Journal of the American Heart Association · 2026
Hemorrhage Pattern and Amyloid Burden in Cerebral Amyloid Angiopathy.
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Gokcal Elif, Becker J Alex, Horn Mitchell J, Rotschild Ofer, Das Alvin S, Fouks Avia Abramovitz, Rosand Jonathan, Viswanathan Anand, Johnson Keith A, Gurol M Edip, Greenberg Steven M
Аннотация
BACKGROUND: Cerebral 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.
METHODS: Sixty-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.
RESULTS: Global 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; P=0.007 and P=0.006, respectively), and these associations remained independent after adjustment (odds ratio [OR], 1.8 [95% CI, 1.1-2.8]; P=0.009 and OR, 1.6 [95% CI, 1.1-2.5]; P=0.020). Compared with the nondominant group, high-degree centrum semiovale-enlarged perivascular spaces were independently associated with both cerebral microbleed-dominant (OR, 9.3 [95% CI, 1.6-52]; P=0.011) and cortical superficial siderosis-dominant (OR, 10 [95% CI, 1.6-62]; P=0.013). In the full cohort, Pittsburgh compound B distribution volume ratio was independently associated with high-degree centrum semiovale-enlarged perivascular spaces (P=0.016) and white matter hyperintensity volume (P=0.049). Findings were unchanged in sensitivity analyses, adjusting for intracerebral hemorrhage.
CONCLUSIONS: Amyloid 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.
METHODS: Sixty-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.
RESULTS: Global 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; P=0.007 and P=0.006, respectively), and these associations remained independent after adjustment (odds ratio [OR], 1.8 [95% CI, 1.1-2.8]; P=0.009 and OR, 1.6 [95% CI, 1.1-2.5]; P=0.020). Compared with the nondominant group, high-degree centrum semiovale-enlarged perivascular spaces were independently associated with both cerebral microbleed-dominant (OR, 9.3 [95% CI, 1.6-52]; P=0.011) and cortical superficial siderosis-dominant (OR, 10 [95% CI, 1.6-62]; P=0.013). In the full cohort, Pittsburgh compound B distribution volume ratio was independently associated with high-degree centrum semiovale-enlarged perivascular spaces (P=0.016) and white matter hyperintensity volume (P=0.049). Findings were unchanged in sensitivity analyses, adjusting for intracerebral hemorrhage.
CONCLUSIONS: Amyloid 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.