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(Stroke. 2002;33:1181.)
© 2002 American Heart Association, Inc.

Letters to the Editor

Multiple Panel of Biomarkers for TIA/Stroke Evaluation

Svetlana A. Dambinova, PhD, DSc Guerman A. Khounteev, MD

Institute of the Human Brain, Russian Academy of Sciences, St. Petersburg, Russia

Alexandr A. Skoromets, MD, PhD, DSc

Department of Neurology and Neurosurgery, I.P. Pavlov’s Medical University, St. Petersburg, Russia

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 excitatory membranes containing glutamate receptors and may be involved in the neurotoxicity process as well.³ Consequently, the appearance of elevated levels of aPL in blood represents an additional indicator of NMDA neuroreceptor damage under ischemic conditions.

The development of a multiple panel of biomarkers for stroke analogous to that now in use for MI would be beneficial for the emergency bedside diagnosis of stroke and may help differentiate ischemic from hemorrhagic stroke. We assessed 3 proposed biomarkers⁵: glutamate and homocysteine as correlates of large and middle artery dysfunction, and NR2A aAb as a criterion of . . . [Full Text of this Article]

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