• Jorge Tapia.
• Departamento de Neurología, Facultad de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile.
• Rev Med Chil. 2021 Jan 1; 149 (1): 76-87.

AbstractAmyloid angiopathy (AA) is a selective deposition of amyloid in the walls of the brain vessels. It is a form of sporadic and localized amyloidosis, constituted by the Aβ4 protein, the same of Alzheimer's disease senile plaques. The most consistent clinical effect of AA is spontaneous brain hemorrhage (BH). It is the second most common cause of BH after arterial hypertension (HT). Other clinical manifestations are cognitive impairment and transient focal neurological episodes. AA BH is characteristically localized in the cerebral cortex and subcortical white matter (lobar hemorrhage), consistent with the preferential deposit of amyloid in the walls of leptomeningeal and intracortical small cerebral vessels. Other types of AA hemorrhagic complications are microbleeds (MB), cerebral convexity subarachnoid hemorrhage (cSAH) and superficial hemosiderosis (cSS). The diagnosis of AA BH is based on the Boston criteria. Using these criteria, several non-hemorrhagic biomarkers of AA have been identified that can be useful in its diagnosis. The principal AA BH risk factor is age, followed by cSS, MB, Apolipoprotein E gen ε2 and ε4 alleles, HT and the use of antithrombotics. This condition has a high recurrence rate that shares the same risk factors. There is no specific treatment for AA BH. It has a better prognosis than HT BH during the acute period, but worse on the long term, due to its high recurrence rate and cognitive impairment.

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