N-acetylaspartate: serum marker of reperfusion in ischemic stroke

Abstract

Conventional ways of monitoring reperfusion in acute ischemic stroke have several limitations. In searching for an alternative, we evaluated biochemical serum markers of stroke change in relation to reperfusion. N-acetylaspartate (NAA) is a small amino acid synthesized by neuronal mitochondria, which can be released in the extracellular space after reperfusion in animal models of brain ischemia. S100B is a well-known peripheral marker of brain damage in various neurologic diseases, including stroke. Serum samples were analyzed from 13 patients with ischemic stroke who were either treated conservatively or with recombinant tissue plasminogen activator. Blood was drawn at baseline; after 30 minutes; after 1, 2, 4, and 8 hours; and between 12 to 24 hours. Serum concentrations of NAA were analyzed using a gas chromatography-mass spectrometry method. S100B was analyzed using an automated immunoluminometric assay. Reperfusion was assessed using transcranial Doppler and clinical criteria. Reperfusion (n = 4) was associated with a transient rapid increase in serum NAA levels. Such an early rapid increase of NAA was not observed for patients with persistent occlusion at 12 to 24 hours (n = 4) and patients with no occlusion on baseline transcranial Doppler (n = 5). NAA peak levels and area under the curve values were significantly higher after reperfusion in comparison with normal transcranial Doppler findings or persistent occlusion (P = .003 and P = .05, respectively). No differences were found between these groups for S100B levels. In patients with acute ischemic stroke, serum NAA levels transiently raise after reperfusion.