Is postoperative cognitive decline after cardiac surgery associated with plasma beta amyloid 1–42 levels?

Abstract

Background Postoperative cognitive decline following cardiac surgery is one of the frequently reported complications affecting postoperative outcome, characterized by impairment of memory or concentration. The aetiology is considered multifactorial and the research conducted so far has presented contradictory results. The proposed mechanisms to explain the cognitive decline associated with cardiac surgery include the neurotoxic accumulation of β-amyloid (Aβ) proteins similar to Alzheimer's disease. The comparison of coronary artery bypass grafting procedures concerning postoperative cognitive decline and plasmatic Aβ1-42 concentrations has not yet been conducted. Methods The research was designed as a controlled clinical study of patients with coronary artery disease undergoing surgical myocardial revascularization with or without the use of a cardiopulmonary bypass machine. All patients completed a battery of neuropsychological tests and plasmatic Aβ1-42 concentrations were collected. Results The neuropsychological test results postoperatively were significantly worse in the cardiopulmonary bypass group and the patients had larger shifts in the Aβ1-42 preoperative and postoperative values than the group in which off-pump coronary artery bypass was performed. Conclusions The conducted research confirmed the earlier suspected association of plasmatic Aβ1-42 concentration to postoperative cognitive decline and the results further showed that there were less changes and lower concentrations in the off-pump coronary artery bypass group, which correlated to less neurocognitive decline. There is a lot of clinical contribution acquired by this research, not only in everyday decision making and using amyloid proteins as biomarkers, but also in the development and application of non-pharmacological and pharmacological neuroprotective strategies.

Persistent Depletion of Neuroprotective Factors Accompanies Neuroinflammatory, Neurodegenerative, and Vascular Remodeling Spectra in Serum Three Months after Non-Emergent Cardiac Surgery

“…We observed an increase in serum amyloid levels, as previously described, but our study cohort is significantly more extensive and accounts for several peri-operative variables [ 22 , 25 , 78 , 81 ]. Our prior study also showed changes in serum total tau, but a much more sensitive technique was used [ 19 ].…”

“…Our data are consistent with some prior observations. Amyloid elevations post-surgery were reported previously in a study enrolling 54 male patients undergoing on and off-pump revascularization [ 22 ]. Interestingly, patients subjected to the off-pump procedures experience a lower value change in amyloid levels than the presurgical levels.…”

“…Cardiac surgery patients may also experience cognitive-related post-surgical effects due to surgery-associated inflammation, peri-operative hypoperfusion, and free radicals creating a neurotoxic environment as evidenced by the peri-operative release of neurofilament light (NF-L) and protein S100 [ 10 , 11 , 12 , 13 ]. Furthermore, the persistence of local post-surgical neuroinflammation compounds neuronal damage and may lead to shrouded neurodegeneration as part of the chronic process of postoperative neurocognitive decline (POCD) [ 9 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 ].…”

“…This process is self-sustained even after an initial insult resolution, creating a risk of long-term neurodegeneration. Therefore, peri-operative insult, peripheral inflammation, and neuroinflammation synergize, leading to various brain injuries and several POCD subtypes [ 9 , 13 , 22 , 68 ]. This heterogeneity may be reflected in the composition and dynamic resolution of the classical and non-classical neurodegenerative markers.…”

Recent progress on the role of non-coding RNA in postoperative cognitive dysfunction

“…There is increasing evidence for these proteins role in POCD. In a clinical trial with the aim to investigate the association between POCD and plasmatic Aβ1-42 concentrations, Požgain et al (2022) demonstrated the earlier suspected relationship between plasmatic Aβ1-42 concentration and POCD, implicating Aβ proteins in the pathogenesis of early POCD (Požgain et al, 2022). Furthermore, a pre-clinical study showed that isoflurane exposure increased the levels of Aβ and phosphorylated tau protein in brain, and lead to the impairment of spatial memory, probably through the activation of the A1A receptor (Zuo et al, 2018).…”