Not All Brain Bleeds Are Equal: An Etiology-First Framework for Stroke Prevention After Intracerebral Hemorrhage

Stroke prevention after intracerebral hemorrhage (ICH) in patients with atrial fibrillation (AF) requires balancing cardioembolic protection against recurrent cerebral bleeding. Randomized evidence indicates that direct oral anticoagulants (DOACs) substantially reduce ischemic stroke compared with no anticoagulation but may increase recurrent ICH in susceptible patients. Importantly, previous ICH does not represent a uniform biological risk. Deep hemorrhage related to hypertensive arteriopathy, lobar hemorrhage associated with cerebral amyloid angiopathy (CAA), mixed small-vessel disease, and hemorrhage from a treatable cause have different recurrence profiles. Magnetic resonance imaging (MRI) markers, including cerebral microbleed distribution, cortical superficial siderosis, convexity subarachnoid hemorrhage, lacunes, and enlarged perivascular spaces, can help characterize cerebral bleeding vulnerability, although no single marker should determine treatment. This editorial proposes an etiology-first, MRI-informed framework for selecting among restarting a DOAC, considering left atrial appendage closure (LAAC), and withholding long-term antithrombotic therapy. LAAC is not a risk-free alternative because it carries procedural risks and generally requires short-term antithrombotic treatment. Until prospective trials validate phenotype-specific pathways, ICH etiology and MRI phenotype should inform multidisciplinary, individualized, and preference-sensitive decisions.