Evidence map›Paper›PMID 42089159›Full record

ArticleJournal of the American Heart Association2026

Hemorrhage Pattern and Amyloid Burden in Cerebral Amyloid Angiopathy.

Elif Gokcal, J Alex Becker, Mitchell J Horn, Ofer Rotschild, Alvin S Das, Avia Abramovitz Fouks, Jonathan Rosand, Anand Viswanathan, Keith A Johnson, M Edip Gurol and 1 more

Abstract read
In one paragraph

Article in Journal of the American Heart Association, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Elif GokcalJ. Philip Kistler Hemorrhagic Stroke Research Program, Massachusetts General Hospital, Harvard Medical School Boston MA USA.ORCID 0009-0009-2264-1603
J Alex BeckerDepartment of Radiology Massachusetts General Hospital, Harvard Medical School Boston MA USA.ORCID 0000-0001-7435-1338
Mitchell J HornJ. Philip Kistler Hemorrhagic Stroke Research Program, Massachusetts General Hospital, Harvard Medical School Boston MA USA.
Ofer RotschildJ. Philip Kistler Hemorrhagic Stroke Research Program, Massachusetts General Hospital, Harvard Medical School Boston MA USA.
Alvin S DasDepartment of Neurology Massachusetts General Hospital, Harvard Medical School Boston MA USA.ORCID 0000-0003-2313-977X
Avia Abramovitz FouksJ. Philip Kistler Hemorrhagic Stroke Research Program, Massachusetts General Hospital, Harvard Medical School Boston MA USA.
Jonathan RosandDepartment of Neurology Massachusetts General Hospital, Harvard Medical School Boston MA USA.ORCID 0000-0002-1014-9138
Anand ViswanathanJ. Philip Kistler Hemorrhagic Stroke Research Program, Massachusetts General Hospital, Harvard Medical School Boston MA USA.ORCID 0000-0001-5398-1816
Keith A JohnsonDepartment of Neurology Massachusetts General Hospital, Harvard Medical School Boston MA USA.
M Edip GurolJ. Philip Kistler Hemorrhagic Stroke Research Program, Massachusetts General Hospital, Harvard Medical School Boston MA USA.ORCID 0000-0002-2169-4457
Steven M GreenbergJ. Philip Kistler Hemorrhagic Stroke Research Program, Massachusetts General Hospital, Harvard Medical School Boston MA USA.ORCID 0000-0003-1792-8887

Funding

Molecular and Physiological Mechanisms of Hypertensive Cerebral MicroangiopathyR01NS114526 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI GUROL, MAHMUT EDIP · 2020 to 2024
$4.4M
NINDS NIH HHS R01 NS114526
6 · The paper itself

Abstract

backgroundCerebral amyloid angiopathy (CAA), a cerebral small vessel disease characterized by vascular amyloid deposition, presents with heterogeneous imaging features, but the biological mechanisms underlying hemorrhagic markers remain unclear. We assessed hemorrhage patterns in CAA to determine their associations with amyloid burden and related imaging markers.

methodsSixty-two patients with probable CAA underwent Pittsburgh compound B-positron emission tomography and structural magnetic resonance imaging. Participants were classified by dominant hemorrhagic pattern: lobar cerebral microbleed-dominant (n=31), cortical superficial siderosis-dominant (n=17), and nondominant (n=14). Global cortical amyloid burden was quantified as Pittsburgh compound B distribution volume ratio. White matter hyperintensity volume and high-degree centrum semiovale-enlarged perivascular spaces were assessed. Associations were tested using age- and sex-adjusted regression models.

resultsGlobal Pittsburgh compound B distribution volume ratio was significantly higher in the cerebral microbleed-dominant (1.40±0.23) and cortical superficial siderosis-dominant (1.45±0.27) groups than nondominant group (1.20±0.17;

conclusionsAmyloid burden in CAA is associated with hemorrhage-dominant patterns, high-degree centrum semiovale-enlarged perivascular spaces, and greater WMH volume. These findings support a close link between vascular amyloid deposition and downstream vascular brain injury, underscoring its relevance as a therapeutic target in CAA.

Indexed as

Cerebral Amyloid AngiopathyCerebral HemorrhageAgedAged, 80 and overAniline CompoundsFemaleHumansMagnetic Resonance ImagingMaleMiddle AgedPositron-Emission TomographyPredictive Value of TestsRadiopharmaceuticalsSiderosisThiazoles2-(4'-(methylamino)phenyl)-6-hydroxybenzothiazoleAniline CompoundsRadiopharmaceuticalsThiazolesamyloidcerebral amyloid angiopathycortical superficial siderosislobar cerebral microbleedsPET

Identifiers

PMID42089159
PMCPMC13279345

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.