Purpose Ever-increasing noncardiac surgeries are performed in patients aged 80 years or over with coronary artery disease (CAD). The objective of the study was to explore the incidence and risk factors of perioperative cardiac complications (PCCs) for the oldest-old patients with CAD undergoing noncardiac surgery, which have not been evaluated previously. Patients and Methods A total of 547 patients, aged over 80 years, with a history of CAD who underwent noncardiac surgery were enrolled in this retrospective study. Perioperative clinical variables were extracted from the electronic medical records database. The primary outcome was the occurrence of PCCs intraoperatively or within 30 days postoperatively, defined as any of the following complications: acute coronary syndrome, heart failure, new-onset severe arrhythmia, nonfatal cardiac arrest, and cardiac death. Multivariate logistic regression analysis and multivariate Cox regression model were both performed to estimate the risk factors of PCCs. The incidence of PCCs overtime was illustrated by the Kaplan–Meier curve with a stratified Log-rank test. Results One hundred six (19.4%) patients developed at least one PCC, and 15 (2.7%) patients developed cardiac death. The independent risk factors contributing to PCCs were age ≧85 years; body mass index ≧30 kg/m 2 ; the history of angina within 6 months; metabolic equivalents <4; hypertension without regular treatment; preoperative ST-T segment abnormality; anesthesia time >3 h and drainage ≧200 mL within 24 h postoperatively. Conclusion The incidence of PCCs in elderly patients over 80 years with CAD who underwent noncardiac surgery was high. Comprehensive preoperative evaluation, skilled surgical technique, and regular postoperative monitoring may help to reduce the occurrence of PCCs in this high-risk population.

Intraoperative hypothermia is a common complication during operations and is associated with several adverse events. Postoperative cognitive dysfunction (POCD) and its adverse consequences have drawn increasing attention in recent years. There are currently no relevant studies investigating the correlation between intraoperative hypothermia and POCD. The aim of this study was to assess the effects of intraoperative hypothermia on postoperative cognitive function in rats undergoing exploratory laparotomies and to investigate the possible related mechanisms. We used the Y-maze and Morris Water Maze (MWM) tests to assess the rats’ postoperative spatial working memory, spatial learning, and memory. The morphological changes in hippocampal neurons were examined by haematoxylin-eosin (HE) staining and hippocampal synaptic plasticity-related protein expression. Activity-regulated cytoskeletal-associated protein (Arc), cyclic adenosine monophosphate-response element-binding protein (CREB), S133-phosphorylated CREB (p-CREB [S133]), α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor 1 (AMPAR1), and S831-phosphorylated AMPAR1 (p-AMPAR1 [S831]) were evaluated by Western blotting. Our results suggest a correlation between intraoperative hypothermia and POCD in rats and that intraoperative hypothermia may lead to POCD regarding impairments in spatial working memory, spatial learning, and memory. POCD induced by intraoperative hypothermia might be due to hippocampal neurons damage and decreased expression of synaptic plasticity-related proteins Arc, p-CREB (S133), and p-AMPAR1 (S831).

Intraoperative hypothermia is very common and leads to memory decline. The hippocampus is responsible for memory formation. As a functional core area, the cornu ammonis 1 (CA1) region of the hippocampus contains abundant blood vessels and is susceptible to ischemia. The aim of the study was to explore vascular function and neuronal state in the CA1 region of rats undergoing intraoperative hypothermia. The neuronal morphological change and activity-regulated cytoskeleton-associated protein (Arc) expression were evaluated by haematoxylin-eosin staining and immunofluorescence respectively. Histology and immunohistochemistry were used to assess vascular function. Results showed that intraoperative hypothermia inhibited the expression of vascular endothelial growth factor and endothelial nitric oxide synthase, and caused reactive oxygen species accumulation. Additionally, the phenotype of vascular smooth muscle cells was transformed from contractile to synthetic, showing a decrease in smooth muscle myosin heavy chain and an increase in osteopontin. Ultimately, vascular dysfunction caused neuronal pyknosis in the CA1 region and reduced memory-related Arc expression. In conclusion, neuronal disorder in the CA1 region was caused by intraoperative hypothermia-related vascular dysfunction. This study could provide a novel understanding of the effect of intraoperative hypothermia in the hippocampus, which might identify a new research target and treatment strategy.