Relation of antiphospholipid antibodies to postmortem brain infarcts in older people Academic Article Article uri icon


MeSH Major

  • Algorithms
  • Heart Ventricles
  • Hypertrophy, Left Ventricular
  • Image Processing, Computer-Assisted
  • Magnetic Resonance Imaging
  • Ventricular Remodeling


  • © 2015 American Heart Association, Inc. 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, communitydwelling 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-phosphatidylserine) 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.

publication date

  • January 2015



  • Academic Article


Digital Object Identifier (DOI)

  • 10.1161/CIRCULATIONAHA.114.012479

PubMed ID

  • 25301832

Additional Document Info

start page

  • 182

end page

  • 189


  • 131


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