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Ann Thorac Surg 2004;78:52-53
© 2004 The Society of Thoracic Surgeons

Invited commentary

Duke University Medical Center, Box 3094, Durham, NC 27710, USA

e-mail: h.grocott{at}duke.edu

In this study by Fazio and colleagues, an important mystery in the field of peripheral marker detection of cardiac surgery-associated neurologic injury is answered. In an ideal world, the use of serum markers would provide an attractive means to diagnose brain injury in a setting where the clinical diagnosis is frequently hampered by the residual effects of anesthesia and imaging diagnostic techniques that either lack specificity and sensitivity or present logistical problems.

Indeed, a great deal of work has been published regarding the relationship of S100ß to neurologic injury in this setting. S100ß was once thought to be an ideal marker of cardiac surgery-associated neurologic injury because its glial cell origin made it brain specific. However, subsequent reports that there may be extra-cerebral sources for S100ß led to the questioning of its specificity as a marker to identify cerebral injury in this setting [1]. This led to considerable dampening of enthusiasm for its continued investigation and also presented a perplexing problem. That is, if S100ß was allegedly brain specific, why was it present in such high concentration in the blood present in the cardiotomy return?

This present study addresses the reasons responsible for this apparent extra-cerebral S100ß. What the authors now demonstrate is that the S100ß immunodetection techniques that previously identified S100ß in high concentration in the blood from the pericardial cavity (that was returned to the venous reservoir via the cardiotomy suction), and thus was detectable in high quantities in the peripheral blood, did so due to a cross-reactivity of S100ß with several other high molecular weight proteins. As a result, although S100ß is detectable using the commercially available ELISA, proteins other than S100ß were actually being detected.

This new finding, however, does not fundamentally change the fact that although there may be a relationship—albeit weak—between early S100ß elevations and neurologic injury, the relationship is, at best, an indirect one. That is, if S100ß is present in the cardiotomy return and, as demonstrated by Brooker and colleagues, the cardiotomy return is an important source of cerebral emboli which themselves can be injurious [2], then the link between these early elevations in S100ß and neurologic injury is likely nothing more than an epiphenomenon. Although there are multiple sources for the emboli that cause injury to the brain, it is clear that the lipid and other debris constituents present in the cardiotomy return bear a more direct relationship to neurologic injury. The S100ß, whether real or erroneous, is simply an innocent bystander that is likely to only reflect the load of material being returned via the cardiotomy. The S100ß, in and of itself, also does not represent any direct relationship to injury.

It should be noted, however, that this study does in no way negate the potential diagnostic (although still poorlydefined) value of late increases in S100ß after cardiac surgery, long after the chest is closed and cardiotomy influences have dissipated (24 hours or more), or its role in other settings of cerebral injury. It simply provides a previously unknown answer to the question of why S100ß was detectable in such high quantities after cardiac surgery, and contributes to our understanding of why the early increases related so weakly to neurologic injury. In addition, it makes it clear that one of the major roadblocks in trying to use peripheral markers to diagnose cerebral injury in the setting of cardiac surgery remains specificity. The search for the ideal marker of cardiac-associated cerebral injury continues.

References

1. Anderson R.E., Hansson L.O., Liska J., et al. The effect of cardiotomy suction on the brain injury marker S100ß after cardiopulmonary bypass. Ann Thorac Surg 2000;69:847-850.[Abstract/Free Full Text]
2. Brooker R.F., Brown W.R., Moody D.M., et al. Cardiotomy suction: a major source of brain lipid emboli during cardiopulmonary bypass. Ann Thorac Surg 1998;65:1651-1655.[Abstract/Free Full Text]

This article has been cited by other articles:

				D.C. Whitaker, A.J.E. Green, J. Stygall, M.J.G. Harrison, and S.P. Newman Evaluation of an alternative S100b assay for use in cardiac surgery: relationship with microemboli and neuropsychological outcome Perfusion, July 1, 2007; 22(4): 267 - 272. [Abstract] [PDF]

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Add to Personal Folders Download to citation manager Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Grocott, H. P. Search for Related Content PubMed Articles by Grocott, H. P. Related Collections Cerebral protection