Arterial hypertension in diabetic patients exacerbates impaired carbohydrate and lipid metabolism. Thus, hypercholesterolemia, obesity, hyperinsulinemia are registered, respectively, in 85%, 75%, 50% of patients. The presence of these basic disorders increases the risk and accelerates the course of atherosclerosis in both types of diabetes, and the risk of developing coronary heart disease (CHD) in such patients increases by a factor of 14 over 10 years of life. In this regard, a natural consideration of the relationship of diabetes, hypertension and atherosclerosis.
Data from recent experimental studies indicate a strong similarity between the effects of hypertension and prolonged hyperlipidemia on the intima of the arteries. Hyperlipidemia in diabetes mellitus should be divided into secondary, associated with decompensation of diabetes mellitus, and primary, due to primary disorders of lipid metabolism. In patients with newly diagnosed type 2 diabetes mellitus and not receiving any treatment, the concentration of cholesterol, triglycerides, LDL, and VLDL is significantly increased and the level of HDL cholesterol is reduced compared with these indicators in healthy individuals and patients with diabetes without diabetes. Moreover, the HDL content has a negative correlation with body weight and the level of triglycerides.
In addition, in patients with diabetes mellitus with angiopathies, complexes or aggregates consisting of VLDL, insulin, and antibodies to insulin were found. This suggests that VLDL in diabetic patients can serve as a kind of carrier of an excessive amount of insulin, antibodies and immune complexes into the vascular wall. VLDL undergoing oxidation is a fairly significant factor causing damage to the inner lining of the arteries. Large particles of VLDL secreted by the liver are not atherogenic, but after they are delipidized and become smaller and more dense, they become atherogenic.
At the same time, VLDL, isolated from patients with hypertriglyceridemia, are absorbed by fibroblasts and macrophages, then turning into “foamy” cells. All this indicates the possible participation of macrophages in the mechanisms of atherosclerosis. LDL accumulates in the arterial wall, interacting with classical LDL receptors. In the case of chemical and biological modification of LDL, there is a significant accumulation of cholesterol esters in macrophages. Glycosylation significantly alters the biological reactivity of LDL, which leads to a decrease in the absorption of LDL and their metabolism in cells.
Hypercholesterolemia in diabetes mellitus, regardless of the original cause (metabolic or exogenous food), is accompanied by an increase in LDL, VLDL and chylomicrons, which come from the blood plasma into the artery wall. Changing the physicochemical properties of LDL leads to their accumulation in the vascular endothelium, increased adherence to monocytes and platelets, their uptake by macrophages and smooth muscle cells to form foamy cells. Disruption of carbohydrate metabolism causes hyperlipidemia and the listed changes in the metabolism of LDL, VLDL, triglycerides, cholesterol. Hyperglycemia is also responsible for an increase in the content of glucosamines and glycosylated lipoproteins in the arterial wall.
Thus, diabetes lipid metabolic disturbance or dyslipidemia, characterized hypertriglyceridemia, reduction in HDL holes- Terina and increase LDL containing an excessive amount of triglycerides, LDL violation kinetics and increased LDL content, glycosylated and oxidated lipoproteins, as well as “small” lipoprotein .
The most important cause of death in patients with diabetes is a high incidence of atherosclerosis and coronary heart disease caused by it, leading to a 4-fold increase in the mortality rate of patients with diabetes compared with the general population. Atherosclerosis of the coronary arteries is characterized by much earlier development and spread. Well-known risk factors for CHD, such as hypercholesterolemia, hypertension, obesity, and smoking, are 3 times more likely to cause death in diabetes patients. At the same time, even in the absence of these risk factors, the frequency of development and progression of atherosclerosis in diabetes suggests additional mechanisms for its development. The increased risk of developing the progression of atherosclerosis in diabetes is associated with factors such as hyperinsulinemia, hyperglycemia, impaired blood clotting and the development of obesity.Researchers pay close attention to lipid metabolism disorders in the pathogenesis of atherosclerosis. Studies of recent years have proved a causal relationship between hyperlipidemia, or rather, dyslipidemia, and the incidence of cardiovascular disease, in particular, IHD. Hyperlipidemia, accompanied by an increase in the concentration of low-density lipoproteins (lipoproteins), today is regarded as the main pathogenetic factor in the development of atherosclerosis. However, an equally important link in pathogenesis is the reduction of high-density lipoproteins (A-lipoproteins), which have anti-atherogenic properties, due to their ability to enhance catabolism of triglyceride-rich lipoproteins.
The role of triglycerides in the development of CHD today seems somewhat controversial. With the exception of cases of primary hyperlipidemia class III, characterized by hypertriglyceridemia and associated with a high risk of atherosclerosis, hypertriglyceridemia is considered not an independent, but rather a secondary violation of lipid metabolism, accompanied by a risk of cardiovascular disease. At the same time, according to the results of the Paris study, among patients with diabetes, compared with the general population, secondary hypertriglyceridemia plays a more important role in the development of atherosclerosis than cholesterol levels.
In the case of diabetes, lipid metabolism disorders depend on several factors, and, first of all, on the degree of hyperglycemia, severity of insulin resistance, obesity, albuminuria, and nutritional factors.
In recent years, insulin resistance and the compensatory hyperinsulinemia associated with it has been recognized as a central element of the mechanisms leading to the development of the “X” syndrome (metabolic syndrome), components