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From the Department of Neurology (Drs. Ritter, Droste, Nabavi, and Ringelstein), University of Münster, Münster, Germany; Departments of Neurology (Drs. Ritter and Csiba) and Neuropathology (Drs. Hegedüs and Szepesi), University Medical School of Debrecen, Debrecen, Hungary.
Address correspondence and reprint requests to Dr. Martin A. Ritter, Klinik und Poliklinik für Neurologie, Universitätsklinikum Münster, Albert-Schweitzer-Str. 33, D-48129 Münster, Germany; e-mail: ritterm{at}uni-muenster.de
Objective: To assess the interaction of cerebral amyloid angiopathy (CAA) and arterial hypertension as cofactors for intracerebral hemorrhage (ICH).
Methods: The authors investigated 129 postmortem brains of hypertensive patients with and without ICH. Sixty-four patients had had deep (n = 40) or lobar (n = 24) ICH. Sixty-five patients without ICH served as controls. Established risk factors for ICH (age, gender, severity of hypertension, bleeding disorders, intake of anticoagulants, and chronic alcoholism) were identified from medical records. Four specimens per brain were stained with hematoxylin-eosin and Congo red. The entire ICH cohort and subgroups were compared with controls using single-factor and multiple logistic regression analyses.
Results: CAA was found in 15 of 64 subjects (23%) with ICH and in five of 65 controls (8%; p = 0.026). In single-factor analysis, CAA was more prevalent in lobar ICH compared with controls (p = 0.007) but not in deep ICH. Poor control of hypertension was more prevalent in the entire ICH group (p = 0.01) and in deep ICH (p = 0.016) but not in lobar ICH. ICH was predictive of the presence of CAA (odds ratio: 5.6, 95% CI: 1.8 to 19.5, p = 0.003), and CAA was more likely to be found in lobar ICH in multivariable-adjusted analysis. After adjustment for conventional risk factors, there was a weak association between CAA and deep ICH.
Conclusion: Cerebral amyloid angiopathy plays a major role in the pathogenesis of intracerebral hemorrhage even in patients with more evident risk factors.
M.A.R. was supported by grant HUN 00-007 from the German Ministry of Education and Research) and grant ETT 122/2003 of the Hungarian Science and Technology Foundation).
All authors are employees of the general health system of Germany or Hungary.
Received May 28, 2004. Accepted in final form December 13, 2004.
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Neurology 2005 64: 1106-1107.
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