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Brugada syndrome is a disease known to cause ventricular fibrillation with a structurally normal heart and is linked to SCN5A gene mutation. However, the mechanism by which ventricular fibrillation develops in cases of Brugada-type electrocardiogram without SCN5A mutation has remained unclear. Recently, oxidative stress has been implicated in the pathophysiology of cardiac arrhythmia. We also investigated oxidative stress levels in the myocardia of patients with Brugada-type electrocardiogram.Endomyocardial biopsy samples were obtained from 68 patients with Brugada-type electrocardiogram (66 males and two females). We performed histological and immunohistochemical analyses for CD45, CD68, and 4-hydroxy-2-nonenal-modified protein, which is a major lipid peroxidation product.SCN5A mutation was detected in 14 patients. Ventricular fibrillation was documented in three patients with SCN5A mutation and in 11 without SCN5A mutation. In patients with SCN5A mutation, 4-hydroxy-2-nonenal-modified protein-positive area was not significantly different between the documented ventricular fibrillation (VF) group (VF+ group) and the group without documented VF (VF- group). However, in patients without SCN5A, the area was significantly larger in the VF+ group than that in the VF- group (P.05). All other parameters (fibrosis area, CD45, and CD68) were not different between the VF+ and VF- group in both SCN5A+ and SCN5A- patients.Oxidative stress is elevated in the myocardium of patients with Brugada-type electrocardiogram who have VF episodes and do not have SCN5A gene mutations. Oxidative stress may be associated with the occurrence of VF in patients with Brugada-type electrocardiogram without SCN5A mutation.

症例は82歳の女性で，食欲不振と体重減少を主訴に近医にてCTを受けS状結腸癌を疑われた．精査目的で注腸検査を受け，検査後に腹痛が出現し翌日の画像検査でS状結腸穿孔によるバリウム腹膜炎の診断で当院紹介となった．緊急開腹術の所見で後腹膜腫瘍のS状結腸への浸潤と穿破によるバリウム腹膜炎，腫瘍による左尿管・左総腸骨動静脈の途絶，後腹膜腔に膿瘍形成を認めた．ハルトマン手術と左腎瘻造設を施行した．病理検査で後腹膜腫瘍は高分化扁平上皮癌であり原発巣を検索した．原発部位としては腎盂尿管が最も強く疑われたが確定診断には至らなかった．

The number of released free cholesterol crystal emboli (fCCE) and their role during percutaneous coronary intervention (PCI) in acute coronary syndrome (ACS) have not been documented yet. Furthermore, fCCE manifesting in the coronary lumen following plaque rupture has been historically overlooked owing to the standard tissue preparation for light microscopy which uses ethanol as a dehydrating agent that can dissolve fCCE, leaving behind empty tissue. In this case report, we evaluated fCCE released during PCI for ACS and their relationship with myocardial injury and coronary artery obstruction on the H&E-stained sections by using polarised light microscopy. To our knowledge, there has been no mention of the visibility of fCCE on H&E-stained frozen polarised sections before.

Serum amyloid P component (SAP) is a member of pentraxins. Previous studies indicate that SAP exists in human atherosclerotic aortic intima and the plasma SAP levels are associated with cardiovascular disease. In this study, we characterized SAP in normal and atherosclerotic intima, investigated the source of SAP in atherosclerotic lesions, and assessed the effect of SAP on HDL function. Immunohistochemical staining and electroimmunoassay indicated that SAP is not present in normal aortic intima which excludes the possibility that SAP non-specifically deposits in aortic intima via its binding to microfibrils. Notably, SAP levels are correlated with the severity of atherosclerotic lesions. Fast protein liquid chromatography (FPLC) and Western blot analysis revealed that SAP exists in atherosclerotic lesions in multiple forms. Soluble SAP accumulates in the lesions as decamer in free or bound forms via ligand-binding to its ligand(s). Insoluble SAP accumulates in the lesions in covalent-bound forms conjugated to collagen/collagen-like substances via disulfide (-S-S-) bonds. In situ hybridization and RT-PCR analysis revealed that SAP is generated in atherosclerotic lesions, at least partly, by macrophages and smooth muscle cells in neointima. Functional analysis demonstrated that SAP associated with HDL promotes SR-BI-dependent cholesterol efflux and lipid-free SAP enhances ABCA1-dependent cholesterol efflux. In conclusion, our findings demonstrate that SAP is specifically accumulated and expressed in atherosclerotic lesions. SAP may be involved in cholesterol clearance through its role in promoting cholesterol efflux.

We report a rare case of inflammatory pseudotumor/inflammatory myofibroblastic tumor (IPT/IMT) of the heart, involving the mitral valve. A 58-year-old woman presenting with dyspnea was immediately admitted to the hospital, and found to have congestive heart failure due to the invagination of a tumor-like mass of the mitral valve. This mass arose from and involved almost the entire posterior leaflet of the mitral valve and occupied almost the entire mitral valve orifice. The tumor was a yellowish-white well-circumscribed mass with a smooth surface. The excised mass was 3.0 x 2.3 x 1.8 cm, and consisted of abundant Sudan III-positive foam cells, histiocytes, lymphocytes, plasma cells, and loosely arrayed spindle cells, in vascular-rich fibrous tissue. Immunohistochemistry showed that the spindle cells were positive for vimentin and alpha-smooth muscle actin, and negative for desmin, CD34, and human muscle actin (HHF-35), suggesting they were myofibroblastic cells. The plasma cells and lymphocytes showed no monoclonality. There were few mitotic cells, and, except for the lymphocytes, few Ki-67-positive cells. The findings suggested IPT/IMT. The 39 cardiac IPT/IMT cases appearing in the English-language literature are discussed.

SummaryA 62-year-old man presented to hospital with chest oppression. Coronary angiography revealed total occlusion of the right coronary artery and inferior myocardial infarction was diagnosed. He was treated by percutaneous coronary intervention with stenting for myocardial infarction. After four months, echocardiography revealed a huge aneurysm protruding below the inferior surface of the left ventricle. It was considered to be a pseudoaneurysm from the echocardiographic findings. The patient had no symptoms and he refused surgery, so progression of the aneurysm was monitored carefully. At seven months after revascularization, the aneurysm showed a marked increase in size, with a maximal diameter of 48mm and orifice diameter of 22mm. Accordingly, the patient agreed to undergo surgical excision. The aneurysm was resected and the defect was closed with a pericardial patch. Pathological examination revealed all of the myocardial elements in the aneurysm wall and thrombus in its lumen. In conclusion, this was a rare case of venricular subepicardial aneurysm.

An 80-year-old woman with acute myocardial infarct received intracoronary thrombolysis by a large dose of urokinase four hours after the onset of chest pain. Despite the patient having no chest pain after intracoronary thrombolysis and her general condition being stable, she died suddenly on the 4th hospital day. Autopsy revealed hemopericardium due to cardiac rupture, which occurred at the center of the transmural hemorrhagic infarction of the anteroseptal wall. The massive hemorrhagic infarction was promoted by reperfusion from thrombolytic therapy. She had also classic risk factors for cardiac rupture, such as hypertension, senility, female gender, and first acute myocardial infarct. Therefore, the present case demonstrated that hemorrhagic infarction increased the incidence of cardiac rupture.

An association between ergot-derived dopamine agonists and asymptomatic valvular heart disease in Parkinson's disease has been established. For safe use of these agonists, it is important to specify those at high risk for valvular heart disease among patients with Parkinson's disease. We performed a nested case-control study of 223 patients with Parkinson's disease. In results of multivariable logistic analyses, use of pergolide, use of cabergoline, age, male sex, and hypertension were independent significant risk factors for left-sided valvular regurgitation. In patients receiving cabergoline or pergolide, elderly (or=70 years) hypertensive patients had a markedly high risk for valvular regurgitation (odds ratio 94.5) as compared to non-elderly (70 years) patients without hypertension. The risk of valvular regurgitation caused by pergolide or cabergoline was found to be highly enhanced by comorbid hypertension or aging, suggesting that special attention should be paid when prescribing cabergoline or pergolide for those patients.

Objective This study was designed to determine the histopathological characteristics of cardiac and vascular lesions responsible for various subtypes of ischemic stroke. Methods Postmortem pathological examination was performed on 142 patients who died within 30 days of the onset of ischemic stroke in the National Cardiovascular Center, Osaka, Japan. Results The numbers of cases with autopsy-proven diagnoses of atherothrombotic, cardioembolic, and lacunar strokes, ischemic stroke of other determined causes, and ischemic stroke of undetermined cause were 17, 107, 2, 12, and 4, respectively. Thrombi that developed at the culprit plaques of the cerebral arteries were responsible for atherothrombotic stroke. In 70% of the cases with cardioembolic stroke, the presence of thrombi as potential embolic sources were confirmed in the heart or, in some cases, in the venous circulation of patients with patent foramen ovale and tetralogy of Fallot. Interpretation In most atherothrombotic strokes, fibrin- and platelet-rich thrombi of various thicknesses develop at the culprit plaques of the cerebral arteries, which are finally occluded with fibrin- and red-cell–rich thrombi (red thrombi). In most cardioembolic strokes, red thrombi generated in the heart or peripheral veins are dislodged to embolize the cerebral arteries. Ann Neurol 2008

Objective Oxygen-derived free radicals are responsible in part for reperfusion injury in globally ischemic myocardium. In this study, the efficacy for resuscitation of nonbeating donor hearts of MCI-186, a free-radical scavenger and antioxidant, was investigated in a pig transplantation model. Methods Cardiac arrest was induced by asphyxiation. After 30 minutes of global ischemia, the hearts were excised and immediately reperfused from the aortic root with normoxemic blood cardioplegia (P o 2 100 mm Hg) for 20 minutes, followed by perfusion with hyperoxemic blood (P o 2 300 mm Hg). MCI-186 (3 mg/kg) was administered into the aortic root for the first 30 minutes of reperfusion in the treated group (n = 6), and untreated hearts were used as a control group (n = 6). Transplantation was performed with the heart beating. Results Posttransplantation recovery of cardiac output, end-systolic pressure–volume ratio, and first derivative of pressure of the left ventricle in the treated group were significantly better than those in the control group. The coronary sinus–aortic root difference in malondialdehyde levels remained low throughout reperfusion in the treated group but abruptly increased after initiation of oxygenated blood perfusion in the control group. The MCI-186–treated hearts showed low degree of edema and well-preserved ultrastructure with normal-appearing organelles, whereas the untreated hearts had marked swelling of mitochondria and scant glycogen granules. Conclusion MCI-186 exerts a cardioprotective action at least partly by inhibition of lipid peroxidation. Antioxidant therapy at the initial reperfusion is essential to successful resuscitation of nonbeating hearts by continuous myocardial perfusion.

Background In patients with cardiovascular disease (CVD), renal dysfunction is a risk factor for the prognosis, but substantial evidence is still lacking about the relationship between clinical characteristics and renal histology. The aim of our study was to evaluate the relationship between the extent of renal parenchymal damage, renal artery stenosis (RAS) and clinical characteristics in autopsy subjects with stroke. Methods During the 17-year period 1980-1997, 2167 subjects were autopsied at the National Cardiovascular Center. We studied retrospectively all the autopsy cases aged 40 years and older who had a history of stroke. Thus, 346 subjects remained and they were classified into two groups. Thirty-six subjects had RAS (group A). Three hundred and ten subjects had no RAS, and we randomly chose 102 subjects among them (group B). We evaluated renal parenchymal damage using a semi-quantitative chronic damage score. Results The average overall chronic damage score was significantly higher in the stenosed kidneys of group A than in the non-stenosed kidneys of group B (9.0+/-2.6 vs 7.0+/-2.7). The contralateral kidneys of group A had a tendency to have milder renal damage than stenosed kidneys. Furthermore, the total score was higher in the subjects with hypertension, diabetes mellitus, proteinuria, renal insufficiency and CVD than in the subjects without such complications. The total score had a significant association with RAS, proteinuria, renal insufficiency, CVD and weight of the kidney. Conclusions In autopsy subjects with stroke, we demonstrated that co-existing renal parenchymal damage was more severe in the subjects with RAS, hypertension, diabetes mellitus, proteinuria and renal insufficiency than those without such complications. The presence of RAS, impaired renal function and proteinuria was closely correlated with the severity of renal parenchymal damage.

This paper reports the results of the largest autopsy-based comparative study of atherosclerotic lesions between young Japanese and Americans, aged 15-34 years and autopsied between 1987 and 1995, by analyzing the data from the Japanese second nation-wide study of atherosclerosis and Pathobiological Determinants of Atherosclerosis in Youth study in the USA. In the right coronary arteries, in Japanese, fatty streaks were well established in the second decade of life with very little increase in the remaining age groups up to age of 34 years. In contrast, in American subjects, the average percentage of surface involvement of fatty streaks and raised lesions proceeded steadily with age without an obvious plateau throughout the 20-year period. The extent and prevalence of the raised lesions was much greater in Americans than in Japanese in 25-29 and 30-34-year age groups. Moreover, the rate of progression of raised lesions was much more rapid in Americans. These findings are in keeping with the fact that coronary heart disease (CHD) death rates are much higher in the USA than in Japan. In light of data showing that the risk factor profiles for CHD have become very similar between the two countries, these differences need to be explained.

Background: The aim of this study was to evaluate the clinical features of patients with congenital complete heart block (CCHB) who developed dilated cardiomyopathy (DCM) after pacemaker implantation (PMI) and to determine factors predicting DCM development. Method: A total of 15 patients were reviewed retrospectively. They were classified into two groups, one consisted of four patients who were diagnosed as having CCHB in utero or at birth and who developed DCM after PMI (DCM group) and the other consisted of 11 patients who did not (non-DCM group). Results: Maternal autoantibodies were found in two of the DCM group and in five of the non-DCM group. Perfusion defects in myocardial imaging were detected in all DCM patients and in five non-DCM patients. DCM developed 2 to 43 months after PMI and three DCM patients died of heart failure 7 to 48 months after PMI. In pathological studies, endocardial or interstitial fibrosis was present in all DCM patients and in one of two in the non-DCM group. No significant differences between the two groups were found in age at PMI, atrial or ventricular rate, end-diastolic dimension and ejection fraction of the left ventricle before PMI, and width of QRS after PMI. Conclusion: Although it was suspected that the patients with CCHB had myocardial involvement before PMI, there was no significant factor predicting the risk of DCM after PMI. In addition to cardiac rhythm abnormalities, careful attention should be paid to cardiac function in CCHB patients after PMI.

BACKGROUND The present study examined whether a bioengineered polyglycolic acid cloth (PGAC) impregnated with bone marrow cells (BMC) improved the function and angiogenesis of the infarcted heart. METHODS AND RESULTS The coronary artery was ligated in Lewis rats and the infarcted area was covered with a PGAC in group 1 (n=8), with a PGAC containing basic-fibroblast growth factor (b-FGF) in group 2 (n=11) and a PGAC containing b-FGF and freshly isolated BMC in group 3 (n=10). In addition, BMC derived from transgenic mice expressing green fluorescent protein (GFP)-BMC were seeded into a PGAC, which was sutured over the infarcted area of C57BL/6 mice (n=5). In the rat study, developed and systolic pressures, dp/dt max and dp/dt min) were the highest in group 3, as were the capillary density in the PGAC and infarcted area. In the mouse study, there were few GFP-BMC in the PGAC, but none in the infarcted area. CONCLUSIONS A PGAC with BMC improved cardiac function by inducing angiogenesis without migration of BMC. Freshly isolated BMC work as angiogenic inducers and a PGAC is useful as a "drug delivery system".

Background Our recent study showed that granulocyte-colony stimulating factor (G-CSF) promoted bone-marrow cells (BMC) to migrate into the infarcted heart and that they differentiated into cardiomyocytes. However, we still do not know to what degree bone-marrow-derived cardiomyocytes contribute to myocardial regeneration after injury. In this study, we verified the proportional contribution of cells from bone marrow (BM) and from non-bone marrow (n-BM) in regenerating neomyocardium after myocardial infarction. Methods Eight C57BL/6 mice were irradiated (900 cGy), and green fluorescent protein (GFP) mouse-derived BMCs (GFP-BMC, 1 × 10 6 cells) were injected. Four weeks later, the left descending coronary artery was ligated. Recombinant human G-CSF (200 μg/kg/day, 8 days) was injected. At 4 weeks after ligation, hearts were fixed for histology. We calculated the proportions of cardiomyocytes derived from BM and n-BM after taking the chimeric rate into consideration. Results The chimeric rate was 54.6% ± 5.9%. At the infarcted border area, the total cell number was 1000.3 ± 56.5/mm 2 , and mobilized BM-derived GFP-BMC was 103.3 ± 13.1/mm 2 . After compensation with the chimeric rate, we found BM-derived troponin I-positive cells at 23.9 ± 4.1/mm 2 , nestin-positive cells at 12.9 ± 2.6/mm 2 , and Ki67-positive cells at 18.3 ± 2.6/mm 2 , respectively. We found significant differences in the contribution of troponin I-(6.7% ± 1.7% vs 93.3% ± 1.7%), nestin- (2.4 ± 0.5 vs 97.6 ± 0.5), and Ki67-positive (3.9 ± 1.0 vs 96.1 ± 1.0) cells derived from BM and n-BM. Conclusions Bone marrow was one of the origins of regenerated cardiomyocytes; however, the contribution of cells from BM was very small compared with those of n-BM origin in the infarction model.

The proliferation of vascular smooth muscle cells (VSMCs) and alterations of their phenotype are implicated in the pathogenesis of atherosclerosis. Arterial wall injury induces the expression of proto-oncogenes, leading to the proliferation of VSMCs. In particular, c-Myc and c-Myb play a central role in cell cycle progression and are essential for VSMC replication. The protooncogene Pim-1 cooperates with c-Myc and enhances the transcriptional activity of c-Myb in hematopoietic cells, suggesting that Pim-1 is involved in cell cycle regulation. The aim of this study was to examine the possible involvement of Pim-1 in VSMC proliferation. Pim-1 was substantially induced in neointimal VSMCs of balloon-injured rat carotid arteries, and in vivo infection with a dominant negative Pim-1-expressing adenovirus (Ad-DN-Pim-1) markedly suppressed neointima formation and cell cycle progression in the balloon-injured arteries. In cultured VSMCs, treatment with serum or H(2)O(2) induced Pim-1 expression, and H(2)O(2)- or serum-stimulated cell cycle progression and DNA synthesis were almost completely inhibited by DN-Pim-1 overexpression. Furthermore, we performed immunohisto-chemical staining for Pim-1 in human thoracic aortas and coronary arteries obtained from six individuals at autopsy and found that Pim-1-positive cells are observed predominantly in the thickened intima of the aortas and coronary arteries. To the best of our knowledge, this is the first report showing Pim-1 expression in rodent and human arterial walls. To summarize, Pim-1 expression was observed in the neointima of balloon-injured rat carotid arteries and in human thoracic aortas and coronary arteries showing intimal thickening, and the specific inhibition of Pim-1 function markedly suppressed neointima formation after balloon injury and the proliferation of cultured VSMCs, suggesting that Pim-1 plays a role in VSMC proliferation.

Objective: We traced and evaluated bone marrow-derived cells after granulocyte-colony stimulating factor (G-CSF) treatment in the doxorubicin-induced cardiomyopathic heart in the time course. Methods: C57BL/6 male mice received doxorubicin (15 mg/kg, i.p.). At 1 week after administration of doxorubicin, the mice were irradiated (900 cGy) followed by transplantation of bone marrow cells (BMT) derived from transgenic mice expressing green fluorescent protein (GFP) (1×106) via a tail vein (BMT). G-group (n=22) received G-CSF (50 µg/kg/day×8 days, s.c.) after BMT, while C-group (n=17) received saline. At 4 and 7 weeks after BMT, heart sections were fixed to evaluate bone marrow-derived GFP cells (BMD-GFP) with immunostaining for Troponin I (TnI), atrial-natriuretic peptide (ANP), connexin 43, von Willebrand factor, and Ki67. Result: There were migrated BMD-GFP in the whole heart of all animals. In the time course, migrated BMD-GFP increased in G-group. At 7 weeks the number of migrated BMD-GFP in G-group (56.2±15.6/HPF) was larger than that in C-group (18.9±10.7/HPF) (p

Cell transplantation is a promising therapy for treating end-stage heart failure. Bone marrow mononuclear cells (BMMNC) have been used to enhance angiogenesis in ischemic heart disease. However, the effect of BMMNC transplantation in non-ischemic dilated cardiomyopathy is unknown. In this study, we evaluated the efficacy of BMMNC transplantation in doxorubicin-induced cardiomyopathy in a rat model.Doxorubicin (15 mg/kg, IP) was introduced into 52 Lewis rats. They were divided into 3 groups at 4 weeks after injection: transplant group (TX, BMMNC [1 x 10(6)] implantation, n = 18), control group (CN, saline injection, n = 18), and sham group (SH, thoracotomy, n = 16). At 4 weeks after surgery, we used echocardiography to measure systolic left ventricular diameter (LVDs), diastolic left ventricular diameter (LVDd), fractional shortening (FS), and left ventricular wall thickness/LVDs. We used a Langendorff apparatus to measure systolic, diastolic, and developed pressures. We used radioimmunoassay to measure circulating atrial natriuretic peptide concentration, and we performed histologic study, including electron-microscopic study.Left ventricular wall thickness/LVDs in the TX group was the largest of all groups (p0.05). Systolic and developed pressures in the TX group were the greatest (p0.005). Systolic left ventricular diameter, FS, and end-diastolic pressure in the TX group were smaller than in the SH group (p0.05). These cardiac parameters did not differ significantly between TX and CN groups, but secondary changes (decreased heart weight, developed ascites, and increased atrial natriuretic peptide concentration) caused by doxorubicin-induced heart failure were most attenuated in the TX group. In the TX group, vascular density was greatest (p0.05) in the left ventricular free wall and in the septum. In addition, electron microscopy showed that myocardium in the TX group was most maintained.Bone marrow mononuclear cell transplantation had beneficial effects in doxorubicin-induced cardiomyopathy.

Objective To elucidate epidemiologic and clinical manifestations of Japanese patients with giant cell arteritis (GCA), the first nationwide survey for GCA was conducted in 1998 in Japan. Methods The first questionnaire on GCA for patients treated in 1997 was sent to 10,717 medical departments in Japan. A total of 177 patients were reported. Among the 177 patients, 66 GCA patients with detailed clinical and epidemiologic features on second survey were analyzed. Results Prevalence in patients 50 years of age and older in 1997 was 1.47 per 100,000 population in Japan. The average age at onset was 71.5 years old. The male:female ratio was 1:1.7. The association with permanent and complete visual loss (6.5%), jaw claudication (15.2%), and polymyalgia rheumatica (PMR) (30.3%) were low in frequency compared with those reported from other countries. All patients were treated with corticosteroids. Only 3 (4.5%) patients were reported as deceased due to other causes. Conclusion The prevalence of GCA in Japan was revealed to be extremely low compared with other countries. Clinical findings of permanent and complete visual loss, jaw claudication, and PMR were infrequent among Japanese patients with GCA.

Hypercholesterolemia affects not only the coronary artery, but also the aortic root, particularly the aortic valve. Aortic stenosis is critical in the prognosis for most patients with homozygous familial hypercholesterolemia (FH) and some heterozygous FH patients who result in aortic valve replacement (AVR). Histopathological examination of their valves shows lipid deposition, inflammatory cell infiltration and calcification in the aortic cusps. These pathological findings are common in non-FH patients with AVR. In homozygous FH patients, the aortic valves are injured by extreme hypercholesterolemia in a relatively short period of time, whereas in heterozygous FH patients with additional risk factors, the damage to the valves occurs over an intermediate time period. In the non-FH population with several risk factors, an underlying raised serum cholesterol level results in gradual impairment over a number of years. Aortic valvular dysfunction caused by hypercholesterolemia, which we termed hypercholesterolemic valvulopathy is recognized to be a life-threatening complication as the primary clinical characteristic of malignant atherosclerosis.

✓ A 58-year-old woman harboring a partially thrombosed giant aneurysm of the vertebral artery (VA) presented with lower cranial nerve palsies and cerebellar ataxia. The authors initially attempted to reduce the mass effect by obliterating the lumen of the aneurysm as well as by trapping of the parent artery with coils. Although there was no angiographically demonstrated evidence of filling, the aneurysm continued to enlarge. Magnetic resonance imaging revealed a marked enhancement around the packed coils close to the neck of the aneurysm. Aneurysmectomy and removal of the coils were performed and resulted in an almost complete cure of the patient's symptoms. Interestingly, at the time of resection, a marked development of vasa vasorum on the occluded VA and the neck of the aneurysm was noted. When the occluded VA was cut, there was blood oozing through the coils packed within its lumen on the side where the aneurysm lay. Histological examination showed the presence of inflammatory cells and neovascularization of a partially organized thrombus around the packed coils in both the aneurysm and occluded VA. The proliferation of vasa vasorum was also recognized histologically. This unique case provides insight into the growth mechanisms of a partially thrombosed giant aneurysm after an apparently complete occlusion by endovascular treatment, especially the role of vaso vasorum on the occluded parent artery in the dynamic process of neovascularization in the incomplete organization of thrombus around the packed coils.

A 73-year-old man with a history of bronchial asthma and atrial fibrillation was admitted to our hospital because of dyspnea and back pain. Blood analysis revealed a marked increase in total blood cell and eosinophil counts. The creatine kinase and creatine kinase-MB increased slightly. The ECG demonstrated significant ST-segment depression that mimicked acute posterior myocardial infarction. Emergent coronary angiography showed no stenotic lesions. The histological findings in endomyocardial biopsy showed thickened endocardium associated with significant eosinophilic infiltration, which was compatible with Loffler's endocarditis. After the administration of prednisolone, the patient's general condition, eosinophilia, ECG abnormalities, and histological findings were improved dramatically. The endomyocardial biopsy in the acute phase was helpful for diagnosis and therapeutic decision-making.

Introduction : Tissue factor plays a key role in the extrinsic coagulation pathway and is induced by inflammatory cytokines. Atrial myocarditis has been detected recently in some patients with lone atrial fibrillation. Virchow's triad of low blood flow, hypercoagulability, and endothelial dysfunction, enhances thrombus formation. The present study was designed to elucidate the role of endothelial dysfunction in thrombogenesis associated with nonvalvular atrial fibrillation. Material and methods : We investigated tissue factor expression in the endothelia of left atrial appendages obtained from seven patients with nonvalvular atrial fibrillation and cardiogenic thromboembolism. Tissues were divided into 7–13 sections and compared with control specimens from four patients who died of noncardiac events. Expression of tissue factor, von Willebrand factor and tissue factor pathway inhibitor was evaluated by immunohistochemistry. Results : Histopathologically, inflammatory cells infiltrated the endocardium and all seven patients showed features of persistent myocarditis. Activated T cells [15.3±9.4 cells/high power field (HPF, mean±S.D.) vs. control 2.2±4.4/HPF ( P =0.0294)] and a few macrophages [5.1±8.4 cells/HPF vs. control 2.4±3.5 cells/HPF ( P =NS)] infiltrated the endocardium. Tissue factor was overexpressed in the endothelia particularly in tissues containing inflammatory cells and denuded matrix of the endocardium, compared with the control group. Von Willebrand factor, but not tissue factor pathway inhibitor, was also overexpressed in these tissues. Conclusion : Tissue factor expression induced by local inflammation is involved in the pathogenesis of thrombosis in patients with nonvalvular atrial fibrillation.

Cerebral amyloid angiopathy (CAA) has two major clinical manifestations: intracerebral hemorrhages and ischemic lesions. Among these, the lobar type of intracerebral hemorrhage (ICH) is a well-known clinical manifestation, while the CAA-related diffuse deep white matter degeneration known as leukoencephalopathy is thought to be rare. The characteristics of CAA-related leukoencephalopathy are still incompletely understood, and the relationship between lobar ICH and leukoencephalopathy in patients with CAA has not been properly clarified. The main purpose of this study is to elucidate the clinical and histopathological features of CAA-related lobar ICH and leukoencephalopathy in order to determine whether the degree of deep white matter degeneration parallels the severity of CAA-associated vasculopathies that lead to vascular wall rupture. We studied 64 Japanese patients with histopathologically proven amyloid beta protein (A beta) type CAA presenting with lobar ICH (52 biopsy and 12 autopsy). In this study, a total of 106 hematomas were observed. CAA-related cerebral hemorrhages tend to occur recurrently and multifocally. Multiple simultaneous labor hemorrhages occasionally developed (9.4%). CAA-related ICH in the sixth decade was not rare (14.1%). Although most patients suffered relapsing and/or multiple severe ICH, no patient in our series presented with diffuse leukoencephalopathy. In conclusion, A beta type cerebrovascular amyloid deposition causes recurrent, multifocal, and often multiple simultaneous ICH even in relatively younger elderly patients, but rarely produces diffuse leukoencephalopathy. This suggests that CAA-associated vasculopathies that cause vascular wall rupture do not always lead to ischemic deep white matter degeneration, and that there may be another unknown pathogenetic mechanism producing the latter CAA-related white matter lesion.

The mortality rate due to rupture of aortic dissection and aortic aneurysm is approximately 90%. Acute aortic rupture can be fatal prior to hospitalization and has proven difficult to diagnose correctly or predict. The in-hospital mortality rate of ruptured aortic aneurysm ranges from 53 to 66%. Emergency surgical and endovascular treatments are the only options for ruptured aortic dissection and aortic aneurysm. No method of systematic early detection or inspection of vessel injury is available at the prevention stage. Regardless of the improvement in many imaging modalities, aortic diameter has remained a major criterion for recommending surgery in diagnosed patients. Previous reports have suggested a relationship between vulnerable plaque and atherosclerotic aortic aneurysm. Non-obstructive angioscopy is a new method for evaluating intimal injury over the whole aorta. It has been used to identify many advanced atherosclerotic plaques that were missed on traditional imaging modalities before aneurysm formation. Non-obstructive angioscopy has shown that atherosclerosis of the aorta begins before that of the coronary artery, which had been noted on autopsy "in vivo". Strong or repetitive aortic injuries might cause sudden aortic disruption. Aortic atheroma is also a risk factor of stroke and perivascular embolism. Detecting aortic vulnerable atherosclerotic plaque on non-obstructive angioscopy may not only clarify the pathogenesis of acute aortic rupture and "aortogenic" thromboemboli and atheroemboli but also play a role in the pre-emptive medicine.

Atrial fibrillation (AF) is a risk factor for cerebral embolism, with the left atrial appendage (LAA) being considered as the source of emboli. However, the relationship between the histologic properties of LAA thrombi and the occurrence of cerebral embolism is not known. Seventy-six hearts from patients who died within 1 month after cerebral embolism were studied at autopsy. Patients were grouped according to the presence of AF and the presence of valvular disease (VD). We determined whether the LAA thrombi adhered to the trabecular region or the remainder of the LAA. LAA thrombi were grouped into three stages: a fresh stage in which thrombi consisted of fibrin and platelets, an organizing stage in which angiogenesis was observed in the thrombi, and an organized stage in which endothelial cells covered the surface of the thrombi. The AF+/VD– group included 19 patients (25.0%), the AF+/VD+ group 8 (10.5%), the AF–/ VD– group 37 (48.7%), and the AF–/VD+ group included 12 patients (15.8%). LAA thrombi were observed in 15 patients (78.9%) in the AF+/VD– group, and all of the thrombi adhered to the trabecular region. Thrombi in the fresh and the organizing stages were observed in 10 patients (66.7%). Patients in the AF+/VD– group accounted for about 25% of the cases of cerebral embolism. All of these thrombi were attached to the trabecular region, and about 70% of them could represent an embolic source.

OBJECTIVES We hypothesized that the plasma atrial natriuretic peptide (ANP) level reflects atrial degenerative change and may predict the outcome of the maze procedure. BACKGROUND Although a larger preoperative left atrial dimension and longer duration of atrial fibrillation (AF) have been reported in patients with persistent AF than in those with sinus rhythm (SR), these individual factors were not enough to predict the outcome of the maze procedure. METHODS Preoperative plasma ANP levels were measured in consecutive 62 patients who underwent the Kosakai's modified maze procedure. Moreover, we performed histological and molecular biological examinations in the resected left atrial tissues. RESULTS The preoperative plasma ANP was lower in the AF group (n = 13) than it was in the SR group (n = 49) (p < 0.001). Multiple logistic regression analysis revealed that duration of AF and plasma ANP were independently associated with postoperative cardiac rhythm. Among 41 patients with a higher plasma ANP or shorter duration of AF than the median value, SR was restored in 95% of patients. In contrast, in 21 patients with a lower plasma ANP and a longer duration of AF than the median value, SR was restored only in 48% of patients. Histological examination revealed that the collagen volume in the left atrial tissue was higher in AF than it was in SR and inversely correlated with plasma ANP. In addition, the messenger RNA expressions of ANP, collagen type I and type III were lower in AF than they were in SR. CONCLUSIONS These results suggest that a combination of plasma ANP and/or duration of AF may predict the success rate for the maze operation. Advanced atrial degenerative change may result in a decrease of atrial ANP secretion.

The purpose of this study was to clarify whether or not a change in the clinical characteristics of cardiac myxoma has occurred during the past 2 decades. The clinical records of 57 patients (22 men, 35 women; age, 52±14 years) with myxoma that had been surgically treated between May 1978 and July 1997 at the National Cardiovascular Center in Japan were reviewed. All myxomas were discovered by transthoracic echocardiography. They were divided into an early group (n=30) treated in the first decade (1978-1987) and a late group (n=27) treated in the second decade (1988-1997). The incidence of myxoma, patient characteristics, preoperative symptoms and echocardiographic features did not differ between the 2 groups. In contrast, the maximal dimensions of myxoma in the early group were significantly larger than those in the late group (6.3 ±2.7 cm vs 4.3±1.3 cm, p=0.012). The weight of myxoma in the early group tended to be heavier than that in the late group (76±80 g vs 25±18 g, p=0.054). The incidence of patients with asymptomatic myxoma also tended to increase in the late group (7% vs 26%, p=0.07). Although there was no difference in the incidence of myxoma, smaller and asymptomatic myxomas were more frequent during the last decade, probably as a result of the development of cardiac imaging, particularly echocardiography. (Circ J 2002; 66: 1008 - 1013)

Background Ghrelin is a novel growth hormone (GH)-releasing peptide, isolated from the stomach, that may also cause a positive energy balance by stimulating food intake and inducing adiposity. We sought to investigate the pathophysiology of ghrelin in the cachexia associated with chronic heart failure (CHF). Methods and Results Plasma ghrelin was measured in 74 patients with CHF and 12 control subjects, together with potentially important anabolic and catabolic factors, such as GH and tumor necrosis factor (TNF-α). Patients with CHF were divided into two groups, those with cachexia (n=28) and those without cachexia (n=46). Plasma ghrelin did not significantly differ between all CHF patients and controls (181±10 versus 140±14 fmol/mL, P =NS). However, plasma ghrelin was significantly higher in CHF patients with cachexia than in those without cachexia (237±18 versus 147±10 fmol/mL, P r =0.28, P r =0.31, P r =−0.35, P Conclusions Plasma ghrelin was elevated in cachectic patients with CHF, associated with increases in GH and TNF-α and a decrease in body mass index. Considering ghrelin-induced positive energy effects, increased ghrelin may represent a compensatory mechanism under catabolic-anabolic imbalance in cachectic patients with CHF.

Calcitonin receptor–like receptor/receptor activity–modifying protein 2 (CRLR/RAMP2) and CRLR/RAMP3 complexes have been reported to be specific adrenomedullin (AM) receptors. In the present study, we evaluated the pathophysiological significance of renal AM and its receptor system in aortocaval shunt (ACS) rats. Renal AM levels were measured serially during 5 weeks after the operation. Renal gene expressions of AM, CRLR, RAMP2, and RAMP3 were measured at 2 weeks (decompensated phase) and 5 weeks (compensated phase) after the operation. Immunohistochemical localizations of renal AM were also evaluated. Furthermore, the relations between urinary sodium excretion (UNaV) and renal AM levels were evaluated. Renal AM levels were higher in ACS than in control animals only at 1, 2, and 3 weeks after the operation. At 2 weeks after the operation, renal AM mRNA expression was also higher in ACS than in control animals. CRLR, RAMP2, and RAMP3 mRNAs were expressed in the kidney, but there were no differences between the 2 groups. Immunohistochemistry revealed the positive AM immunostaining within the renal tubular cells, and it was more intense in ACS than in control animals. There were significant correlations between UNaV and renal AM levels. At 5 weeks after the operation, there were no differences in mRNA levels of AM, CRLR, RAMP2, and RAMP3 between the 2 groups. There was a significant correlation between UNaV and medullary AM levels. The present findings suggest that increased renal AM levels in decompensated heart failure, presumably due to increased AM production in renal tubules, in part, are involved in the regulation of sodium excretion.

Tissue factor pathway inhibitor (TFPI) is a protease inhibitor that regulates tissue factor (TF)--initiated coagulation. We report here that cardiomyocytes express TFPI and the expression could be increased by Interleukin-1(IL-1beta). The TFPI expression in cardiomyocytes was confirmed by Northern blotting with rat cardiomyocytes and also by immunostaining with anti-TFPI antibody on human heart specimens from patients either with sarcoidosis, myocarditis or myocardial infarction. The regulation of TFPI expression in cardiomyocytes differs from that in endothelial cells because TFPI expression is not induced in human endothelial cells by IL-1beta.

Staged coronary embolization, causing myocardial microinfarctions, has been shown in dogs and sheep to cause chronic ischemic heart failure (HF) that resembles the hemodynamics of the human condition. However, its histopathological basis remains unclear. We examined the hypothesis that the ventricular remodeling seen in such sheep resembles the histopathology of human ischemic cardiomyopathy (ICM). Understanding the pathophysiology of this model will determine its place in the development of treatment strategies for HF. Global left ventricular (LV) damage resulting in HF was induced by staged coronary embolization in 11 sheep. Six others served as controls (normal control, NC). In HF sheep, the heart was harvested 6 months after LV ejection fraction (EF) had stabilized at35%. Histopathological profiles were compared in biventricular transverse sections at midpapillary level using computed image analysis. LV end-diastolic volume increased in the HF group from 84.9+/-29 to 122.4+/-30.3 ml (n=11, P.05), but myocytes across the LV wall in noninfarcted zones decreased (435.7+/-38.2 NC; 297.8+/-48.4/unit area HF; n=11, P.0001) as did myocyte nuclear density (990.5+/-51.5 NC; 677.5+/-121.1/mm(2) HF, n=11, P.0001). In contrast, LV replacement and interstitial fibrosis increased as did myocyte diameter in noninfarcted zones: 0.1+/-0.1 to 6.2+/-4.5% (P=.0049); 2.0+/-1.0 to 7.6+/-4.9% (P=.0149); and 10.0+/-0.5 to 15.9+/-2.2 microm (P.0001), respectively. Although LV myocyte nuclear length increased (10.2+/-1.0 NC; 12.2+/-0.9 microm HF, n=11, P=.0006), right ventricular (RV) myocyte nuclear density and length did not alter. In this ovine chronic HF model, LV dilation and interstitial and myocyte remodeling resemble human ICM.

We studied whether differences exist between hearts having rheumatic mitral valves and those having myxomatous mitral valves, in functional, geometrical, and mass changes in the left ventricle after mitral valve replacement.Patients who underwent mitral valve replacement without preservation of annular-papillary continuity for pure mitral incompetence were classified into rheumatic and myxomatous based on valvular histopathology. Echographic data measured before surgery was compared to that about 3 weeks after surgery.In the rheumatic group, ejection fraction decreased from 57.5 +/- 10.8 to 47.7 +/- 12.0, indexed left ventricular internal dimension in systole (mm/m2) from 24.7 +/- 6.8 to 20.7 +/- 6.2 (P = 0.0001), and left ventricular mass index (g/m2) from 205 +/- 55 to 138 +/- 54 (P = 0.0002). In the myxomatous group, ejection fraction decreased from 60.4 +/- 11.6 to 39.7 +/- 14.5 (P = 0.0001), indexed left ventricular internal dimension in systole from 24.2 +/- 5.6 to 23.1 +/- 5.5, and left ventricular mass index from 195 +/- 83 to 111 +/- 72 (P = 0.0004). Mean wall thickness index and relative wall thickness showed significant differences between the two groups postoperatively but no significant difference preoperatively.Hearts dilated due to chronic mitral incompetence respond differently after valvular replacement with total chordal excision depending on whether a rheumatic or myxomatous mitral valve is involved.

The aim of this study was to analyze the cellular composition of the arterial wall in Takayasu's disease and to investigate the contribution of the various cell types to the immunoinflammatory processes and degenerative alterations of the vessel wall in this disease. Specimens of aorta were obtained at operation from 10 patients with Takayasu's arteritis. The duration of disease ranged from 2 months to 13 years. Immunohisto chemical investigation was carried out using the antibodies CD3 (to identify T-cells), CD20 (B-cells), S-100 (dendritic cells), CD68 (macrophages), CD15 (granulocytes), von Willebrand factor (endothelial cells), and alpha-smooth muscle actin (smooth muscle cells). All specimens showed distinctive histologic features of Takayasu's arteritis and contained inflammatory infiltrates, but the degree of their accumulation within the aortic wall varied. Inflammatory infiltrates within the deep part of the intima, around areas of neovascularization and within the adventitia contained T-cells colocalizing with dendritic cells. Nodules formed by large numbers of intermingling T-cells and B-cells enriched with dendritic cells were observed in the adventitia. Massive accumulation of granulo- ( continued on next page) cytes and their destruction within the adventitia were prominent in all cases. This is the first study that establishes the presence of dendritic cells and granulocytes in Takayasu's disease. Dendritic cells are probably involved in the immunoinflammatory processes through their interaction with T-cells and B-cells. The present observations may help understanding of the pathogenesis of Takayasu's disease.

Two monoclonal antibodies that specifically detect human prion protein (PrP) were developed. The epitope of both antibodies was mapped using fusion proteins of glutathione-S-transferase and PrP peptides to the C-terminal region encompassing the polymorphic 219 residue. The antibodies recognized human PrP with 219Glu but not that with 219Lys. The unique property of the antibodies was utilized to determine the allelic origin of abnormal PrP deposited in the brain of a patient with Gerstmann-Straussler syndrome (GSS) with 102Leu/219Lys encoded by the same allele. Abnormal PrP was exclusively of mutant allelic origin, suggesting that 219Lys may be permissive to the formation of abnormal PrP in GSS. The antibodies may help to explore the relationship of 219Glu/Lys polymorphism to the pathogenesis of human prion diseases.

The present study was undertaken to examine the cellular composition of the aortic wall in Takayasu's arteritis and to investigate the association of different cell types in the immuno-inflammatory reactions of this disease. Specimens of aortic wall affected by Takayasu's arteritis were obtained from 10 patients (five male, five female), aged 32 to 68 years (mean 49.5 years) at elective operation. The mean duration of disease was 6.5 years (range 2 months to 13 years). Specimens were embedded in paraffin and the sections stained with antibodies to CD3 (to identify T cells), CD20 (B cells), S-100 (dendritic cells), CD15 (granulocytes), CD68 (macrophages), alpha-SMA (smooth muscle cells) and von Willebrand factor (endothelial cells). Immunohistochemical examination demonstrated that all specimens showed histological alteration with the replacement of the muscular and elastic layers of the media and adventitia by dense fibrous tissue, and were characterized by varying degrees of inflammatory cell infiltration. In five cases, inflammatory nodules consisting of numerous T cells and B cells were observed in the adventitia. Within the inflammatory nodules, as well as around areas of neovascularization in the deep portion of the intima, lymphocytes were co-localized with dendritic cells. In addition, in the adventitia, the accumulation of a large number of granulocytes was observed. The present study demonstrates that immune inflammation is a typical feature of Takayasu's disease, and that the interactions between dendritic cells and lymphocytes may be important in the control of the immune reactions in this vascular pathology.

BACKGROUND: Primitive neuroectodermal tumors (PNETs) are very rare. Malignant tumors of the cerebrum in young individuals are composed predominantly of undifferentiated cells, with moderate differentiation along either neuronal or glial lines. To our knowledge, cerebral PNETs in adults are extraordinarily rare and have been reported in only 11 cases, with little cytologic documentation in the literature. The cytopathologic, immunohistochemical and ultrastructural features of cerebral PNET arising in an adult male are presented. CASE: A cystic tumor, on computed tomography and magnetic resonance imaging, arose from the left frontal lobe in a 39-year-old man and contained histopathologic features of PNET. Specimens obtained from surgery revealed the presence of an undifferentiated type of PNET with moderate neuronal and glial differentiation and mild characteristic findings of peripheral PNET. The cytologic and histologic specimens showed evidence of a scattered pattern of blastic and undifferentiated tumor cells and a neural arrangement with Homer-Wright-like rosettes. Immunohistochemically, the tumor cells were glial fibrillary acidic protein, neuron-specific enolase, synaptophysin and CD-99 positive and epithelial membrane antigen, S-100 protein and vimentin negative. Ultrastructurally, neither microtubular structures nor intermediate filaments, except neurosecretory granules, were found in the tumor cells. CONCLUSION: Both immunohistochemical and ultrastructural studies on cytologic and histologic slides were important for the diagnosis of PNET because of establishing not only undifferentiated tumor cells but also neural and glial differentiation.

Striatocapsular infarction is a distinct form of stroke, but few histopathological studies have been performed concerning acute lesions. We report the postmortem findings of a patient with an infarct who died shortly after onset. A 72-year-old man died of acute myocardial infarction 6 days after the onset of left-sided striatocapsular infarction. Autopsy revealed thrombus formation of the left middle cerebral artery (MCA) trunk. The lateral striate arteries irrigating the area of the infarct branched off distal to the arterial segment occluded with a thrombus. The cortical vessels were perfused by leptomeningeal collaterals. This report histopathologically confirmed thrombus formation of the MCA resulting in striatocapsular infarction.

Cardiac transplantation has been established as a therapeutic strategy for patients with end-stage heart failure. In Japan, however, cardiac transplantation has not been performed since the first case in 1968, and even now, after legislation for the approval of brain death was passed in 1997, it is still not performed regularly. Following long and steady efforts to enlighten Japanese society about the concept of brain death and the importance of organ transplantation, the first cardiac transplantation under the new legislation was successfully performed at Osaka University Hospital on February 1999. The patient was 47-year-old male in the dilated phase of hypertrophic cardiomyopathy who had been supported with an implantable left ventricular assist device. This article briefly reviews the situation prior to the first case of cardiac transplantation under the new legislation and discusses the current status of the therapy in Japan.

Pathologically, restenotic lesions after stenting were investigated by use of atherec tomized 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 α-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.

Cases of hypoplastic left heart syndrome (HLHS) were studied angiographically in 18 patients and pathologically in 22 patients. They were divided into three subgroups according to the morphological features of the left heart: mitral atresia with aortic atresia (MA/AA), mitral stenosis with aortic atresia (MS/AA) and mitral stenosis with severe aortic stenosis (MS/AS). Patients with MS/AA had a significantly lower right ventricular end-diastolic volume index and more hypokinesis of the right ventricular posterior wall than those with MA/AA. MS/AA not only increased the thickness of the left ventricular posterior wall and interventricular septum but also increased endocardial thickness compared with MA/AA. Myocardial histology revealed more frequent abnormal findings such as myocardial necrosis, calcification and interstitial fibrosis in the mitral stenosis groups (i.e., MS/AA and MS/AS) than in MA/AA. Right ventricular function appeared to be greatly influenced by left heart structure. The presence of larger left ventricular muscle bulk and frequent myocardial damage seen in MS/AA seems disadvantageous to right ventricular end-diastolic volume and right ventricular wall motion.

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.

The determination of the malignancy of an endometrioid adenocarcinoma arising in the lower uterine segment (LUS) is difficult because of the high degree of differentiation of adenocarcinoma. The cytopathological and immunohistochemical features of endometrioid adenocarcinoma arising in the LUS of a young adult female are presented. The preoperative cytopathological examination of a 27-yr-old female could not enable an accurate diagnosis of malignancy. Hysterectomy specimens revealed the presence of an endometrioid-type adenocarcinoma with minimal atypia and myometrial invasion, which was located in the LUS. This tumor was consistent with a histological diagnosis of endometrioid minimal-deviation adenocarcinoma (MDA). Immunohistochemically, the tumor's glands were p53-, proliferating cell nuclear antigen-, and carcinoembryonic antigen-positive, and estrogen receptor-, progesterone receptor-,and vimentin-negative. The cytological and surgical specimens showed a remarkable association of squamous metaplasia. Although cytopathological difficulties in determining malignancy of MDA endometrioid adenocarcinoma arising in the LUS are well-known, the following features worth noting include: 1) squamous metaplasia on cytological and histological slides; 2) epithelial cells incorporating polymorphic nuclear neutrophils on cytological slides; and 3) positive immunohistochemistry of p53 protein. Diagn. Cytopathol. 1999;21:117-121.