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Department of Anesthesiology, Duke University Medical Center, Durham, NC, h.grocott{at}duke.edu
To the Editor:
The recent report by Kofke et al. (1) outlining a relationship between apolipoprotein E genotype and serum markers of "cerebral injury" after cardiac surgery raises some interesting issues. At first glance, the hypothesis that biochemical markers of brain injury after cardiac surgery demonstrate larger increases in patients possessing the Apo
4 allele, an allele previously associated with worse neurologic outcome after cardiac surgery, (2) seems logical. However, their explanation that this relationship relates to the increased susceptibility of Apo4 patients to cerebral ischemia during major vascular and cardiac surgery has some inherent flaws. The weakness in this argument stems from the fact that extracerebral sources for S100ß have been identified; mediastinal blood aspirated by cardiotomy suction has been shown to have high concentrations of S100ß (3). As a result, the use of the cardiotomy grossly contaminates the blood with S100ß, making serum levels an unreliable surrogate of cerebral injury. Furthermore, the recent work by Fazio et al. has largely explained the true reason for the apparent extracerebral source for S100ß (4). The commercially available assays used by Kofke et al. and others lack sufficient specificity for S100ß, with the S100ß signal representing other high molecular proteins (such as heptaglobin precursor I).
However, this does leave the question as to how the authors found this apparent relationship. A potential, although admittedly not exclusive, explanation for this may lie in an enhanced inflammatory response to cardiopulmonary bypass previously demonstrated in Apo4-positive patients (5). An augmented inflammatory response may lead to increased bleeding (6) and if the Apo4 patients bled more, they likely would have had more mediastinal and pericardial blood (with high S100ß levels) returning to the venous reservoir via the cardiotomy suction and, as a result, have higher blood levels of S100ß (7). Therefore, the link between S100ß and Apo4 is most likely unrelated to cerebral injury per se but may represent an indirect link to an enhanced inflammatory response.
References
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