Acute myocardial infarction (AMI) remains the major cause of hospitalization, disability, and mortality of the able-bodied population of Ukraine, despite serious advances made in recent decades in the treatment of acute coronary syndromes (ACS). In the era of modern methods of interventional cardiology in the treatment of AMI, mortality in the presence of type 2 diabetes is still 2-3 times higher compared to patients without carbohydrate metabolism disorders. It has been proved that accurate stratification of patients, taking into account the risk of adverse course of AMI, can determine the effectiveness of further management of the patient. Metabolic disorders associated with type 2 diabetes, such as hyperglycemia, insulin resistance, dyslipidemia, oxidative stress, lead to impaired vasodilatory, adhesive and protective function of the endothelium. Among many pathogenic mechanisms of vascular injury in ischemic heart disease and type 2 diabetes, endothelial dysfunction is crucial. Disruption of nitric oxide (NO) synthesis is a leading factor in the development of endothelial dysfunction in acute myocardial infarction. The NO synthetase (NOS) system is involved in the regulation of vascular wall remodeling, inhibiting the activation, secretion, adhesion, and platelet aggregation, migration and proliferation of smooth muscle cells. Damage to the NOS system in diabetes was shown to result in a decrease in NOS level in the endothelium and impairment of vascular endothelium-dependent dilation. Asymmetric dimethylarginine (ADMA) is an endogenous competitive inhibitor of NO synthesis. There is a link between an increase in ADMA levels and an increased risk of coronary heart disease, hypercholesterolemia, high blood pressure, and impaired glucose tolerance. ADMA is also considered an indicator of insulin resistance.
The plasminogen activator inhibitor-1 (IAP-1) suppresses the action of tissue plasminogen activator and urokinase-like plasminogen activator. Upregulation of IAP-1 occurs in patients with diabetes mellitus and endothelial dysfunction.
Insufficient fibrinolysis due to increased levels of plasminogen activator-1 inhibitor is associated with a high risk of myocardial infarction. At the same time, it has been shown that an increase in IAP-1 levels correlates positively with the risk of cardiovascular events in patients with insulin resistance. Moreover, high plasma concentrations of IAP-1 are considered to be predictors of myocardial infarction.
