Cerebral Microbleeds and Antiplatelet Therapy

• Deep/basal ganglia distribution -> hypertensive small vessel disease
• Strictly lobar/cortical distribution -> cerebral amyloid angiopathy (CAA)

Does the presence of CMBs contraindicate antiplatelet therapy?

• The RESTART trial (Lancet Neurology) randomized patients with a prior symptomatic ICH who had a strong indication for antiplatelet therapy to start vs. avoid antiplatelets. Resuming antiplatelet therapy did not increase recurrent ICH risk, and there was a trend toward lower recurrent ICH with antiplatelet use.
• Pre-specified subgroup analyses by CMB burden and location (including patients with numerous or strictly lobar microbleeds, i.e. probable CAA) showed the effect of antiplatelet therapy was consistent regardless of microbleed number or anatomical distribution - CMBs did not modify the treatment effect.
• The rationale: absolute risk of recurrent ischemic stroke on antithrombotic therapy generally exceeds the absolute risk of recurrent ICH, even in patients with imaging markers of small vessel disease, so CMBs "should not influence use of antiplatelet or anticoagulant drugs" for secondary prevention in most patients (subgroup analysis, RESTART trial, Lancet Neurology 2019).

When caution/individualization is still warranted

• High CMB burden (>10) prior to IV thrombolysis for acute ischemic stroke: symptomatic ICH risk rises sharply (30-47% vs. 1-4% with fewer/no CMBs), so the benefit of thrombolytics becomes uncertain in this specific acute setting - distinct from routine long-term antiplatelet secondary prevention (Rosen's Emergency Medicine, p. 1439).
• Suspected CAA with heavy lobar CMB burden (>4) and/or cortical superficial siderosis: these features raise recurrent ICH risk and are weighed more heavily in decisions about anticoagulation in particular (e.g., choosing left atrial appendage closure over anticoagulation in AF), and are flagged as risk factors in other bleeding-prone contexts such as anti-amyloid antibody therapy (Goldman-Cecil Medicine; Harrison's Principles of Internal Medicine, 22e). For antiplatelet monotherapy specifically, this is a softer caution rather than an absolute contraindication - decisions should be individualized considering the strength of the ischemic indication.
• Anticoagulation (as opposed to antiplatelet) in patients with high CMB burden or siderosis carries more deliberation in guidelines - MRI markers are used for risk stratification, though their impact on the anticoagulation decision itself remains debated (Fuster and Hurst's The Heart, 15th ed.).

Practical bottom line