The increase of blood anticardiolipin antibody depends on the underlying etiology in cerebral ischemia

Although anticardiolipin antibody (aCL) has been suggested to be a potent risk factor for thrombosis and atherosclerosis in multiple arterial beds, conflicting results still exist between aCL and cerebral ischemia in the general stroke population. To elucidate if this discrepancy relates to the heterogeneity of underlying etiologies, blood beta₂-glycoprotein I dependent-aCL was evaluated in 432 Taiwanese adults associated with cerebral ischemia who were classified into five subtypes according to their causes of cerebral ischemia. The results were compared with those in 100 healthy controls. A definite increase of aCL-IgG isotype was found in 41 patients (9.35%) and four controls (4.0%). The relative risk was 2.52. The frequency of increased aCL-IgG was 12.2%, 12.8%, 8.8%, 3.9%, and 3.5% in patients with large-artery atherosclerotic disease, stroke of unknown etiology, small-artery occlusive disease, cardioembolism, and stroke of other known etiology, respectively. Only patient with large-artery atherosclerotic disease (p<0.025) and stroke of unknown etiology (p<0.05) had a higher frequency of increased aCL than control. The frequencies of abnormal result of activated partial thromboplastin time, antinuclear factor, Coombs' test, and venereal disease research laboratory were 2.84%, 1.22%, 1.02%, and 1.34% in these 41 patients, respectively. Accordingly, aCL-IgG selectively increases in patients with large-artery atherosclerosis and stroke of unknown etiology, reflecting selective activation of humoral immunity for aCL in the pathogenesis of cerebral ischemia.