Cerebral Amyloid Angiopathy and Anticoagulation
A history of lobar intracerebral hemorrhage (ICH) suggestive of cerebral amyloid angiopathy (CAA) is sufficient to tip the balance away from anticoagulation in nonvalvular atrial fibrillation. 1
The Evidence Against Anticoagulation in CAA
The American Heart Association/American Stroke Association guidelines explicitly identify lobar ICH suggestive of CAA as a bleeding risk that outweighs the benefits of anticoagulation in patients with atrial fibrillation. 1 This represents one of the few bleeding risks considered strong enough to contraindicate anticoagulation despite stroke prevention needs.
Decision analysis studies using quality-of-life years as outcomes demonstrate that elderly patients with lobar hemorrhage likely due to amyloid angiopathy have a much higher projected risk of poor outcomes with continuation of warfarin. 1 The risk of recurrent ICH in CAA patients is particularly high and generally precludes use of anticoagulation. 1
Key Clinical Distinctions
Location Matters
- Lobar hemorrhages in elderly nonhypertensive patients characteristically indicate CAA 2
- Deep hemorrhages (basal ganglia, thalamus) typically result from hypertensive arteriopathy and carry different recurrence risks 2
Risk Stratification by Hemorrhage Location
For patients with small deep ICH, the risk of restarting versus withholding warfarin is similar. 1 However, for lobar ICH in elderly patients with probable CAA, antiplatelet agents may be a better choice than warfarin for stroke prevention in lower-risk scenarios (e.g., atrial fibrillation without prior ischemic stroke). 1
MRI Findings That Strengthen the Contraindication
Multiple juxtacortical microhemorrhages on susceptibility-weighted MRI sequences are highly specific for CAA and represent chronic hemorrhagic lesions from amyloid deposition in vessel walls. 2 The presence of:
- Multiple microhemorrhages (≥4) <10 mm in diameter highly predict future bleeding risk and contraindicate anticoagulation 3
- Lobar macrohemorrhages >10 mm in diameter significantly increase recurrent hemorrhage risk with anticoagulation 3
- Superficial siderosis indicates previous subarachnoid hemorrhage with high recurrence risk 3
When Anticoagulation Might Be Reconsidered
The 2018 CHEST guidelines suggest that after acute spontaneous ICH in patients with AF and high ischemic stroke risk, anticoagulation with a NOAC may be considered after careful risk-benefit assessment. 1 However, this comes with critical caveats:
- The balance of net benefit may be more favorable in those with deep ICH or without neuroimaging evidence of CAA 1
- Timing should be delayed beyond the acute phase (approximately 48 hours) and probably for at least 4 weeks 1
- In ICH survivors at high risk of recurrent ICH (e.g., those with probable CAA), left atrial appendage occlusion is suggested instead of anticoagulation 1
Alternative Stroke Prevention Strategy
For patients with CAA and atrial fibrillation requiring stroke prevention, left atrial appendage closure represents a viable alternative to long-term anticoagulation. 1, 4 This mechanical approach avoids the hemorrhagic risks of systemic anticoagulation while still reducing cardioembolic stroke risk.
Common Pitfalls to Avoid
- Do not assume all ICH carries equal recurrence risk: Deep hemorrhages from hypertension have different risk profiles than lobar hemorrhages from CAA 1, 2
- Do not rely on CT alone: MRI with gradient-echo or susceptibility-weighted imaging is mandatory to detect microhemorrhages and superficial siderosis that indicate CAA 3
- Do not restart anticoagulation early: If anticoagulation is considered after ICH, delay at least 4 weeks and preferably use NOACs over warfarin 1
- Do not ignore the CHA₂DS₂-VASc score context: Lower stroke risk (e.g., AF without prior stroke) makes the decision against anticoagulation more straightforward in CAA patients 1