Polyarteritis nodosa (PAN) is a rare systemic necrotizing arteritis that involves small- and medium-sized arteries in various organs. Although aneurysm formation in visceral arteries is a typical finding in PAN, intracranial aneurysms are much less common, and only a few cases of aneurysm rupture associated with this disease have been documented. In this paper, the authors report on a ruptured PAN aneurysm of the anterior cerebral artery; the lesion was trapped and resected. On histological examination, extensive fibrinoid necrosis and an inflammatory infiltration of leukocytes were seen in the aneurysm wall. To the authors' knowledge this is the first report of subarachnoid hemorrhage from a histologically confirmed PAN aneurysm.
We reviewed the cases of 66 patients who underwent 67 tricuspid valve replacements with Carpentier-Edwards pericardial xenografts between April 1985 and January 1994. Average patient age at time of operation was 52 years (range 8 to 71 years). Concomitant mitral or aortic valve replacements were performed in 46 patients. There were 10 operative deaths and 6 late deaths. Actuarial survival at 9 years was 75.4% +/- 5.7%. Prosthetic valve endocarditis occurred twice in one patient. Reoperations for tricuspid regurgitation and for concomitant procedures (maze operation and repair for leak of the mitral prosthesis) were performed in two patients. In both cases, examination of the explanted prostheses showed that the tricuspid regurgitation was the result of nonstructural dysfunction caused by fibrous pannus formation on the cusps of the ventricular side. Among the survivors, 47 patients (92%) were in functional class I or II. Prosthetic valve function was studied by color Doppler echocardiography. Among 38 patients, tricuspid regurgitation more than grade 3/4 or transprosthetic gradient more than 5 mm Hg was found in 11. One patient had right heart failure and the others had no symptoms. In 10 years of experience with the Carpentier-Edwards pericardial xenograft, mortality and morbidity after tricuspid valve replacement were satisfactory. Echocardiographic examination revealed subclinical prosthetic dysfunction in 35% of patients who were followed up for longer than 5 years, however, and we believe that these patients should receive careful follow-up.
In a study of duration of brain death, granular layer autolysis (GLA) of the cerebellar cortex was analyzed in 45 patients who died of acute cerebrovascular diseases (CVDs). Twelve patients who died of causes other than intracranial disease served as controls. Tonsillar herniation occurred in all who died of acute CVDs. More advanced GLA was seen in the central folia adjacent to the central white medullary body of the cerebellum as compared with the peripheral folia. Widespread GLA involving the most of the peripheral folia was found solely in patients in whom brain death had been present over 18 h. Of the 12 control patients, 4 showed GLA only in the central folia. Although GLA of the central folia might develop during immersion fixation of the brain, the alteration of the peripheral folia is assumed to develop in the period of brain death. Widespread GLA extending to the peripheral folia could be a pathological finding characteristic of brain death, where intracranial blood flow could be absent or significantly reduced. Brain death for little less than 1 day would be necessary for GLA to develop.
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