Cerebral Infarction in Alzheimer's Disease Is Associated With Severe Amyloid Angiopathy and Hypertension

doi:10.1001/archneur.1995.00540310076019

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Vol. 52 No. 7, July 1995

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Cerebral Infarction in Alzheimer's Disease Is Associated With Severe Amyloid Angiopathy and Hypertension

John M. Olichney, MD; Lawrence A. Hansen, MD; C. Richard Hofstetter, PhD; Michael Grundman, MD, MPH; Robert Katzman, MD; Leon J. Thal, MD

Arch Neurol. 1995;52(7):702-708.

Abstract

Objective
To determine if severe cerebral amyloid angiopathy (AA) in patientswith Alzheimer's disease (AD) is associated with an increasedprevalence of cerebral infarction diagnosed at autopsy. Amyloidangiopathy is increasingly recognized as a cause of ischemicinfarcts, as well as cerebral hemorrhages. However, the relationshipof AA to cerebral infarction in patients with AD is uncertain.

Design
Retrospective clinicopathological study of autopsy-confirmedcases of AD.

Patients
One hundred forty-five deceased patients with AD confirmed atautopsy.

Main Outcome Measures
Semiquantitative scores of AA severity were done in four brainregions: midfrontal, inferior parietal, superior temporal, andhippocampal. The finding of cerebral infarction at autopsy wasmodeled as a function of AA severity, hypertension, age at death,AD severity, and sex in X² and multiple logistic regressionanalyses.

Results
Severe AA was significantly associated with cerebral infarctionat autopsy in patients with AD (odds ratio [OR], 3.5; 95% confidenceinterval [CI], 1.4 to 8.9). None of the other independent variablesin the multiple logistic regression analysis were significantpredictors. While hypertension was equally common in the severeand mild AA subgroups, the combination of both severe AA andhypertension interacted to increase the risk of infarction (OR,14.2; 95% CI, 3.2 to 63.4) beyond that observed with hypertension(OR, 1.1; 95% CI, 0.4 to 3.2) or severe AA (OR, 1.3; 95% CI,0.3 to 5.3) alone.

Conclusions
Severe AA is associated with an increased frequency of cerebralinfarction in patients with AD. This appears to be largely dueto an interaction between severe AA and hypertension that mayproduce multiplicative injuries on the vasculature. Furtherstudy with regard as to how AA may cause ischemia and its rolein the neuropathologic and clinical progression of AD is needed.

Author Affiliations

From the Alzheimer's Disease Research Center (Drs Olichney, Hansen, Hofstetter, Grundman, Katzman, and Thai) and the Department of Neurosciences (Drs Olichney, Hansen, Grundman, Katzman, and Thai), University of California—San Diego, La Jolla, and the Neurology Service, Veterans Affairs Medical Center, San Diego (Drs Olichney and Thai).

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