Postop Neurocognitive Dip Tied to High CRP Levels


SAN DIEGO — Increased levels of C-reactive protein and other markers of perioperative inflammatory response are associated with neurocognitive decline following cardiac surgery, Dr. Basel Ramlawi said at a congress sponsored by the Association for Academic Surgery and the Society of University Surgeons.

Dr. Ramlawi and his associates prospectively evaluated 41 patients who underwent coronary artery bypass graft and/or valve procedures that used cardiopulmonary bypass. The patients' mean age was 67 years. All patients had neurocognitive testing preoperatively, postoperatively at day 4, and at 3 months. The validated tests took 45 minutes to administer and covered memory, executive function, naming, attention, fluency, and premorbid intelligence, said Dr. Ramlawi of the division of cardiothoracic surgery at Harvard Medical School, Boston. Neurocognitive decline was defined as performing one standard deviation from baseline on at least 25% of tasks.

Study participants also underwent serum testing preoperatively, postoperatively at 6 hours, and at 4 days. Levels of C-reactive protein (CRP) and of interleukin 1β, IL-6, and IL-10 were assessed, and an increase of serum tau protein after surgery was used as a marker of axonal central nervous system damage.

Of the 41 patients, 7 (17%) developed neurocognitive decline. Baseline characteristics and predictors of neurocognitive decline such as age, education level, and perioperative temperature did not differ significantly between patients with and without postoperative neurocognitive decline.

However, patients who experienced postoperative neurocognitive decline had significantly greater increases of CRP, IL-1β, and IL-10 than those who had no decline.

In addition, the level of tau protein was increased 78% in patients with neurocognitive decline, compared with 29% in their counterparts who did not show a decline.

“There exists a significant association [between] the magnitude and persistence of the perioperative inflammatory response and neurocognitive decline in this cohort,” Dr. Ramlawi said. “This association is likely mediated by axonal damage.”

According to the medical literature, the incidence of neurocognitive decline is 20%–60% in the first 2 weeks after cardiac surgery. “It can range from 5% to 40% for periods up to 5 years after surgery,” he said, adding that the etiology of this complication is not known.

“It is likely a multifactorial problem,” Dr. Ramlawi said. “Several theories have been assessed. The most obvious one is ischemia. Any microemboli might cause this.”

Other possible factors include anesthesia, perioperative hypothermia, and low level of education.

“While there have been certain markers of brain injury following cardiopulmonary bypass, very few have been associated with clinical outcomes and neurocognitive decline,” he said. “Tau protein, on the other hand, assesses axonal damage and has not been [studied] in cardiac surgery before.”

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