The combination of hypertension, obesity and non-alcoholic fatty liver disease occurs in medical practice very often. A number of studies have shown that non-alcoholic fatty liver disease increases the risk of cardiovascular disease independently of other predictors and manifestations of the metabolic syndrome. Current issues of research and identification of common pathogenic relationships of obesity, hypertension, and liver steatosis are investigated in the article. According to the analysed literature, it is indicated that insulin resistance and compensatory hyperinsulinaemia are considered as one of the key factors in the development of this comorbidity. The processes of chronic inflammation are increasing with the growth of adipose tissue volume. Some researchers believe that non-specific systemic inflammation combines arterial hypertension, increased body weight (especially abdominal obesity), steatosis, dyslipidaemia, atherogenesis and arteriosclerosis into a single syndrome. The role of non-alcoholic fatty liver disease in the growth of the thickness of the intima-media complex was studied. It is known that adipose tissue functions as an endocrine organ, expresses genes encoding bioactive substances, and secretes certain cytokines. A strong link between dysfunction of adipose tissue in patients with non-alcoholic fatty liver disease and in such conditions as metabolic syndrome and cardiovascular disease was demonstrated. The dysfunction of the endothelium is also advisable to consider as the connecting link between liver disease, obesity and hypertension. Despite some understanding of common pathogenic mechanisms for the development of non-alcoholic fatty liver disease and hypertension, this comorbid pathology remains the subject of much debate and a variety of studies. key words: arterial hypertension, obesity, non-alcoholic fatty liver disease, insulin resistance, dyslipidaemia, non-specific systemic inflammation, endothelial dysfunction, atherogenesis.
Background. Mechanisms of activation of the process of vascular wall remodelling in patients affected by arterial hypertension have not been studied in depth and require clarification. Materials and methods. The study included 381 patients with hypertension-212 men and 169 women of the average age 53.0 (47; 60) years. The structural-functional vessel status was determined by the method of duplex scanning and colour duplex mapping of blood flow with the Logiq 500 MO apparatus (GE, USA). Statistical analyses were made using Microsoft Excel software kit , Statistica for Windows 6.0. Results. The patients with hypertension presented some left-right asymmetry of remodelling extracranial carotid arteries. Unlike the impact of remodelling of the right carotid artery, the most essential effect on the left carotid artery was the impact of daytime pulse arterial pressure and variability of the nocturnal systolic arterial pressure (the strength of impact 25.0 and 13.9%, respectively. The processes of remodelling of the right carotid artery are more sensible to the impact of high values of nocturnal diastolic arterial pressure (the strength of impact 16.4%). The beginning of some brain complication is associated with the significant increase in atherosclerotic affection not only of the left, but also of the right carotid artery. Conclusions. Remarkable remodelling of the right carotid artery is often associated with the severity of the disease and to some extent reflects the severity of the flow of the disease and can be regarded as an additional unfavourable feature.
Disorders of the kidneys often occur in cardiovascular diseases. They are connected with the heart by complex hemodynamic and neuroendocrine bonds. The structure, functions, and possibilities of using an endogenous indicator of the functional state of the kidney - cystatin C are discussed in the article. Available data allow the use of cystatin C as a predictor of renal dysfunction in patients with cardiovascular pathology and arterial hypertension, in particular. However, the widespread use of cystatin C in routine clinical practice requires further study and improvement.
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