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Review
. 2017 Jan 20;114(3):37-42.
doi: 10.3238/arztebl.2017.0037.

Cerebral Amyloid Angiopathy in Stroke Medicine

Review

Cerebral Amyloid Angiopathy in Stroke Medicine

Frank Block et al. Dtsch Arztebl Int. .

Abstract

Background: Cerebral amyloid angiopathy (CAA) is a degenerative vasculopathy that is classically associated with lobar intracerebral or sulcal hemorrhage. Its prevalence is estimated at 30% in the seventh decade and 50% in the eighth and ninth decades. In this review, we summarize the risks linked to CAA with respect to the treatment and prevention of stroke.

Methods: This review is based on pertinent publications retrieved by a selective search employing the terms "amyloid cerebral angiopathy," "stroke," "intra - cerebral bleeding," and "acute stroke therapy."

Results: Among patients given systemic lytic treatment for stroke, those who have microhemorrhages tend to have a higher risk of treatment-associated brain hemorrhage. In a meta-analysis, 70% of patients who sustained a hemorrhage after thrombolytic therapy were found to have CAA, compared to only 22% in a control population. Patients with cerebral hemorrhages have microhemorrhages more commonly than patients with transient ischemic attacks (TIA) or infarcts. This was observed among persons under treatment with vitamin K antagonists (odds ratio, 2.7) or platelet aggregation inhibitors (odds ratio, 1.7). Moreover, the apolipoprotein E2 allele is associated with a higher incidence of intracerebral hemorrhage (ICH) under oral anticoagulation. Strict treatment of arterial hypertension can lower the risk of ICH in persons with probable CAA by 77%. On the other hand, the use of statins after a lobar ICH increases the risk for a clinically manifest recurrent hemorrhage from 14% to 22%.

Conclusion: In patients with CAA, arterial hypertension should be tightly controlled. On the other hand, caution should be exercised in prescribing oral anticoagulants or platelet aggregation inhibitors for patients with CAA, or statins for patients who have already sustained a lobar ICH.

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Figures

Figure 1
Figure 1
Cranial computed tomogram of a 69-year-old patient with cerebral amyloid angiopathy, showing lobar hemorrhage in an atypical location
Figure 2
Figure 2
Cranial computed tomogram of a 79-year-old patient with cerebral amyloid angiopathy, showing sulcal hemorrhage (cortical, nontraumatic subarachnoid hemorrhage)
Figure 3
Figure 3
Cranial magnetic resonance images (T2*-weighted) of two patients with cerebral amyloid angiopathy. (a) Residues of sulcal hemorrhage (tram-track sign) and stigmata of older parenchymal hemorrhage and (b) multiple temporo-occipitally accentuated microbleeds are seen.

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