Chikao Yutani

Imprint cytology of primary cardiac sarcomas: a report of 3 cases

Primary cardiac sarcomas are rare instances and only occasionally documented in the cytologic literature. Usually, the diagnosis of these rare lesions can be made at echocardiography, aspiration biopsy cytology, cardiac biopsy, and open cardiac surgery (intraoperative diagnosis). In this study, cytologic configurations and immunohistochemistry for 3 primary cardiac sarcomas (rhabdomyosarcoma, angiosarcoma, and malignant fibrous histiocytoma) were revealed. In rhabdomyosarcoma (right ventricle), the tumor cells exhibited an anisocytotic spindle-shaped nuclei with hyperchromasia and an obscure cytoplasmic margin. Vimentin and myosin were positive throughout the cytoplasm for the tumor cells. In angiosarcoma (right atrium), small clusters of anisocytotic spindle-shaped tumor cells appeared as vascular-like structures and hemosiderin-laden macrophages in many erythrocyte-rich backgrounds. Nuclei showed round to oval shape with hyperchromasia and prominent large nucleoli. Cytoplasm was obscure and elongated. Factor VIII related antigen and CD34 were strongly positive throughout the cytoplasm for the tumor cells. In malignant fibrous histiocytoma (right ventricle), the tumor cells exhibited oval to spindle-shaped and elongated nuclei and coarse granular chromatins with hyperchromasia. The nuclear margin was thin. A few small round nucleoli appeared. Elongated obscure and foamy cytoplasm was stained pale blue. Vimentin and alpha(1)-antitrypsin were positive throughout the cytoplasm for the tumor cells. This study elucidated the cellular characteristics and immunohistochemistry for cardiac sarcomas using imprint smears as an aid to cytopathologic diagnosis.

Elevated oxidative stress is associated with ventricular fibrillation episodes in patients with Brugada-type electrocardiogram without SCN5A mutation

BACKGROUND 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. METHODS 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. RESULTS 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. CONCLUSION 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.

Histopathological Study of Multiple Organ Failure Following Open Heart Surgery

Although the recent development of intensive care unit (ICU) has made it possible to reduce the mortality due to failure of one vital organ, it is reported that multiple organ failure (MOF), defined as serious and sequential disturbances in more than two organs [1], is associated with most postoperative deaths.

Clinicopathological Aspects of Chronic Pulmonary Thromboembolic Hypertension with Special Reference to Pulmonary Thromboendarterectomy in Japan

The incidence of chronic pulmonary thromboembolic hypertension (CPTEH) has been gradually increasing in Japan. Pulmonary thromboendartectomy has been recently performed, but the success rate of this operation is not as good as that in the San Diego group. To clarify the factors leading to a satistactory outcome in this operation, we have clinicopathologically compared seven autopsy cases, including three patients with CPTEH who died after operation, to 11 surgically successful patients. We have classified CPTEH to assess operative indication.

Morphology of Left Ventricular Hypertrophy in the Human

The hypertrophied heart typically exhibits various changes in architecture as well as in histology, according to the cause and stage of hypertrophy. The macroscopic and histologic changes in hypertrophied hearts are briefly described. The various dimensions of the autopsied hearts, width of myocytes, contents of myocytes, and extent of fibrosis were compared between one group of patients who seemed to have hypertrophied hearts secondary to arterial hypertension in adaptive growth or a prolonged state of successful adaptation, and a second group of patients who appeared to have almost normal hearts. There were significant differences in heart weight, the length of the inflow portion of the left ventricle, the wall thickness of the left ventricle and interventricular septum, the width of myocytes, and the extent of fibrosis.