Postmortem pathological examination of a case one month after carotid artery stenting.

SUMMARY: There have been few pathological reports on human carotid stenting. A 73-year-old diabetic male with 80% stenosis in the left carotid bifurcation. Despite no neurological events, he died of pneumonia one month after. Findings pathological examination revealed: successful dilatation without deformity of the stent, eccentric compression and partial disruption of the plaque by struts, thrombi around disrupted plaque, and neointimal growth. Findings were generally compatible with those reported on coronary stenting. Case accumulation is required to clarify an exact pathological process and establish a procedure to reduce complications.

Angiographic classification of cerebral embolism. Relation with the response to local intra-arterial thrombolysis.

Since 1994, we have treated 62 cases with hyperacute cerebral embolism with local intraarterial thrombolysis (LIT), but not all cases showed recanalization. We tried to classify these cases by angiographic results. Angiographically they could be classified into four types; tapering type, fading type, stump type, and edge type. The tapering and fading type had a significantly higher tendency to recanalize than the stump and edge type. We think these classifications indicate the dissolubility of the cerebral emboli; the former two types dissoluble, the latter two types indissoluble. The tapering and fading type are the good indicators for LIT, but the stump and edge type may not be.

Angiographic A-V Shunt during Interventional Thrombolysis for Acute Cerebral Embolism. A New Predictive Sign for Hemorrhagic Complication.

SUMMARY: In order to predict the post-therapeutic hemorrhagic complication of interventional thrombolysis, we retrospectively examined angiographic findings and other factors in 44 patients with acute cerebral embolism. All patients were super selectively catheterized within 5 hours of onset and received a fixed regimen of urokinase or t-PA, unless recanalization was achieved or deterioration was apparent before total infusion. Immediate post-therapeutic CT scan revealed hematoma within the basal ganglia in 10 patients (group 1) and no hemorrhage in the remaining 34 (group 2). A series of angiograms during the therapy showed A-V shunt from lenticulostriate arteries to thalamostriate vein in 7 of 10 cases in group 1; no case in group 2 was accompanied by such abnormal shunt. Prognosis after the therapy was worse in group 1 than in group 2. No other factors, such as therapeutic timing after the disease onset or total doses of urokinase or t-PA infused, differed between the two groups. These findings indicate that angiographic A-V shunt during therapy is a predictive sign of a high incidence of hemorrhagic complication. We recommend performing several angiographic controls during therapy and when A-V shunt is detected, the therapy should be discontinued to prevent hemorrhage which leads to a poor prognosis.

Histopathological analysis of the mechanisms of intracranial hemorrhage complicating infective endocarditis.

BACKGROUND AND PURPOSE: We conducted the present study to elucidate the pathological mechanisms leading to intracranial hemorrhage complicating infective endocarditis. METHODS: Neurological, neuroradiological, and histopathological analyses were performed in 16 patients (one surgical and 15 autopsy cases), 12 men and four women 26-68 years of age, who had demonstrated central nervous system complications during the course of infective endocarditis. RESULTS: Intracranial hemorrhage was found in all cases; parenchymal hematomas were found in 12 cases, hemorrhagic infarcts in four cases, and primary subarachnoid hemorrhages in two cases. Chronological analysis of neurological examination and computed tomographic scan of the brain confirmed that antecedent cerebral ischemic events had occurred in five of 12 patients showing parenchymal hematomas at autopsy. Hemorrhagic infarct, indicated by petechial or diffuse hemorrhages within the infarct, was seen in another four patients, so that hemorrhagic transformation of the ischemic infarct was confirmed in nine patients. Although mycotic aneurysms were found in five patients, only three of these were ruptured; the other two were occluded with septic emboli. Pyogenic arteritis without aneurysm was found to be distributed in the small cortical arterial branches located in the spaces of cortical sulci, with rupture occurring in five patients. CONCLUSIONS: These results suggest that hemorrhagic transformation of the ischemic infarct due to septic emboli is the most frequent mechanism leading to intracerebral hemorrhage encountered in patients dying of infective endocarditis and that rupture of pyogenic arteritis may be responsible for such hemorrhage in many cases, with ruptures of mycotic aneurysms as an alternative mechanism.

Hemorrhagic infarct induced by arterial hypertension in cat brain following middle cerebral artery occlusion.

The purpose of this experiment was to determine whether an acute rise in brain perfusion pressure causes hemorrhagic transformation of an infarct without a reopening of the occluded artery. We raised the blood pressure of 22 cats by aortic obstruction 5-24 hours after transorbital middle cerebral artery clipping; hemorrhagic infarcts were induced in 11. Mean arterial blood pressure increased by 57.2 +/- 16.9 mm Hg (mean +/- SD) in the 11 cats with hemorrhagic infarcts and by 40.4 +/- 16.9 mm Hg in the 11 remaining cats with pale brain infarcts (p less than 0.05). Induction of hypertension increased regional cerebral blood flow in the ischemic cortical gray matter more in three cats with hemorrhagic infarcts than in seven with pale infarcts. Our results demonstrate that hemorrhagic transformation of an infarct can be induced by a rapid increase in perfusion pressure to brain tissue already exposed to focal ischemia. We also suggest that the restoration of blood flow through leptomeningeal collaterals plays an important role in the pathogenesis of hemorrhagic infarction in cases without reopening of occluded arteries.

Prospective, controlled, randomized trial of naloxone infusion in early hyperdynamic septic shock.

To determine whether naloxone infusion is efficacious in severe hyperdynamic septic shock, we conducted a prospective study of 22 patients randomly assigned to a naloxone or placebo group. Patients were treated 12 +/- 2 h (SEM) after the onset of shock, with a mean arterial pressure (MAP) of 63 +/- 3 mm Hg. All patients had clinical evidence of an infectious process and required dopamine 20 +/- 2 micrograms/kg.min. Five (46%) of 11 patients in the naloxone group and one (9%) of the other 11 patients in the placebo group responded clinically. The MAP among the five responders increased from 62 +/- 5 to 89 +/- 4 mm Hg within 20 min of naloxone treatment (p less than .01). This favorable hemodynamic response was sustained throughout the patients' clinical course. In contrast, the MAP did not change significantly in the nonresponders who received naloxone, nor did it change in the placebo group. More patients in the naloxone group than in the placebo group received steroids concurrently. Survival rate was 100% in those who responded to naloxone clinically. However, overall survival rate in each group was essentially the same. No adverse effects were observed, except for mild agitation in some of the patients receiving naloxone. We conclude that naloxone infusion is clinically efficacious in improving the hemodynamic profile of a subgroup of patients with severe early hyperdynamic septic shock, but does not appear to improve the overall survival rate.

Autolysis of the granular layer of the cerebellar cortex in brain death.

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.

Cerebro-spinal infarction caused by atheromatous emboli.

Cholesterol embolization to the abdominal viscera is common, but rare in the central nervous system. Fourteen cases of atheromatous embolization to the central nervous system were morphologically investigated. Among the 800 consecutive autopsy cases, 38 cases had atheromatous emboli in various organs. Cerebro-spinal infarction caused by atheromatous emboli was found in 11 cases. Infarction rate (11/14) was relatively higher than in other organs and 5 of these cases were thought to be due to direct injury to the erosive surface of the aorta; cardiac catheterization (2 cases), intra-aortic balloon pumping (2 cases), and extra-anatomical bypass graft operation (1 case). These 14 patients consisted of elderly patients (70.1 +/- 6.3 years old) usually associated with hypertension (78.6%) and diabetes mellitus (42.8%). Anatomically, aortic aneurysms were seen in 10 cases (71.4%), in which aortic arch aneurysm was seen in 6 cases. Hence, aortic mechanical procedure is of great importance for denuding atheromatous materials from erosive atherosclerosis to the central nervous system.