based on the principle of optical-pressure conversion used in tactile sensors of robot arms. Its advantages are in measuring sealing forces, contact area, and pressure-distribution patterns of the lips at maximum effort. We used the PDS to evaluate pressure-distribution patterns of long-face subjects with extremely large interlabial distances. The results suggest that the PDS is a useful device for evaluating lip sealing functions and their changes after orthodontic therapy or orthognathic surgery.
A 10-year-old girl was referred to us with a diagnosis of pulmonary atresia and intact ventricular septum with a severely hypoplastic right ventricle and atrial septal defect. Her tricuspid valve diameter (TVD) was 48.5% of normal, with a TVD Z-score of -6.7, while right ventricular end-diastolic volume was 53.4% of normal. As a definitive procedure, one and one half ventricular repair using a bidirectional cavopulmonary shunt (BCPS) was performed instead of a Fontan procedure. The postoperative course was uneventful without episodes of low cardiac output or elevated right atrial pressure. She has been doing well during a follow-up period of 3 years.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
A 10-year-old female child of the Jehovah's Witness faith presented with congenitally corrected transposition of the great arteries (S,L,L), pulmonary atresia, and a ventricular septal defect. A successful surgical correction was performed using an aortic homograft as a valved extracardiac conduit without the use of homologous blood or blood products. We used permanent splinting of the sternum with a methyl methacrylate resin plate to prevent compression of the conduit.