Cerebral amyloid angiopathy (CAA) is a small vessel disease marked by β-amyloid deposition within cortical and leptomeningeal vessels. It is associated with a range of hemorrhagic manifestations, including lobar intracerebral hemorrhage (ICH), cortical superficial siderosis, and convexity subarachnoid hemorrhage (cSAH). In addition to hemorrhagic complications, cerebral ischemic events may occur due to impaired vascular reactivity and reduced cerebral perfusion. The coexistence of ischemic and hemorrhagic strokes in patients with biopsy-confirmed CAA poses significant diagnostic and therapeutic challenges, particularly in relation to antithrombotic use. A 74-year-old woman with type 2 diabetes mellitus and dyslipidemia initially presented with transient focal neurological deficits and subsequently developed left parietal cSAH along with multiple acute infarcts involving the left parietal, temporal, and centrum semiovale regions, for which aspirin and rivaroxaban were initiated. Over the following years, she developed progressive cognitive decline. Three years after her ischemic event, she experienced a lobar ICH in the right frontotemporoparietal region and later suffered another ischemic stroke, prompting treatment with cilostazol. This case illustrates the coexistence of ischemic and hemorrhagic pathology in CAA. Recurrent lobar ICH is a characteristic feature of CAA; however, ischemic events may also occur during its course and can adversely affect prognosis. The lack of clear guidance regarding antithrombotic therapy further complicates management. In this context, cilostazol was selected due to its favorable safety profile in patients at high risk of hemorrhage. This approach underscores the importance of individualized treatment strategies in CAA.
Nobleza et al. (Sat,) studied this question.