Abstract
BackgroundPostoperative 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.MethodsThe 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.ResultsThe 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.ConclusionsThe 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.
Highlights
Postoperative cognitive decline following cardiac surgery is one of the frequently reported complica‐ tions affecting postoperative outcome, characterized by impairment of memory or concentration
The damage of overexpressed Aβ to memory, learning, and hippocampal volume has been related to acetylcholine synthesis and release in the central nervous system (CNS) since nicotine acetylcholine receptors have the key role in the neurotransmission and regulation of memory, consciousness, and learning
Body mass index (BMI) was 28,5 kg/m2 median, ranging from 25 kg/m2 to 31.3 kg/m2, there was no significant difference considering the type of surgery or Postoperative cognitive dysfunction (POCD). 83% of the patients declared as not paying attention to their diet
Summary
Postoperative cognitive decline following cardiac surgery is one of the frequently reported complica‐ tions affecting postoperative outcome, characterized by impairment of memory or concentration. 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. POCD is defined and measured by standardized mental function tests and the decline has been noted even 5 years after surgery, in spite of cerebral recovery. The precise pathophysiologic mechanisms of these factors influencing POCD development have not yet been described, but the proposed mechanisms for explaining the cognitive decline associated with cardiac surgery include the neurotoxic accumulation of β-amyloid (Aβ) proteins similar to Alzheimer’s disease (AD) [2,3,4]. Few studies have demonstrated changes of plasmatic and liquor concentrations of Aβ1-42 in patients with POCD, where the postoperative plasmatic concentration was lower and liquor concentration was higher, the results are contradictory and diverse between the studies [8, 12]
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