Serum biomarkers of brain injury after uncomplicated cardiac surgery: Secondary analysis from a randomized trial

Abstract

Background: Postoperative cognitive dysfunction is common after cardiac surgery.Postoperative measurements of brain injury biomarkers may identify brain damage and predict cognitive dysfunction. We describe the release patterns of five brain injury markers in serum and plasma after uncomplicated cardiac surgery.Methods: Sixty-one elective cardiac surgery patients were randomized to undergo surgery with either a dextran-based prime or a crystalloid prime. Blood samples were taken immediately before surgery, and 2 and 24 h after surgery. Concentrations of the brain injury biomarkers S100B, glial fibrillary acidic protein (GFAP), tau, neurofilament light (NfL) and neuron-specific enolase (NSE)) and the blood-brain barrier injury marker β-trace protein were analyzed. Concentrations of brain injury biomarkers were correlated to patients' age, operation time, and degree of hemolysis.Results: No significant difference in brain injury biomarkers was observed between the prime groups. All brain injury biomarkers increased significantly after surgery (tau +456% (25th-75th percentile 327%−702%), NfL +57% (28%−87%), S100B +1145% (783%−2158%), GFAP +17% (−3%−43%), NSE +168% (106%−228%), while β-trace protein was reduced (−11% (−17−3%). Tau, S100B, and NSE peaked at 2h, NfL and GFAP at 24 h. Postoperative concentrations of brain injury markers correlated to age, operation time, and/or hemolysis. Conclusion:Uncomplicated cardiac surgery with cardiopulmonary bypass is associated with an increase in serum/plasma levels of all the studied injury markers, without signs of This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

The effect of stent and decalcification on mitral annular motion after aortic valve replacement

“…With only three sutures needed to anchor the valve, rapid-deployment valve replacement can shorten cardiopulmonary bypass time, thus reducing the risk for complications associated with cardiopulmonary bypass. 6,7 Major differences in TAVR and RDV are the use of cardiopulmonary bypass and the need for decalcification. Although the effect of cardiopulmonary bypass on physiology are well known, [6][7][8] the effect of decalcification after AVR is not well studied.…”

“…6,7 Major differences in TAVR and RDV are the use of cardiopulmonary bypass and the need for decalcification. Although the effect of cardiopulmonary bypass on physiology are well known, [6][7][8] the effect of decalcification after AVR is not well studied.…”

“…For surgical AVR, rapid‐deployment valve replacement, which uses stent technology similar to TAVR to anchor the valves at the aortic annulus, is another evolving technology used today. With only three sutures needed to anchor the valve, rapid‐deployment valve replacement can shorten cardiopulmonary bypass time, thus reducing the risk for complications associated with cardiopulmonary bypass 6,7 . Major differences in TAVR and RDV are the use of cardiopulmonary bypass and the need for decalcification.…”

Persistent Depletion of Neuroprotective Factors Accompanies Neuroinflammatory, Neurodegenerative, and Vascular Remodeling Spectra in Serum Three Months after Non-Emergent Cardiac Surgery

“…Cardiac surgery patients may also experience cognitive-related post-surgical effects due to surgery-associated inflammation, peri-operative hypoperfusion, and free radicals creating a neurotoxic environment as evidenced by the peri-operative release of neurofilament light (NF-L) and protein S100 [ 10 , 11 , 12 , 13 ]. Furthermore, the persistence of local post-surgical neuroinflammation compounds neuronal damage and may lead to shrouded neurodegeneration as part of the chronic process of postoperative neurocognitive decline (POCD) [ 9 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 ].…”

“…The multiple pathways leading to POCD exacerbate the “classic-markers”-related symptoms of AD. Concomitantly, several non-classical markers of neurodegeneration may also contribute to POCD progression [ 15 , 23 , 24 , 25 ]. While the emergence of clinically apparent cognitive decline may be delayed for years, these same inflammatory processes also contribute to a higher risk of cerebrovascular accidents (CVA) in the peri-operative period [ 9 , 13 , 24 , 68 ].…”