Background The formation of the effect of SGLT 2 inhibitors on the cardiovascular system implies inhibition of the Na+/H+exchanger (NHE) that leads to a decrease in the concentration of Na+, which in turn contributes to a decrease in the concentration of Ca2+ in the cardiomyocyte (S. Verma, J. McMurray, 2018). However, this effect may be different against the background of exposure to empagliflozin and dapagliflozin. A study of A. Baartscheer (2017) demonstrated the reduction of [Na+], systolic and diastolic [Ca+] in cardiomyocyte is affected by Empagliflozin. N.N. Hamouda's research shows that Dapagliflozin reduce [Na+], systolic, but not diastolic [Ca2+] in cardiomyocytes. In this regard, studying the Na+/Na+ exchanger (which is the mode of the NHE operation) activity estimated by the Na+/Li+countertransport (SLC) in the erythrocyte membrane (K. Morgan, M. Canessa, 1990; M. Canessa, 1989) is of great interest. Purpose A study of the impact of Dapagliflozin, and Empagliflozin on SLC in erythrocyte membranes of healthy volunteers in acute drug tests. Materials and methods 10 healthy volunteers (7 men and 3 women) were included in the study. The mean age of the study group was 24±0,6 years. The volunteers took singly Dapagliflozin, and Empagliflozin separately in one-month intervals. The activity of SLC was determined before drug consumption, as well as 2, 12, and 24 hours after consumption by the method of M.Canessa (1980). All data were tested for normality using the Kolmogorov–Smirnov test and statistically tested by paired Student t-test. Results Mean speeds of SLC before the drugs were administered was 289.1±33.1 mmol/L cell*h in the Dapagliflozin group and 287.8±37.3 mmol/L cell*h in the Empagliflozin group (p=0.979). Two hours after Dapagliflozin was administered, the speed of SLC increased to 76.3±17.0 mmol/L cell*h (95% CI: 37.9–114.7) and was maximum 365±41.6 mmol/L cell*h (p=0.002) for observation period. Then after 12 and 24 hours decreasing SLC activity was observed. However, the values were higher than the initial level and amounted to 335.5±39.18 mmol/L cell*h (p=0.024) after 12 hours and 331±31.8 mmol/L cell*h (p=0.001) after 24 hours. Two hours after Empagliflozin was administered, the speed of SLC not significantly changed and amounted to 287.8±37.3mmol/L cell*h (p=0.7). After 12 hours, the speed not significantly increased to 23.4±11.9 (95% CI: 4.6–51.4) mmol/L cell*h and amounted to 311.1±39.2 (p=0.08), with the subsequent decrease of speed within 24 hours to 277.6±40.5 mmol/L cell*h (p=0.5). Thus Dapagliflozin and Empagliflozin have different effects on the function of Na+/Na+ exchanger which may differently affect the changing of the [Na+] and [Ca2+] in the cardiomyocyte. Conclusions 1. When Dapagliflozin was administered the SLC speed reached its maximum level after 2h and maintained higher than initial level after 12h and 24h. 2. When Empagliflozin was administered no significant change in SLC speed was observed. Funding Acknowledgement Type of funding source: None
Aim. Iron has a protective effect on cardiomyocytes during hypoxia, while iron deficiency (ID) directly affects its function, disrupting mitochondrial respiration, reducing their contractility and relaxation. Some studies have shown that ID is a predictor of adverse outcomes in patients with acute coronary syndrome (ACS). However, the impact of ID and its treatment, quality of life and prognosis of patients with ID and myocardial infarction (MI) has not been fully established. The study aim is to determine the effectiveness of intravenous ferric carboxymaltose (FCM) compared with oral iron (ferrous sulfate) in relation to left ventricular (LV) systolic function, assessed by echocardiography.Material and methods. This open-label, prospective, randomized study includes 360 patients with or without ID who were hospitalized with acute myocardial infarction (MI). Patients with ID will be randomized (1:1) to intravenous FCM and oral ferrous sulfate therapy. Treatment in groups will be started at the time of hospitalization. Patients without ID will form the control group. The follow-up period for patients will be 1 year. The primary endpoint was a reduction in LV wall motion score index (WMSI) in the FCM group compared to the ferrous sulfate group. The key secondary endpoint is a composite endpoint of cardiovascular death, non-fatal MI and stroke, and hospitalization for decompensated heart failure.Conclusion. The OPERA-MI study will determine the effect of ID treatment with intravenous FCM compared with oral ferrous sulfate on WMSI, which reflects LV systolic function.
A number of studies have demonstrated the negative impact of iron deficiency (ID) on the prognosis and course of heart failure. The prevalence of patients with coronary artery disease (CAD) in these studies was 39,4-65%, while the proportion of patients who had myocardial infarction reached 60%. The effect of ID on CAD course requires further study. The aim of this review was to analyze the available data on the effect of ID on heart function, quality of life, and prognosis in patients with CAD. This literature review analyzed 359 publications and systematized information on ID prevalence in patients with CAD, pathophysiological effects of ID on the function and structure of cardiomyocytes, the impact of ID on the course, prognosis, and quality of life in patients with CAD. The influence of ID and its correction on cardiomyocytes and left ventricular systolic function were studied.
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