Açık Kalp Cerrahisi Geçiren Erişkin Hastalarda Intraoperatif Gelişebilecek Mikroserebral Hasarın Belirlenmesinde Preoperatif Adropin, Nöron Spesifik Enolaz (Nse) ve Nörofilament Hafif Zincir (Nfl) Düzeylerinin Postoperatif Nse ve Nfl Düzeyleri ile İlişkisi
xmlui.mirage2.itemSummaryView.MetaDataShow full item record
Atherosclerotic cardiovascular disease is the most common non-communicable cause of death in the world. Coronary artery and cerebrovascular diseases are the most common forms of atherosclerosis. Despite the advances in the management of those diseases, open heart surgery still stays as the primary treatment modality, in which, cardiopulmonary bypass (CPB) is usually utilized. One of the most CPB-related devastating complications is central nervous system injury. Although, major complications such as cerebral injury-which might be caused by micro-and macro-emboli are commonly seen; minor complications like confusion, stupor, and coma can also be seen as a result of low-pressure in CPB. Thus, it is crucial to predict the risk of neurological injury preoperatively to intervene promptly when these complications occur. Adropin is a biomarker that is negatively correlated with the prevalence of atherosclerotic vascular diseases. Preoperative and postoperative 1st-hour levels of Adropin, a biomarker whose correlation with the extent of atherosclerotic vascular disease has been proven by studies, were compared in terms of adropin level course. Then, the correlation of neuron-specific enolase and neurofilament light chain levels, which indicate nerve damage, with their levels at the postoperative 1st, 24th, and 72nd hours were examined. Forty-two patients who were undergone open heart surgery were included in the study. No findings in favor of significant stenosis were found in the carotid arteries and other vascular structures related to the head and neck, according to the physical examination and imaging techniques. No postoperative major neurologic complications nor death were observed. Confusion in 1 patient and lethargy in 1 patient were observed. Since the patients were followed up until discharge, it was not possible to evaluate them in terms of cognitive impairment. All of the patients were diagnosed with CAD and therefore all patients underwent CABG operation. It was observed that there was no significant relationship and correlation between the preoperative and postoperative 1st-hour adropin levels. Therefore, comparisons of parameters were made with the preoperative adropin level. The patients were divided into two groups as low (<4.7 pg/dl) and high preoperative adropin levels. Postoperative NSE levels of those with low adropin levels were found to be higher than the other group (P>0.05). There was no correlation between NFL levels and adropin levels. The patients were followed up with NIRS monitoring throughout the surgery. NIRS levels were recorded at pre-CPB, during CPB when the aorta was clamped and declamped, and at post-CPB. No significant decrease in NIRS levels was observed. When the relationship between NIRS values at post-CPB and preoperative adropin levels were examined, the NIRS levels of those with low adropin levels were found to be lower than the other group, but the relationships were not statistically significant. The insignificance of our results does not mean that adropin cannot be a predictive parameter of atherosclerotic involvement of cerebral vascular structures. CPB-related neurological complications will always remain as a major problem. For this reason, we think that controlled, randomized trials with larger sample sizes are needed to determine the presence of specific predictive markers preoperatively in patients with atherosclerotic cardiovascular diseases. As a result, these markers may reduce the incidence of neurological complications.