Article

Serologic markers of brain injury and cognitive function after cardiopulmonary bypass

Division of Cardiothoracic Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.
Annals of Surgery (Impact Factor: 8.33). 11/2006; 244(4):593-601. DOI: 10.1097/01.sla.0000239087.00826.b4
Source: PubMed

ABSTRACT To examine the association between biochemical markers of brain injury (MBI) and the inflammatory response in relation to neurocognitive deficiency (NCD) after cardiopulmonary bypass (CPB).
In cardiac surgery, NCD is a common but underdiagnosed complication with an unclear pathophysiology leading to significant morbidity. Despite extensive investigation, identification of a MBI for clinical use and clarifying the pathophysiology of NCD have not been achieved.
Forty patients undergoing CABG and/or valve procedures using CPB were administered a validated neurocognitive battery preoperatively and postoperatively at day 4 and 3 months. S-100b, neuron specific enolase (NSE), and tau protein were assayed as MBIs preoperatively and postoperatively at 6 hours and day 4. C-reactive protein (CRP), interleukin (IL)-6, C3a, and total peroxide levels were also quantified from serum. Impact of cardiotomy suction and antifibrinolytics on markers of brain injury was assessed.
The incidence of early NCD was 40% (16 of 40). NSE and tau protein at the 6-hour time point were both significantly elevated in the presence of NCD (NCD group) compared with those without NCD (NORM group) (8.69 +/- 0.82 vs. 5.98 +/- 0.61; P = 0.018 and 68.8 vs. 29.2%; P = 0.015; respectively). S-100b increase was not different between the NCD and NORM groups. Cardiotomy suction significantly elevated S-100b levels, whereas NSE and tau were not significantly influenced. Aprotinin did not have an effect on NCD or levels of MBIs. Also, the NCD group had significantly elevated CRP and peroxide levels compared with the NORM group at postoperative day 4 while C3a was significantly elevated at 6 hours.
NSE and tau are better associated with NCD and less influenced by cardiotomy suction compared with S-100beta. Inflammatory and oxidative stress is associated with NCD post-CPB.

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    • "It is possible that NT4/5 acts as a shielding factor by decreasing oxidative status and thus protects neuronal synapses, which in turn facilitates better functioning. Although not widely investigated, this is in line with studies suggesting a relationship between oxidative stress and neurocognition in a variety of other clinical populations [63-66]. Nevertheless, there is only one study in the literature that examined the relationship between oxidative damage and neurocognition in schizophrenia. "
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    • "In addition, the pathophysiological mechanism by which systemic inflammation results in the observed decrease of NSE is not clear. Increased levels of NSE are associated with deterioration of CF after cardiac surgery [46]. Also, increased NSE levels are associated with brain injury in septic patients, but an association between NSE and CFs in septic patients has not been examined. "
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