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.