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Background: Atherosclerotic stenosis of large intracranial arteries, especially the middle cerebral artery (MCA), is a common cause of stroke in Chinese patients. We aimed to describe the morphological features of atherosclerotic stenosis in the MCA and to investigate their relationship with cerebral infarcts from a postmortem series., Methods: We studied the morphological features of the MCAs in consecutive postmortem adults aged 45 years or above. The following parameters were evaluated by a single observer blinded to the clinical history: (1) thickness of fibrous cap; (2) extent of lipid area; (3) degree of luminal stenosis; (4) presence of intraplaque hemorrhage, neovasculature, thrombus and calcification. A semiquantitative assessment of macrophage and T lymphocyte infiltration was made by immunohistochemical staining for CD68 and CD45RO., Results: Seventy-six cases were recruited. Atherosclerotic plaques of more than 40% cross-sectional area luminal narrowing stenosis were found in 69 MCAs (45.4%, 69/152). The results demonstrated that the degree of luminal stenosis, the percentage of the plaques containing more than 40% lipid area and the prevalence of intraplaque hemorrhage, neovasculature and thrombus were higher in those plaques associated with infarct, and the mean index of both CD45RO and CD68 was higher among those associated with infarct (p < 0.01). Binary logistic regression showed that stenosis (p = 0.003; odds ratio, OR = 1.050), lipid area (p = 0.048, OR = 1.698) and presence of neovasculature (p = 0.040, OR = 3.471) were independent risk factors of MCA infarcts., Conclusions: Luminal stenosis caused by atherosclerotic plaque, percentage of lipid area and presence of intraplaque neovasculature may play a key role in leading to ischemic stroke., ((c) 2007 S. Karger AG, Basel.)

Islet amyloid has been suggested to be an important link between insulin resistance and beta-cell dysfunction in type 2 diabetes. To investigate the prevalence and clinicopathological characteristics of islet amyloid, we examined consecutive autopsies of 235 Chinese patients with type 2 diabetes and 533 nondiabetic subjects. Islet amyloid deposits were identified using Congo red staining and quantitated by image analysis. We found that 3.0% of the nondiabetic subjects versus 39.6% of the diabetic patients displayed islet amyloid (P < 0.001). In diabetic patients, the amyloid deposits occupied a mean islet area of 36.2%, which was positively associated with BMI, blood pressure, and glycemic control. Pancreatic fibrosis and fat infiltration were more frequently found in diabetic patients with islet amyloid than those without islet amyloid, whereas pancreatic arteriosclerosis was identified in all diabetic patients. These findings suggest that islet amyloid deposits reflect greater insulin resistance and islet failure in a subgroup of type 2 diabetic patients. Islet failure may also have been exacerbated by fat infiltration, fibrosis, and arteriosclerosis. Optimal blood pressure and metabolic control may reduce these pathological changes and help preserve islet cell mass.