The state of the membrane potential of the mitochondria of blood leukocytes in acute coronary syndrome

Abstract

Purpose: to assess the state of mitochondrial membrane potential of blood leukocytes in acute coronary syndrome (ACS) depending on the presence and absence of type 2 diabetes mellitus (T2DM).Material and Methods. The study involved 100 people hospitalized at the regional vascular center (RCC) of the Vladivostok Clinical Hospital No. 1 with a diagnosis of ACS, aged 35 to 65 years. The control group consisted of 30 apparently healthy volunteers of the same age and sex. At the time of admission, all patients underwent studies for the diagnosis of ACS, including an assessment of the content of troponin I (TrI), and the marker of the precursor of the cerebral natriuretic peptide (NTproBNP) and the membrane potential of mitochondria (MPM) of blood leukocytes were determined.Results. Indicators of the state MMP made it possible to assess the content of dead and living cells in the blood of the examined persons. An increase in non-viable leukocytes in the blood patients with all types of ACS, including myocardial infarction (MI) and unstable angina (UA), was established. A direct relationship was found between the increase in the number of these cells and the content of TrI in MI and a direct relationship between it and NTproBNP both in MI and NS. In patients with ACS, no significant difference was found between the MMP values of leukocytes depending on the presence of T2DM.Conclusion. An increase in the MPMP of blood leukocytes in patients accompanies of the redox balance disturbance in ACS. The established relationship between MPMP indices in MI and the content of TrI can be considered as a confirming fact of the participation of cells with mitochondrial dysfunction in the development of ischemic necrosis. The found relationship between the increase in blood leukocyte MPMP in patients with ACS and the level of NTproBNP indicates a certain contribution of mitochondrial dysfunction of leukocytes to the development of myocardial remodeling, regardless of the clinical form of ACS and the presence of DM2.