# Effect of Carotid Stenosis Severity on Patterns of Brain Activity in Patients after Cardiac Surgery
## 4 Discussion  
As found in our study, the frequency of POCD was higher in patients with less than 50% CA stenoses in comparison to the patients without them (76% vs. 61%). However, the frequency was comparable in combined coronary and carotid surgery and isolated CABG (63% vs. 61%). The POCD structure both in the patients with CA stenosis of less than 50% and in patients with hemodynamically significant CA stenoses (70-99%) consisted of executive function decline, which was determined as the non-successful performance of neurodynamic tasks in these patients. Previously, it has been shown that for the correct assessment of the signal sequence in neurodynamic tests, a high level of indicative activity is required. This causes increased brain energy consumption [40]. It can be assumed that highly organized cognitive activity is disrupted by the deterioration of cerebral blood flow in patients with CA stenoses. We also demonstrated that the patients with CA stenosis of less than 50% had more pronounced signs of brain dysfunction as compared with patients without stenoses. These changes were diffuse and expressed as higher power values of resting state EEG in the frequency band from 6 to 13 Hz. Earlier, it has been shown that an increase in the slow rhythm power is associated with a decrease in the level of cortical activation and may be a reflection of chronic cerebral ischemia [41, 42]. It should be noted that these pathological EEG signs were observed in patients with CA stenosis of less than 50% already in the preoperative period and persisting after surgery. One of the possible causes of neurological complications in patients with hemodynamically insignificant CA stenoses may be the instability of small atherosclerotic plaques with the development of vasoconstrtor and procoagulant effects [43]. There is an assumption that the atherosclerosis in patients with multiple vascular lesions may proceed more aggressively [44]. We may propose that such patients probably develop a more pronounced systemic inflammatory response associated with cardiopulmonary bypass. Earlier experiments showed that the combined effect of ischemia and hypoxia induces an increase in the production of pro-inflammatory cytokines (TNF-\(\alpha\), IL-1\(\beta\) and IL-6) in the brain, which contributes to damage and increased permeability of the blood-brain barrier, and as a consequence, the development of brain edema [45, 46]. In addition, cerebral blood flow autoregulation may be disrupted more often in patients with CA stenoses, leading to the decrease in the brain's resistance to acute ischemia and hypoperfusion associated with cardiopulmonary bypass [36, 47]. The state of the circle of [PERSON] and the density of leptomeningeal collaterals also contribute to brain  
Figure 5: The topography of the postoperative theta1 rhythm power changes in the patients undergoing isolated CABG and simultaneous intervention (CABG+CEA): (**a**) left hemisphere; (**b**) right hemisphere; error bars denote SE, *—\(p<0.05\) Newman–Keuls multiple comparison test for between-group differences. -hemodynamic parameters [48; 49]. On the other hand, the interaction between macro- and microcirculation requires attention in regard to postoperative neurophysiological changes in the patients after cardiac surgery. Earlier, it has been found that carotid atherosclerosis, white matter hyperintensities and lacunar infarction are associated with and commonly contribute to the deterioration of neurological function [50; 51]. Additionally, one conclusion we reached was that patients with CA stenoses of less than 50% are vulnerable to the effects of the factors that accompany cardiac surgery using cardiopulmonary bypass compared with patients without CA lesions. The presence of even hemodynamically insignificant stenoses in cardiac surgery patients makes it possible to include them in the group at increased risk of brain damage in the perioperative period.