Introduction
Although there have been many advances in technology to help with intraoperative neurocognitive protection, the adverse effects from cardiopulmonary bypass (CPB) during cardiac surgery remain a major threat to patient outcomes. Advances in risk stratification, CPB, anesthesia methods, along with pre and postoperative care have changed cardiac surgical outcomes significantly over the past few decades, however optimizing protection of the central nervous system remains an area of ongoing effort. Furthermore, short-term neurocognitive deficits appear to be predictive of both long-term outcomes and quality of life.1
Given that the majority of cardiac surgery is still performed using CPB, it is important to better understand which patients will experience neurocognitive decline, and to what degree, in order to assist in both preoperative and perioperative counseling along with treatment decisions. Previous studies from our group suggest that neurocognitive outcomes in certain patients are related to transcriptional upregulation of specific genes that may play a role in inflammation and immunomodulation.2 Furthermore, activation of the inflammatory response may lead to penetration of the blood-brain barrier by cytokines either directly or via vagal nerve stimulation.3 Additionally, cognitive impairment has been shown to be a result of cytokine-mediated interactions between neurons and glial cells within the CNS.3 It remains unclear whether these inflammatory interactions occur in genetically predisposed patients or if there are risk factors that contribute to this inflammatory response, i.e., hyperglycemia during and after cardiac surgery. The aim of the present study is to elucidate possible risk factors of early NCD in patients undergoing cardiac surgery with CPB.