## 1 Introduction  
Cardiovascular diseases (CVDs) continuously remain the leading cause of death worldwide and are bound to increase as a burden with the aging population [1; 2]. According to the World Health Organization (WHO), approximately 17.9 million people died from CVDs in 2019, representing 32% of global deaths [3]. The vast majority of these disorders would be better managed if early diagnosis and elimination of some common risk factors, including physical inactivity, unhealthy diet, and tobacco or alcohol consumption, were applied [4]. As a dominant cause of CVD, atherosclerosis is responsible for most cardiovascular morbidity and mortality. It is acknowledged as a chronic inflammatory disease resulting in the deposition and accumulation of endogenously modified structures, specifically oxidized lipoproteins beneath the endothelial layer of arterial walls [5]. The lipid lesions can be found in the aorta in the first decade of life, however, they may become the cause of symptoms during later years of the disease [6]. Genetic as well as environmental factors estimate the expansion of the atherosclerotic plaques so that they can be found in various arterial territories such as carotid, cerebral, coronary, or lower limb vessels [7]. Among people aged 30-79 years, approximately 28% have an abnormal carotid intima-media thickness, nearly 21% carotid plaque, and 1.5% carotid stenosis [8; 9]. As atherosclerosis is a diffuse disease, patients with stenosis of the carotid artery (CA) are more expected to have atherosclerotic disease in other arteries [8; 9]. The extensive group of people with carotid plaque or carotid stenosis indicates a potential for cerebrovascular events resulting in a massive load of diseases in the global healthcare system [8].  
Glucocorticoids (GCs) are one of the numerous factors determining CVD pathogenesis. They are steroid hormones synthesized and released by the adrenal cortex in a circadian manner and as a response to stress. GCs are also used as therapeutic agents. Their side effects, such as abdominal obesity, diabetes, and arterial hypertension (HT), are simultaneously CVDs risk factors [10; 11; 12].  
GCs act via the GC receptor (GR), a member of the nuclear receptor superfamily of ligand-dependent transcription factors. GR is encoded by the gene _NR3C1_ located on chromosome 5q31-32 in humans [13]. _NR3C1_ gene genetic variation may contribute to higher body mass index (BMI), elevated plasma lipid levels, insulin resistance, and HT, which are considered atherosclerosis risk factors [14; 15]. However, some reports have shown contradictory results [14; 16; 17]. GR polymorphisms such as ER22/23 EK and GR-98 have been associated with GC resistance syndrome, resulting in a better metabolic profile, including decreased total cholesterol levels [18; 19]. N363S and _BclI_ polymorphisms' carriers have higher BMI and the risk of visceral obesity probably due to GC hypersensitivity [18]. Patients with A3669G polymorphism of the GR gene, which has been connected with GC resistance, have been reported to be at elevated risk of enlarged heart, systolic dysfunction, CAD, and heart failure (HF) [20; 21].  
In this study, we discussed the possible influence of the genetic polymorphisms Thh111I, N363S, and ER22/23 EK of the GR gene _NR3C1_ on the incidence of CA stenosis in a group of Polish patients subjected to carotid angiography.