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Biomedical subjects

C Yutani

Publications and source records attributed to C Yutani.

At least 55 records · Page 3Linked to original sources
PubMed1999

Sutured wound in myxomatous mitral valve one month after repair surgery: report of two cases.

There have been no reports concerning wound healing at the site of the suture line in myxomatous leaflets. We microscopically studied the sutured wounds in two myxomatous posterior mitral leaflets which underwent quadrangular resection of the frail middle segment followed by primary suture. The sutured wounds had a thick scar which was abundant in collagen fibers about 1 month after the repair surgery. This suggests that severe myxomatous degeneration itself would not be a cause of wound dehiscence, and that a sutured wound could be a cause of rigidity and deformity of leaflets.

Humans↗
PubMed1999

Characteristic cardiovascular manifestation in homozygous and heterozygous familial hypercholesterolemia.

BACKGROUND: The aortic valve dysfunction of patients with homozygous familial hypercholesterolemia (FH) suggests that hypercholesterolemia affects not only coronary arteries but also the aortic valve. We studied the aortic root of patients with homozygous FH and those of patients with heterozygous FH to characterize the premature atherosclerotic lesions by using histopathologic specimens. METHODS AND RESULTS: The aortic roots of 10 patients with homozygous FH, age 9 to 58 years, were studied by cardiac catheterization with several angiographies. The aortic roots of 39 patients with heterozygous FH under age 60 years were also examined for aortic and mitral valvular functions by color Doppler echocardiography, and 30 normocholesterolemic patients with coronary artery disease were examined as control subjects. In addition, in 22 patients with FH and 20 control subjects, the internal diameter of the aortic annulus and the aortic ridge in cardiac cycles were measured. Of the 10 homozygotes with FH, 8 patients had aortic regurgitation demonstrated by aortography; 3 of them showed significant transvalvular pressure gradients. Stenotic changes of coronary ostia were observed in 8 of the 10 homozygotes with moderate coronary atherosclerosis. Of the 39 heterozygotes with FH, 10 patients had aortic regurgitation shown by Doppler echocardiography, as did only 1 of the 30 control subjects (P <.05). The average diameter and distensibility of the ascending aorta were significantly reduced in the heterozygotes compared with the control subjects. The surgically resected cusp specimens of aortic valves obtained from 1 homozygous and 1 heterozygous patient showed significant thickening of the cusp with foam cell infiltration. CONCLUSIONS: Premature atherosclerosis in FH had a characteristic distribution, affecting the aortic root dominantly. The involvement of the aortic valve indicating "hypercholesterolemic valvulopathy" was a peculiar feature of FH, especially its homozygous form, but was reminiscent of ubiquitous processes caused by hypercholesterolemia.

Adolescent↗
PubMed1999

Parvovirus B19 infection induces apoptosis of erythroid cells in vitro and in vivo.

OBJECTIVE: intrauterine parvovirus B19 infection is related to non-immune hydrops fetalis, the pathogenesis of which is based on the strict tropism of B19 for erythroid precursor cells and the massive destruction of the infected erythroid cells, although the mechanism of beta19-induced cytotoxicity has not been studied in detail. The purpose of this study is to provide empirical evidence that beta19 induces apoptosis of erythroid cells both in vitro and ill vivo. METHODS: we analysed culture cells infected in vitro by B19 and tissues of nine cases of hydrops fetalis caused by B19 intrauterine infection by histological and biological methods. RESULTS: cells infected iil vitro by B19 showed nuclear changes characteristic of apoptosis by light microscopic examination and DNA extracted from the infected cells was fragmented. Electron microscopic examination showed the nuclei of infected cells contained crescent-shaped clumps of heterochromatin with increased density and double staining with anti-B1 9 antibody and terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine triphosphate-digoxigenin nick-end labeling (TUNEL) confirmed apoptosis of individual cells. Tissues of cases of hydrops fetalis caused by B19 contained erythroid cells with nuclear inclusions and characteristic nuclear changes of apoptosis by light microscopy. The double-staining confirmed apoptosis of erythroid cells in the tissues. Immunohistochemical analysis with antibodies against cellular factors involved in apoptosis showed that caspase3, p53 and p21 were positive in infected cells.

Apoptosis↗
PubMed1999

Ultrasonic tissue characterization in patients with dilated cardiomyopathy: comparison with findings from right ventricular endomyocardial biopsy.

AIM: The clinical usefulness of integrated backscatter (IB) imaging was compared with right ventricular endomyocardial biopsy for assessing myocardial damage in patients with dilated cardiomyopathy (DCM). METHODS: We examined 15 patients with DCM and 20 healthy controls. In addition to the conventional M-mode echocardiographic parameters, we determined the cyclic variation in IB values (CV-IB) obtained from parasternal short axis views of the left ventricle just under the transducer for both the interventricular septum (IVS) and the left ventricular posterior wall (PW). The per cent fibrosis area (%) and the transverse diameter of myocytes (microm) were measured in right ventricular endomyocardial biopsy specimens by computer image analysis. To analyze the relationship between pathological findings and CV-IB, we divided patients into four subgroups on the basis of the pathological characteristics of endomyocardial biopsy specimens as follows: degeneration dominant group (n = 5), fibrosis dominant group (n = 5), dilated phase hypertrophic cardiomyopathy (n = 2), and mixed type (n = 3). RESULTS: CV-IB in the IVS and the PW was lower in patients with DCM (8.8 +/- 2.9, 8.3 +/- 2.7 dB, respectively) than in normal subjects (14.4 +/- 2.9, 13.6 +/- 2.6 dB, respectively). Biopsy findings showed a mean per cent fibrosis area of 24.0 +/- 12.3%, and a mean myocyte diameter of 14.3 +/- 2.9 microm in patients with DCM. CV-IB was correlated with both of these findings: per cent fibrosis area (r = -0.56 in IVS, r = -0.56 in PW) and myocyte diameter (r = 0.67 in IVS, r = 0.71 in PW). CV-IB was decreased in all DCM subgroups compared with normal subjects, but there was no significant difference between subgroups. CONCLUSIONS: CV-IB was correlated with both the extent of fibrosis in myocardial tissue and the myocyte diameter. These findings suggest that ultrasonic tissue characterization is a good indicator of the severity of fibrosis and myocyte atrophy in patients with DCM.

Biopsy↗
PubMed1999

Coronary atherosclerosis and interventions: pathological sequences and restenosis.

The primary cause of cardiac morbidity and mortality in developed countries is ischemic (coronary) heart disease. The incidence of this disease is virtually all due to atherosclerosis, and ischemic heart disease is also the most prevalent disease in the industrialized world, causing over 40% of all deaths in the United States and Western Europe. In Japan, the incidence of ischemic heart disease due to coronary atherosclerosis is gradually increasing as well. Compared with the classical nomenclature of atherosclerosis; that is, fatty streak, fibrous plaque and complicated lesions, the term Stary's classification has been universally accepted because it reflects the more recently acquired knowledge about the morphological and biochemical details of the processes in coronary atherosclerosis, which have been obtained by new strategies such as angioscopy, intravascular ultrasound and molecular biological methods. The term Stary's classification has been applied for the coronary atherosclerosis of patients with acute coronary syndrome at the National Cardiovascular Center, for the analysis of predisposing atherosclerosis of these patients. The recent findings regarding acute coronary syndrome resulting from a rupture of coronary atherosclerotic plaques indicate that this syndrome is probably the most important mechanism underlying the sudden onset. It has been found that the risk of plaque rupture may depend more on plaque composition than on plaque size. Plaques rich in soft extracellular lipids and macrophages are possibly more vulnerable to plaque rupture. Two of the goals of the present review are to clarify how plaque disruption occurs and to elucidate the relationship between plaque disruption and coronary risk factors in elderly Japanese patients with acute coronary syndrome. Coronary stents have been shown to be efficacious in the treatment of acute and threatened closure complicating percutaneous transluminal coronary angioplasty (PTCA) and have produced encouraging initial results in the prevention of restenosis. In the autopsy study of restenosis after PTCA, it was observed that dense caps of collagen fibers in the adventitia in the vicinity of the disrupted internal elastic laminae were present in all of the remodeling lesions. It is suggested that remodeling, which resulted in adventitial scarring, is one of the major causative factors of restenosis after PTCA. The long-term success of stenting, however, remains limited by the occurrence of late in-stent restenosis, with an incidence of 20-42% depending on the stent design and the patient population studied. Another aim of the present review is to describe the pathological mechanism of restenosis after PTCA and/or stent replacement and, consequently, the vascular remodeling that occurs around adventitial tissue after PTCA and intimal hyperplasia that is chronically irritated by a foreign body granulomatous reaction after stenting. Finally, the results of the investigation of the effect of a tissue factor pathway inhibitor on the prevention of interventional restenosis is described.

Angioplasty, Balloon, Coronary↗
PubMed1999

Epithelioid hemangioma of the temporal artery clinically mimicking temporal arteritis.

A rare case of epithelioid hemangioma (angiolymphoid hyperplasia with eosinophilia) arising in the right temporal artery of a 68-year-old Japanese woman was investigated. The patient had been treated with corticosteroids (Predonine 5 mg/day p.o.) for 4 years for idiopathic thrombocytopenic purpura. Headaches in the right temporal region with repeated high fevers first appeared 1 year prior to the biopsy of a nodule at the artery. The clinical diagnosis was temporal arteritis (giant cell arteritis). The specimen consisted of a short segment of the superior arterial branch having a sheet-like proliferation of the epithelioid endothelial cells in the lumen, which was almost occluded, focal rupture of the media, and marked proliferation of the capillaries (neovascularization) radiating out from the media to the adventitia. There were scattered foci of inflammatory cell infiltration composed mainly of small lymphocytes in the adventitia, but there were no histological changes suggestive of giant cell arteritis. The lesion was thus characterized by the proliferation of epithelioid endothelial cells in the lumen of the artery, and neovascularization between the media and adventitia. The histological features were very close to epithelioid hemangioma except for the absence of an eosinophilic reaction. The long-term administration of corticosteroids may have suppressed it. The authors believe this is the first case of epithelioid hemangioma arising from the temporal artery without a history of trauma. It showed some unique features both clinically and histopathologically, which contributed to the study of the yet not clearly classified vascular proliferative lesion, epithelioid hemangioma.

Aged↗
PubMed1999

A case of hereditary amyloidosis transthyretin variant Met 30 with amyloid cardiomyopathy, less polyneuropathy, and the presence of giant cells.

Transthyretin-Met 30 (TTR-Met 30) is a variant of transthyretin and is usually associated with familial amyloid polyneuropathy. It is rare that patients with TTR-Met 30 will primarily develop amyloid cardiomyopathy. This report presents a patient with late-onset TTR-Met 30 who primarily developed amyloid cardiomyopathy, with less amyloid polyneuropathy in the peripheral nervous system than is usually seen. An autopsy was performed, and histological examination revealed many foreign-body giant cells and macrophages in the area of amyloid deposition that was found in nearly all of the organs.

Aged↗
PubMed1999

A case of interleukin-6-producing malignant fibrous histiocytoma originating in the heart.

Primary cardiac malignant fibrous histiocytoma is extremely rare and its pathophysiological characteristics remain largely unknown. We treated a female patient with persistent fever and disseminated intravascular coagulation. Since ultrasonic echocardiography revealed the presence of a cardiac tumor and her serum interleukin-6 level was elevated, we speculated she had a cardiac myxoma. Histological examination of the surgically resected specimen, however, revealed that the tumor was malignant fibrous histiocytoma. Although her disseminated intravascular coagulation and heart failure were transiently improved after operation, local recurrence and systemic metastasis occurred and she died 7 weeks after operation. Using the autopsied specimen, we examined whether the malignant fibrous histiocytoma constitutively synthesized interleukin-6. The interleukin-6 content in the tumor was high, consistent with interleukin-6 production by the tumor. This was confirmed by immunohistochemical analysis. To our knowledge, this is the first report demonstrating interleukin-6 production by a cardiac malignant fibrous histiocytoma.

Aged↗
PubMed1999

Histologic evidence of foreign body granulation tissue and de novo lesions in patients with coronary stent restenosis.

OBJECTIVES: We examined the relative contributions of foreign body granulation and de novo lesions to neointimal hyperplasia in atherectomized specimens of restenosis after coronary stenting. BACKGROUND: Clinicopathological studies have suggested that smooth muscle cell (SMC) hyperplasia is the most likely cause of restenosis after coronary stenting. It is not yet fully understood how SMC hyperplasia occurs or how SMCs stimulation can lead to intimal hyperplasia. Although inflammation has been postulated to be a major contributor to restenosis after coronary stenting, there is a paucity of data on the relationsip between inflammation and subsequent neointimal formation in humans. Only in a porcine experimental model of stent restenosis, foreign body granulation tissue as a cause of inflammation in stent restenosis was reported. METHODS: Tissue specimens were retrieved by directional atherectomy from 11 patients in whom stent restenosis developed after percutaneous revascularization of coronary artery disease. For specimens preserved in 10% buffered formalin, analysis of cellular composition was performed quantitatively after cell-specific immunostaining, i.e. CD68, UCHL-1, HLA-DR, smooth muscle actin, vimentin, desmin, PCNA and TGF-beta. RESULTS: Five of the 11 patients showed granulation tissues 3-6 months after stent implantation, of whom 3 patients revealed foreign body multinucleated giant cells around the stent struts where PCNA- and vimentin-positive SMCs were demonstrated. Calcification and de novo lesions in medial and adventitial tissues were observed in 3 other patients, and fresh and/or organized thrombi were documented in 3 of the 11 patients. CONCLUSIONS: These findings support the notion that stent restenosis results from SMC hyperplasia and suggest that the foreign body granulation tissue against metals of the stents and de novo lesions could play an important role in chronic inflammation leading to intimal hyperplasia and subsequently to stent restenosis in some patients. Clinicians should thus consider whether a patient may be allergic to stent components with unknown reaction, e.g. haptens.

Aged↗
PubMed1999

Histologic comparison of coronary and iliac atherectomy tissue from cases of in-stent restenosis.

Pathologically, restenotic lesions after stenting were investigated by use of atherectomized tissues of seven coronary and seven iliac arteries. The mean interval of the stent deployment to restenosis was 9.1 months for the coronary artery and 33.7 months for the iliac artery, indicating a 3.7-fold longer interval for the latter. This study does not include cases of acute thrombotic occlusion. The atherectomized tissue from restenotic coronary arteries showed abundant neointima with alpha-actin-positive and ultrastructually synthetic-type smooth muscle cells in a rich myxomatous extracellular matrix. In the iliac arteries, the predominant component of restenosis consisted of organized thrombi. The neointima of the iliac arteries was mature, and only a small amount of spindle cells were observed in the hyalinized matrix. The tissue that developed restenosis after stenting was different in the coronary and iliac arteries included in this series. This study on the atherectomized tissue suggests that even in the chronic stage, a major cause of in-stent restenosis among the larger caliber vessels such as the iliac artery is not neointima but stent thrombosis.

Aged↗
PubMed1999

Expression of MEF2 genes during human cardiac development.

To better understand the regulatory mechanisms in gene expression of human cardiomyocytes, we studied the expression of MEF2 genes encoding transcription factors during the course of cardiac development. Expression of all four MEF2 transcripts (MEF2A, MEF2B, MEF2C, and MEF2D) were detected in all developmental stage of the human heart, while Mef2b transcripts were down-regulated in mouse heart development. Although none of the MEF2 genes, besides mouse Mef2b, exhibited any remarkable quantitative change in their transcripts, qualitative changes in MEF2 transcripts were found during the course of cardiac development. In particular, MEF2D transcripts showed prominent changes by alternative splicing in the perinatal period. MEF2D transcripts containing the 21-base exon (exon b) were predominantly expressed after birth. At the same time, transcripts of the alpha myosin heavy chain (alphaMHC) gene increased after birth, as the splicing pattern in transcripts of the cardiac troponin T (cTnT) gene changed to decrease the transcripts of cTnT1 after birth. These changes seemed to be correlated with the alternative splicing changes of MEF2 genes, especially MEF2D. The alternative splicing as well as transcriptional regulation in MEF2 genes might be important for regulating the alphaMHC gene and the maturation of cardiomyocytes.

Animals↗
PubMed1999

[Multiple cavities in myocardium of left ventricle after irradiation therapy for breast cancer: a case report].

A 68-year-old woman was admitted to our hospital with congestive heart failure. She had been diagnosed with hypertrophic cardiomyopathy 12 years ago in another hospital. She had received irradiation therapy for left breast cancer 33 years ago after resection of her left breast. Echocardiography revealed left ventricular hypertrophy and wall motion hypokinesis, and multiple cavities in the myocardium of the left ventricle, interventricular septum, and anterior wall. Some cavities were observed to connect to the left ventricular cavity and Doppler echocardiography showed slow velocity flows in them different from that of the coronary artery. The pathologic diagnosis was severe sclerosis of the left coronary artery, especially the left descending artery and its branch, which was the area with irradiation. Histopathology revealed sclerotic changes of the coronary artery causing acute and chronic myocardial infarction, and incomplete regeneration and hypertrophy of cardiac cells. There was no sign of hypertrophic cardiomyopathy. Myocardial degeneration and deciduation were present next to the cavities connected to left ventricle-like fistulas.

Aged↗
PubMed1998

Diagnostic value of plasma levels of brain natriuretic peptide in arrhythmogenic right ventricular dysplasia.

BACKGROUND: Arrhythmogenic right ventricular dysplasia (ARVD) is characterized by local or diffuse wall motion abnormalities in the right ventricle (RV), associated with recurrent ventricular tachycardia (VT) of RV origin. Brain natriuretic peptide (BNP) was first isolated from a porcine brain extract. In humans, BNP is expressed predominantly in the ventricles of failing hearts, and its expression has been observed primarily in myocytes in the interstitial fibrous area in dilated cardiomyopathy. We hypothesized that BNP is increasingly secreted from the residual myocytes within the atrophic tissue in patients with ARVD. METHODS AND RESULTS: Plasma BNP levels were measured in 17 patients with ARVD, 12 patients with idiopathic RV outflow tract tachycardia (RVOT), and 120 control subjects. We performed cardiac catheterization, RV endomyocardial biopsy, electron- beam CT, and biventricular endomyocardial mapping in the ARVD patients. There was a significant increase in plasma BNP levels in the ARVD patients compared with the RVOT patients and control subjects (61.4+/-59.6 pg/mL versus 8.3+/-5. 5 pg/mL and 9.3+/-5.8 pg/mL; P<0.0001, respectively). The plasma BNP levels had no correlation with any of the hemodynamic data, but they had a significant correlation with the RV ejection fraction (r=-0. 588, P=0.025) and with the fractionated-area scores (r=0.705, P=0. 005). Light microscopic immunohistochemistry showed strong BNP immunoreactivity in residual myocytes with fibrofatty replacement. CONCLUSIONS: These results suggest that plasma BNP levels were not increased in RVOT patients but were increased in ARVD patients, and that the increased BNP levels indicate the severity of both the RV dysfunction and the arrhythmogenic substrate.

Adolescent↗
PubMed1998

Chronic infusion of adrenomedullin reduces pulmonary hypertension and lessens right ventricular hypertrophy in rats administered monocrotaline.

A novel vasorelaxant peptide, adrenomedullin, its messenger ribonucleic acid (mRNA), and the mRNA for its receptor are highly expressed in the lung, suggesting that adrenomedullin may play a role in the regulation of the pulmonary circulation. We investigated whether the chronic infusion of rat adrenomedullin would affect pulmonary hypertension and right ventricular hypertrophy produced by the administration of monocrotaline. Four-week-old male Wistar rats received a single subcutaneous injection of 60 mg/kg monocrotaline and were then chronically and subcutaneously infused with rat adrenomedullin (PH + AM group, n = 8) or saline (PH group, n = 10) by an osmotic minipump for a period of 21 days. Plasma levels of adrenomedullin were significantly higher in the PH vs. the control group. The chronic infusion of adrenomedullin in rats with pulmonary hypertension increased the plasma levels of adrenomedullin to a value 94% greater than that of the control group and 55% greater than that of the untreated PH group. Chronic infusion of adrenomedullin significantly lessened the increase in right ventricular systolic pressure and the ratio of right ventricular weight to body weight seen after monocrotaline treatment. Histological examination revealed that adrenomedullin also attenuated the medial thickening of the pulmonary artery. These results suggest that chronic infusion of adrenomedullin attenuates the pulmonary hypertension and right ventricular hypertrophy seen in rats treated with monocrotaline.

Adrenomedullin↗
PubMed1998

Serum amyloid P component associates with high density lipoprotein as well as very low density lipoprotein but not with low density lipoprotein.

Serum amyloid P component (SAP) is a glycoprotein in human plasma. We previously showed that SAP is specifically localized in human atherosclerotic lesions, suggesting that SAP may play a role in atherogenesis. In this study, the interactions between human SAP and high density lipoprotein (HDL), low density lipoprotein (LDL) and very low density lipoprotein (VLDL) were investigated by using a solid phase plate assay. Biotinylated SAP bound to immobilized HDL and VLDL in a calcium-dependent, saturable manner. The SAP-HDL and SAP-VLDL bindings reached saturation at 4 nM and 16 nM of SAP, respectively. The bindings were inhibited by native SAP in a dose-dependent manner. No binding between SAP and LDL was found in the presence of calcium or EDTA, which indicates the specificity of SAP-lipoproteins interactions. These results suggest that the function of SAP is related to its capability to interact with lipoproteins and this may have important implications in atherosclerosis and in amyloidosis.

Binding, Competitive↗
PubMed1998

Aneurysmal pouch on left coronary cusp accompanied by bacterial endocarditis.

A 58-year-old male was admitted to our hospital with a preliminary diagnosis of bacterial endocarditis. After admission, echocardiography indicated the presence of vegetation-like tissues on both the left coronary cusp and the anterior mitral leaflet, although retrograde aortography two months earlier hadn't indicated an abnormal finding on the aortic cusp. The vegetation-like tissues had gradually enlarged despite the administration of antibiotics at another hospital, and aortic and mitral regurgitation had become severe. We decided to perform replacements of the aortic and mitral valves on the day of admission. During the operation, the aortic valve was found not to have vegetation, but an aneurysmal pouch on the left coronary cusp. It was supposed that either bacterial endocarditis or catheter injury had made a part of the aortic cusp weak and intolerant of diastolic pressure gradient, and as a result, the weakened part of the cusp progressively dilated into the left ventricle forming an aneurysmal pouch. To our knowledge, there have been only two previous reports of an aneurysmal pouch on the aortic cusp documented in the literature.

Aortic Valve↗