Zoe Arvanitakis1, Robin L Brey2, Jacob H Rand2, Julie A Schneider2, Ana W Capuano2, Lei Yu2, Sue E Leurgans2, David A Bennett2, Steven R Levine2. 1. From the Rush Alzheimer's Disease Center (Z.A., J.A.S., A.W.C., L.Y., S.E.L., D.A.B.), Department of Neurological Sciences (Z.A., J.A.S., A.W.C., L.Y., S.E.L., D.A.B.), and Department of Pathology (J.A.S.), Rush University Medical Center, Chicago, IL; Department of Neurology, University of Texas Health Science Center at San Antonio, San Antonio (R.L.B.); Department of Pathology, Montefiore Medical Center, Bronx, NY (J.H.R.); and Departments of Neurology and Emergency Medicine, State University of New York Downstate Medical Center, Brooklyn, NY, and Department of Neurology, Kings County Hospital Center, Brooklyn, NY (S.R.L.). zarvanit@rush.edu. 2. From the Rush Alzheimer's Disease Center (Z.A., J.A.S., A.W.C., L.Y., S.E.L., D.A.B.), Department of Neurological Sciences (Z.A., J.A.S., A.W.C., L.Y., S.E.L., D.A.B.), and Department of Pathology (J.A.S.), Rush University Medical Center, Chicago, IL; Department of Neurology, University of Texas Health Science Center at San Antonio, San Antonio (R.L.B.); Department of Pathology, Montefiore Medical Center, Bronx, NY (J.H.R.); and Departments of Neurology and Emergency Medicine, State University of New York Downstate Medical Center, Brooklyn, NY, and Department of Neurology, Kings County Hospital Center, Brooklyn, NY (S.R.L.).
Abstract
BACKGROUND: There are few data on the relationship of antiphospholipid antibodies (aPLs) to pathologically proven brain infarcts. We tested the hypothesis that aPLs are associated with a higher odds of brain infarcts among older, community-dwelling individuals who came to autopsy. METHODS AND RESULTS: Specimens and clinical and pathological data were derived from 607 deceased subjects (mean age at death, 89 years; 66% women) who were participating in 1 of 2 cohort studies of aging (Rush Memory and Aging Project and Religious Orders Study) and had agreed to brain autopsy. Brain infarcts were identified on gross and microscopic examinations, and severity of cerebral vessel disease (atherosclerosis, arteriolosclerosis) was graded. Four clinically used aPLs were measured longitudinally: 3 in serum (anticardiolipin antibodies, β2-glycoprotein I, and anti-phosphatidyl-serine) and 1 in plasma (lupus anticoagulant). A quarter of subjects (142 of 607, 23%) had at least 1 aPL present at baseline (median time interval from baseline to death, 4.6 years), and three quarters of these subjects had persistently positive measures over time. In a logistic regression analysis, baseline aPL positivity did not increase the odds of brain infarcts (odds ratio=1.08; 95% confidence interval, 0.74-1.58; P=0.19) or of gross or microscopic infarcts separately. Findings were essentially unchanged when considering number of baseline aPLs, aPLs proximate to death, and persistence of aPLs. Associations did not differ among subjects with increased severity of vessel disease. CONCLUSION: Overall, we did not find evidence that aPLs increase the odds of pathological brain infarcts in older people.
BACKGROUND: There are few data on the relationship of antiphospholipid antibodies (aPLs) to pathologically proven brain infarcts. We tested the hypothesis that aPLs are associated with a higher odds of brain infarcts among older, community-dwelling individuals who came to autopsy. METHODS AND RESULTS: Specimens and clinical and pathological data were derived from 607 deceased subjects (mean age at death, 89 years; 66% women) who were participating in 1 of 2 cohort studies of aging (Rush Memory and Aging Project and Religious Orders Study) and had agreed to brain autopsy. Brain infarcts were identified on gross and microscopic examinations, and severity of cerebral vessel disease (atherosclerosis, arteriolosclerosis) was graded. Four clinically used aPLs were measured longitudinally: 3 in serum (anticardiolipin antibodies, β2-glycoprotein I, and anti-phosphatidyl-serine) and 1 in plasma (lupus anticoagulant). A quarter of subjects (142 of 607, 23%) had at least 1 aPL present at baseline (median time interval from baseline to death, 4.6 years), and three quarters of these subjects had persistently positive measures over time. In a logistic regression analysis, baseline aPL positivity did not increase the odds of brain infarcts (odds ratio=1.08; 95% confidence interval, 0.74-1.58; P=0.19) or of gross or microscopic infarcts separately. Findings were essentially unchanged when considering number of baseline aPLs, aPLs proximate to death, and persistence of aPLs. Associations did not differ among subjects with increased severity of vessel disease. CONCLUSION: Overall, we did not find evidence that aPLs increase the odds of pathological brain infarcts in older people.
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