Greater levels of S100β after coronary artery bypass grafting (CABG) surgery are thought to indicate cerebral injury [1]. Lipid peroxidation arising from oxidative stress occurs during cardiopulmonary bypass (CPB), and is indicated by increased malondialdehyde concentration [2]. We report the relationships between malondialdehyde production, S100β, and neurological and cognitive scoring 3 months after CABG.

Eighty-six patients aged 60 ± 10 years (mean ± standard deviation) were studied. A structured neurological examination and a battery of cognitive tests were completed the day before and 3 months after surgery by 68 of these patients. A catheter was positioned in the jugular bulb and blood samples were drawn immediately after CPB (post bypass [PBP]) and 6 h after surgery for estimation of S100β and malondialdehyde levels. Lactated Ringer's was used to prime the CPB circuit in the first 21 patients, and subsequent patients received nonlactated prime. Administration of aprotonin was noted. Intervariable relationships was assessed by two-tail Pearson correlation, and stepwise linear regression analysis was used to model malondialdehyde and S100β production.

There was no significant correlation between postsurgical cognitive score and S100β level (r = 0.036; P > 0.1; Table 1).

There is a positive relationship between lipid peroxidation and S100β immediately after CPB. S100β 6 h after surgery is related to neurological score, but not to cognitive score. However, neurological score accounts for only 3% of the variance in S100β, and on the basis of this evidence it can not be recommended as a surrogate marker of subtle neurological outcomes after CABG surgery.