Abstract
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.
Highlights
Rupture of the atherosclerotic plaque is accompanied by a violation of the integrity of the endothelial monolayer
Blood samples were obtained on the 1st and 10th days of AMI under the basal conditions, nitric oxide-synthase (NOS) blood serum level was determined with commercial enzyme linked immunosorbent assay ELISA kit (Bender Medsystem, Austria), Plasminogen activator inhibitor-1 (PAI-1) blood serum level was determined with commercial enzyme linked immunosorbent assay ELISA kit (Technoclone GmbH, Austria), soluble CD40 ligand (sCD40L) blood serum level was determined with commercial enzyme linked immunosorbent assay ELISA kit (YH Biosearch Laboratory, China), according to the manufacturer's instruction, and all these were performed with Auto mated EIA Analyzer «LabLine-90» (Austria)
Analyzing the levels of NOS on the first day of AMI, we found that in the group of patients with concomitant type 2 diabetes mellitus (DM) the median endothelial NOS was 2,6 ng/ml, while in the group of patients without concomitant carbohydrate metabolism disorders — 4,2 ng/ml (р < 0,01), that indicates much more significant violation of vasodilatory function of the endothelium in the cohort of patients with type 2 DM
Summary
Rupture of the atherosclerotic plaque is accompanied by a violation of the integrity of the endothelial monolayer. Metabolic disorders associated with type 2 diabetes mellitus (DM), such as hyperglycemia, insulin resistance, dyslipidemia, oxidative stress, only worsen a degree of endothelial injury [2, 3]. This leads to the release into the general circulation of a number of biologically active substances — endothelium-dependent mediators with wide range of effects. Plasminogen activator inhibitor-1 (PAI-1) plays a crucial role in the pathogenesis of AMI preventing dissolution of thrombi. The authors guarantee absence of competing interests and their own financial interest when carrying out the research and writing the article. Клінічна ендокринологія gulation of fibrinolysis, PAI-1, participating in the reception of insulin, enhances the insulin resistance [7, 8]
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