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The aim of study is to evaluate the levels of endothelium-dependent mediators: endothelial nitric-oxide synthase (NOS), plasminogen activator inhibitor-1 (PAI-1) and circulating soluble CD40 ligand (sCD40L) in patients with acute myocardial infarction (AMI) and concomitant type 2 diabetes mellitus (DM). The study included 255 patients with AMI, who were divided into two groups depending on the presence of concomitant type 2 DM: 1 group — 143 patients with concomitant type 2 DM; 2 group — 112 patients without concomitant disturbances of carbohydrate metabolism. Studied endothelial-dependent indicators were investigated using enzyme-linked immunosorbent assay. Statistical data were processed using the Mann–Whitney U-test, quantitative variables were described by the following parameters: median (Me), 25th and 75th percentiles (Q1; Q3). Analyzing the studied indicators on admission of patients to the hospital, a statistically significant decrease in NOS levels (p < 0,01), as well as an increase in PAI-1 (p < 0,01) and sCD40L (p < 0,01) in the cohort of patients with AMI and concomitant type 2 DM compared with patients without disturbances of carbohydrate metabolism. This indicates a more significant violation of endothelium-dependent vasodilation, thrombin fibrinolysis and activation of intravascular inflammation caused by comorbidity. Over the next 10 days, an increase in NOS levels, a decrease in PAI-1 and sCD40L levels were observed in patients of both groups, indicating a gradual improvement of the endothelial function. However, in patients with AMI and concomitant type 2 DM, the levels of the studied endothelium-dependent mediators continued to differ statistically even on the 10th day after acute occlusion of the coronary artery. In our opinion, this tendency is caused by the negative impact of metabolicdisorders associated with type 2 DM on the endothelium of the coronary arteries in patients with insulin resistance and, apparently, may increase the risk of complications of AMI.

Acute myocardial infarction continues to occupy one of the leading places among the causes of mortality. Some indicators of endothelial dysfunction are also associated with a high risk of cardiovascular complications, which play a key role in the pathogenesis of cardiovascular complications, which makes it relevant to study the relationship between endothelial dysfunction markers and the development and progression of atherosclerotic vascular lesions. Dysfunction of the endothelial vasodilator system is accompanied by a decrease in the level of nitric oxide (NO), which is a characteristic feature of patients who are at risk of coronary artery disease, so coronary vasodilator dysfunction may involve prolonged progression of atherosclerosis and the frequency of cardiovascular events. The high risk of vascular accidents is an incentive to study the pathogenetic mechanisms of thrombotic formation in type 2 diabetes. Plasminogen activator inhibitor type 1, which is a member of the superfamily of serine protease inhibitors and the main inhibitor of fibrinolysis in the plasminogen activator system, plays a key role in the pathogenesis of arterial and venous thrombosis and, therefore, contributes to the occurrence of thrombotic events. The combination of acute myocardial infarction with type 2 diabetes mellitus is characterized by a significant increase in the content of the plasminogen activator inhibitor type 1 in serum compared with those without diabetes. As a result of the study, a close direct correlation between the increase of lipid, carbohydrate metabolism, hemostasis parameters proportional to the high content of the plasminogen activator inhibitor type 1 in serum of patients with acute myocardial infarction with concomitant type 2 diabetes mellitus was proved. The inverse correlation between the level of type 1 plasminogen activator inhibitor and the reduced content of nitric oxide synthase, which increases endothelial dysfunction and atherothrombosis in patients with acute myocardial infarction with concomitant type 2 diabetes mellitus, is proved.