Introduction Neurocognitive decline (NCD) is a common complication in cardiac surgical patients. Its pathophysiology remains unknown; leading to significant morbidity particularly in the elderly. We studied the inflammatory response and CRP in relation to NCD following cardiopulmonary bypass and correlated this to a marker of axonal central nervous system (CNS) injury.
Methods Prospective cohort of 43 low-risk patients undergoing CABG and/or valve procedures using cardiopulmonary bypass were administered a neurocognitive battery preoperatively, postoperatively at day 4 and at 3 months. Battery consisted of eight validated assessments covering memory, executive function, naming, attention, fluency, and premorbid intelligence. Following published STS Consensus Statement, NCD was defined as one standard deviation from baseline on ≥ 25% of tasks. CRP, interleukin-1β (IL-1β), IL-6, and IL-10 were quantified from serum with high sensitivity immunoassay and fold-change(FC) calculated between preoperative/postoperative samples at 6 hrs. Increase of serum tau protein after surgery (dichotomous) was used as a marker of axonal CNS damage.
Results Cohort had an NCD rate of 45% (mean age 72 ± 3.6 years). Baseline characteristics and known predictors of NCD such as age, education level, and perioperative temperature were not significantly different between patients with/without NCD. Patients with NCD had a significantly higher increase of CRP, IL-1β and IL-10 compared to those without NCD, as described in the Table below. Serum tau protein increase was significantly correlated to NCD.
Conclusions Increased CRP and inflammatory response perioperatively is associated with NCD in patients following cardiopulmonary bypass. Inflammation plays a key role in NCD pathophysiology, likely via axonal CNS injury, and could become a target for prevention.
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