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Amyloid Angiopathy in Brain Hemorrhage: A Postmortem Neuropathological-Magnetic Resonance Imaging Study
Celine Guidoux1,2,3, Jean-Jacques Hauw3, Isabelle F Klein4
1INSERM LVTS (Laboratory for Vascular Translational Science) 1148 and Paris-Diderot University, Sorbonne Paris Cité, Paris, France.
Insights
Hypertension and cerebral amyloid angiopathy (CAA) often occur together in patients with intracerebral hemorrhage (ICH). Microbleeds, detected by MRI and confirmed by histology, were more frequent in patients with CAA.
Area of Science:
- Neurology
- Pathology
- Radiology
Background:
- Intracerebral hemorrhage (ICH) is often linked to hypertension and cerebral amyloid angiopathy (CAA).
- Understanding the prevalence and overlap of these risk factors in ICH is crucial.
- Investigating the association between CAA and cerebral microbleeds is important for patient outcomes.
Purpose of the Study:
- To determine the autopsy prevalence of CAA in patients who died from ICH.
- To assess the overlap between CAA, hypertension, and other risk factors in ICH patients.
- To correlate CAA with the presence of cerebral microbleeds.
Main Methods:
- Analysis of 81 consecutive autopsy brains from ICH patients.
- Staining for CAA detection and comparison with age/sex-matched controls.
- Postmortem MRI and histological analysis of microbleeds in 11 ICH brains.
Main Results:
- Hypertension and CAA were present in 69.1% and 24.7% of ICH cases, respectively.
- CAA prevalence was similar in non-hypertensive ICH cases and controls, but higher in hypertensive cases versus controls.
- MRI detected 48 microbleeds, with all 5 CAA-positive brains having microbleeds, compared to 3/6 CAA-negative brains.
Conclusions:
- Hypertension and CAA frequently coexist in intracerebral hemorrhage.
- MRI-detected microbleeds, confirmed histologically, were twice as common in patients with CAA compared to those with hypertensive ICH.
Background:
Risk factors for intracerebral hemorrhage (ICH) include hypertension and cerebral amyloid angiopathy (CAA). The objective of this study was to determine the autopsy prevalence of CAA and the potential overlap with other risk factors among patients who died from ICH and also the correlation of CAA with cerebral microbleeds.
Methods:
We analyzed 81 consecutive autopsy brains from patients with ICH. Staining for CAA detection was performed. We used an age- and sex-matched control group of routine brain autopsies of nonneurological patients to determine the frequencies of CAA and hypertension. Postmortem 3D T2-weighted gradient-echo magnetic resonance imaging (MRI) with a 1.5-T magnet was performed in 11 brains with ICH (5 with CAA and 6 without) and histological correlation was performed when microbleeds were detected.
Results:
Hypertension and CAA were found in 69.1 and 24.7% of cases respectively. Among patients with CAA, 65.0% also had hypertension. The prevalence of CAA was similar among non-hypertensive cases and controls (33.3 and 23.1%; p = 0.54), whereas a significant difference was found between hypertensive cases vs. controls (28.9% vs. 0; p = 0.01). MRI documented 48 microbleeds and all 5 brains with CAA had ≥1 microbleed, compared to 3/6 brains without CAA. Among 48 microbleeds on MRI, 45 corresponded histologically to microbleeds surrounding microvessels (23 <200 µm in diameter, 19 between 200 µm and 2 mm, 3 were hemosiderin granules).
Conclusions:
Both hypertension and CAA frequently coexist in patients with ICH. MRI-detected microbleeds, proven by histological analysis, were twice as common in patients with CAA as in those with hypertensive ICH.
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