Abstract
To the Editor: Brey et al1 reported what is to their knowledge the first study to demonstrate a prospective association between sera cofactor-dependent anticardiolipin antibodies and stroke independent of other risk factors as well as myocardial infarction (MI). In addition to lending support to basic research that has shown the pathogenicity of antiphospholipid-protein antibodies (aPL) in thrombosis,2 this well-conducted epidemiological study of Japanese-American men enrolled in the Honolulu Heart Program and followed for up to 20 years provides evidence for the role of aPL as potentially important markers and/or causes of increased vascular risk associated with ischemic stroke and MI. It is known that stroke is a multisystemic disorder involving mechanisms of thrombotic and neurotoxic coupling.3 Biochemical markers including glutamate, homocysteine (a sulfinic analog of aspartate4), and N -methyl-d-aspartate (NMDA) receptor autoantibodies (aAb) are independently associated with neurotoxicity and can be measured in blood.5 The aPLs are a part of the structural components of …
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