Antiphospholipid Antibodies, Brain Infarcts, And Cognitive And Motor Decline In Aging (ABICMA): Final Cerebral Infarct Results from a Community-Based, Longitudinal, Clinical-Pathological Study (S62.002)

OBJECTIVE: In the ongoing Antiphospholipid Antibodies, Brain Infarcts, and Cognitive and Motor Decline in Aging Study (Arvanitakis Z, et al: Neuroepidemiology 2013) we tested the hypothesis that aPL are associated with an increased risk of brain infarcts (BI) at autopsy and are related to cognitive and motor decline in aging. We present the final results for cerebral infarction. BACKGROUND: Antiphospholipid antibody positivity (aPL+) has been associated with clinical ischemic stroke. DESIGN/METHODS: Baseline and follow-up stored blood assayed for aPL [anticardiolipin antibodies (aCL), lupus anticoagulant, antiphosphatidylserine antibodies, and anti-β2-glycoprotein 1 antibodies] from 2 longitudinal clinical-pathologic cohort studies based at Rush University [Rush Memory and Aging Project (MAP) and Religious Order Study (ROS)]. Standardized neuropathological protocol assessed BI (macro-/microscopic, cortical/subcortical) blinded to aPL status. We had 80% power to detect an odds ratio (OR) of 2. aPL+ was defined as positive on any one of the 4 aPL assays. Multiple logistic regression performed for independent effect of aPL+ on BI. RESULTS: aPL were assayed at baseline (n=572, mean 82±7 yrs., 30% male, 97% Caucasian) ~7yrs. prior to death. BI occurred in 279/572 (49%): macroscopic (37%: cortical 15%, subcortical 28%) and microscopic in 29%. Controlling for age and sex, aPL+ at baseline (OR 1.14, 95%CI 0.77,1.70, p = 0.50) or proximal to death (OR 0.98, (95%CI 0.65,1.48, p = 0.92) was not associated with BI. Neither macro- nor microscopic infarcts were associated with aPL+. Persistence (n= 426) of aPL+ was not associated with BI when aPL+ was defined as either any persistent aPL+ assay (OR 0.89, 95%CI 0.56, 1.41, p = 0.62) as the same aPL+ isotype (OR 0.90, 95%CI 0.55, 1.45, p = 0.66). CONCLUSIONS: Overall aPL+ at baseline, proximal to death, or persistent aPL+ are not independent risk factors for BI in the elderly. Study Supported by: NIH grants R01HL96944, R01AG040039, P30AG10161, R01AG15819, R01AG17917, R01 AG24480 Disclosure: Dr. Levine has received personal compensation in an editorial capacity for MedLink. Dr. Levine has received royalty payments as editor of a book. Dr. Arvanitakis has received personal compensation for activities with Vista Health. Dr. Arvanitakis has received research support from Ceregene, Inc. Dr. Brey has received personal compensation in an editorial capacity for Neurology Now. Dr. Rand has nothing to disclose. Dr. Schneider has received personal compensation for activities with AVID Radiopharmaceuticals, Inc., and GE Healthcare. Dr. Yu has nothing to disclose. Dr. Leurgans has nothing to disclose. Dr. Bennett has received personal compensation for activities with Danone Inc., Dr. Wilmar Schwabe GmbH & Co., KG Pharmaceuticals, and Eli Lilly & Company. Dr. Bennett has received research support from Danone, Inc.