## 4 Discussion
This is an interesting and important finding because studies suggest that there is a link between selenium deficiency and an increased risk of developing atherosclerotic plaques. For example, endothelial cells are more likely to undergo apoptotic destruction due to selenium deficiency, and that contributes to increased atherosclerotic plaque instability [36]. Selenium deficiency negatively affects endothelium-mediated function, as selenium deficiency can lead to increased thromobaxene concentration and decreased prostaglandin concentration, causing vasoconstriction [36]. There is evidence that the addition of selenium to dietary supplements containing antioxidants may reduce the risk of cardiovascular mortality [11]. For example, four years of supplementation with selenium and coenzyme Q10 reduced cardiovascular mortality risk in a group of healthy elderly participants but also in subgroups of patients with arterial hypertension, diabetes mellitus, and myocardial infarction after 12 years [37], but the mechanism is not fully known. Low soil selenium concentrations have been associated with an increased incidence of cardiomyopathy characterized by extensive myocardial fibrosis (Keshan disease) [38]. In addition, low selenium concentrations have been associated with subsequent cardiovascular death in patients with ACS [39], so supplementation of selenium in the daily diet may be an important avenue to prevent various cardiovascular diseases. The consumption of enriched eggs in our study increased serum vitamin E concentrations and improved microvascular and macrovascular reactivity to vasodilator stimuli. It has been previously demonstrated that vitamin E can influence vascular reactivity. For example, oral vitamin E supplementation can ameliorate the transient impairment of endothelial function after smoking by acting on the oxidative status but has no effect on chronic endothelial dysfunction in healthy male smokers [40]. Furthermore, the oral application of a \(\gamma\)-T-rich tocopherol (TmT) mixture during short-term nicotine-replacement-therapy-assisted smoking cessation improved endothelial dysfunction measured by FMD in healthy former smokers [41]. To our knowledge, our study is the first in which vitamin E was administered in the form of a functional food and showed a significant beneficial effect on vascular relaxation in participants with CCS. Selenium supplementation can reduce oxidative stress levels (measured as MDA levels and total antioxidant capacity) [42]. Vitamin E also has antioxidant effects [43]; for example, supplementation with vitamin E (900 IU/day) in combination with vitamin C (1000 mg/day) in subjects with high-salt diets prevented increased oxidative stress [44]. However, in our study, oxidative stress biomarkers were not altered by the diet, even though eggs were fortified with vitamin E and selenium. This could be due to the long duration of CCS in the patients, in which oxidative stress plays a role at baseline but not during the course of the disease. There is increasing evidence suggesting that n-3 PUFA supplementation improves micro- and macrovascular function [45]. In patients with peripheral arterial disease, the intake of n-3 PUFAs improved macrovascular reactivity, as measured by FMD [46]. Studies in animal models suggest that n-3 PUFAs can increase NO levels, causing ex vivo dilation of bovine coronary arteries [47; 48]. In atherosclerosis, there is a disruption of the eNOS system, which decreases the bioavailability of NO in the vessel wall. Moreover, n-3 PUFAs can activate eNOS in cultured human endothelial cells [49]. We found that the consumption of enriched eggs increased the serum protein concentration of iNOS, whereas the levels of eNOS and nNOS did not change. The improvement in endothelial function in our subjects may be explained by changes in iNOS levels. An increase in the expression of the nNOS isoform was found in our previous studies in healthy young adults who consumed Nutri4 eggs [13].