Cerebral beta amyloid angiopathy is a risk factor for cerebral ischemic infarction. A case control study in human brain biopsies

Cerebral amyloid angiopathy (CAA) is conspicuous for its association with A lzheimer disease (AD) and as a cause of lobar hemorrhages in the elderly, b ut its role in cerebral infarction is less clear. There is evidence that CA A may also be a risk factor for ischemic infarction in AD. To further inves tigate CAA as a risk factor for infarction, we studied 108 cases of recent cerebral or cerebellar infarction diagnosed in tissue samples obtained from surgical material. There were 69 males and 39 females with a mean age of 5 2 yr (range 1-86). The majority of biopsies were obtained from the frontal and parietal lobes. Radiological studies demonstrated a lesion confined to a vascular distribution in 12 of the 17 (71%) cases examined. Microscopic s ections stained with hematoxylin and eosin revealed complete, organizing in farction in 107 cases with areas of coagulative necrosis, anoxic-ischemic n euronal injury, inflammation, macrophages, vascular proliferation, gliosis, and swollen axons. One case showed an incomplete infarct. Most cases also exhibited a minor hemorrhagic component with hemosiderin and hematoidin pig ments. CAA, defined as amyloid deposition in the walls of leptomeningeal an d parenchymal arteries, was found by immunohistochemical stains for beta am yloid in 14 (13%) cases of complete cerebral infarct. Cortical beta amyloid plaques were found by immunohistochemistry in 19 (17%) cases. Cerebral or cerebellar tissues containing cortex and leptomeninges obtained from 136 pa tients with a mean age of 52 yr (range 1-85) during surgical procedures for diagnosis of primary or metastatic neoplasms and demyelinating lesions wer e used as age-matched controls. In this control group. CAA was found in 5 ( 3.7%) and beta amyloid plaques in 19 (14%. The results indicate that CAA, b ut not beta amyloid plaque formation, is significantly more common in patie nts with ischemic cerebral infarction than in age-matched controls with non vascular lesions (odds ratio 3.8; 95% confidence interval 1.3-10.9; p < 0.0 1). Our results indicate that CAA is a risk factor for ischemic cerebral in farction in the population studied.