Neurocognitive decline in cardiac surgery—Distraction rather than destruction?

A neurocognitive decline is an undesirable event that can be observed in patients after cardiac surgery. It has been related to the use of cardiopulmonary bypass (CPB). Minor embolic or hyperinflammatory mechanisms are thought to be responsible. In this issue of the Journal of Cardiac Surgery, the neurocognitive decline was observed in 22 of 30 patients after cardiac surgery with CPB. Repeatable neuropsychological status tests were used and scores 4 days after surgery were 5%–15% lower than before. Mechanistic investigations with glycemic control and transcriptomic and cytokine analyses failed to provide an explanation but the frequency of this observation is worrisome.


COMMENTARY
Cardiac surgery became a reproducible treatment option for many patients around 50 years ago. For the following three decades, there were no or few treatment alternatives for many patients and cardiosurgical practice was characterized by the documentation of risks and activities to improve outcomes.
Cardiopulmonary bypass (CPB) is a key component in most surgical procedures, as it provides the basis for the safe conduct of all the different techniques described to address a cardiac condition today. However, CPB has also been associated with undesirable adverse events by causing, for instance, coagulation disorders, inflammatory response syndrome's or neurological events in varying degrees. 1 Even mild changes in neurocognitive function are often attributed to the use of CPB, suggesting that minor particulate or minor air embolism affects cerebral function. For decades such conditions (also known as "air head" or "pump head") were considered a given risk and "part of the package. after surgery were often 5%-15% lower than before surgery. The authors excluded a possible relation to glycemic control but were unable to provide more revealing insights despite sophisticated transcriptomic and cytokine analyses. Irrespective of possible molecular mechanisms explaining this finding, the fact that three-quarters of patients appear to experience neurocognitive decline after cardiac surgery is highly disturbing and requires deeper investigation.
The good news upfront: despite being a frequent clinical condition, the neurocognitive function is usually restored after 3 months, and at 1 year, cognitive function is indistinguishable from matched controls. 4,5 In addition, postoperative neurocognitive dysfunction is common in all kinds of surgery and its incidence has been described to be 5%-15% 6 and in certain high-risk groups (such as hip fracture patients), it may reach over 60%. 7 Thus, the association to the use of CPB may not be as clear as we thought.
The neurocognitive decline has also been reported in interventional patient populations. In patients with NSTEMI, for instance, undergoing percutaneous coronary interventions (PCIs), its incidence has been reported with 28.8%. 8 A recent cohort study from the American Health and Retirement Study on 1680 patients above 65 years of age assessed the change in the rate of memory decline after CABG or PCI. The authors found no difference between the two treatment options in the rate of memory decline. 9 They did not compare the results to a cohort that did not undergo invasive coronary artery diseases treatment, but the lack of differences in this long-term outcome between CABG and PCI questions again a specific technical aspect of surgery as the sole cause of neurocognitive dysfunction.
The current literature suggests that neurocognitive outcomes may be due to a hyperinflammatory state, 10 which may be the common denominator for all these observations. Scrimgeour et al. 3  It may be accidental that the amount of functional decline due to this distraction was similar to the neurocognitive decline measured in the above study 4 days after cardiac surgery using CPB, where a destructive mechanism is entertained. 3 Although the many different tests and characteristics used and assessed may not be directly comparable, such a consideration may be able to explain why postoperatively noted neurocognitive decline is temporary, reversible, not affected by diabetes mellitus, and not different between surgical and other interventional procedures. We, therefore, would like to ask, whether neurocognitive decline after cardiac surgery may be more due to mental distraction than cellular destruction. "May be", but in the absence of convincing evidence, our thoughts may also be a distraction from possible destruction. In any case, the phenomenon is there, but it is not necessarily surgery-specific.