Cerebral amyloid angiopathy (CAA) — deposition of beta-amyloid in the brain's small vessels — is a major cause of haemorrhagic stroke and contributes to cognitive decline and to complications of anti-amyloid immunotherapy. Diagnosis usually rests on MRI showing multiple (micro)bleeds or cortical/leptomeningeal blood products. For cardiovascular practice the key issue is the high recurrence risk: in patients with an indication for antithrombotic therapy, CAA demands a carefully individualised weighing of bleeding versus thrombotic risk. Research focuses on risk prediction, early markers and disease-modifying therapy.
Cerebral amyloid angiopathy is a major cause of hemorrhagic stroke, a frequent contributor to age-related cognitive impairment, and a key component in adverse responses to beta-amyloid (Aβ) immunotherapy. Defined by pathological deposition of Aβ in the small blood vessels of the brain, cerebral amyloid angiopathy is most often diagnosed on the basis of magnetic resonance imaging studies showing multiple hemorrhages or leptomeningeal blood products within or overlying the cerebral cortex. The disorder typically manifests as hemorrhagic stroke or as a contributing factor to cognitive decline and, less commonly, with transient focal neurologic symptoms or a cerebral inflammatory autoimmune syndrome. The high risk of recurrent hemorrhagic strokes associated with cerebral amyloid angiopathy poses a particular challenge in patients with indications for antithrombotic therapy and dictates a carefully individualized weighing of risks and benefits. Ongoing research is focused on tools to aid in risk prediction, early diagnostic markers, and identification of key pathogenic steps as targets for disease-modifying therapies.
