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In recent years, it has been shown that sodium-g lucose co-transporter type 2 inhibitors (SGLT2), drugs for type 2 diabetes mellitus treatment, significantly improve metabolic parameters and have protective effect on the kidneys and heart not only in patients with type 2 diabetes mellitus. New research indicates that the progression of chronic heart failure (CHF) and chronic kidney disease (CKD) involves metabolic reprogramming, which consists of a deterioration in energy metabolism in the heart as a result of a mismatch between glucose uptake and its oxidation, leading to the accumulation of glucose-6-phosphate (G6P), glycogen and activation of the pentose phosphate pathway. This nutrient excess activates the mammalian target of rapamycin (mTOR), thereby promoting pathological myocardial remodeling, and at the same time suppresses the nutrient deficiency sensors SIRT1, AMPK and PGC-1α, which is accompanied by mitochondrial dysfunction, increased oxidative stress and decreased fatty acid oxidation. Similar processes occur in the proximal convoluted tubules of the kidneys in CKD, leading to renal dysfunction, albuminuria, and interstitial fibrosis. SGLT2 inhibitors inhibit the reabsorption of sodium and glucose in the proximal tubule, which leads to increased urinary glucose excretion and moderate osmotic diuresis and natriuresis. Nutrient deficiency resulting from glucose excretion promotes the activation of AMPK, which is involved in the regulation of mitochondrial biogenesis by stimulating PGC-1α, stimulates catabolic metabolism and activates autophagy by inhibiting mTORC1, which is accompanied by antiinflammatory effects, reduced oxidative stress and apoptosis and increased autophagy. These processes are accompanied by a decrease in blood pressure and a decrease in the load on the myocardium, with a simultaneous decrease in the tone of the sympathetic nervous system. Taking SGLT2 inhibitors is accompanied by normalization of tubuloglomerular feedback and a decrease in hyperfiltration, which has a beneficial effect on glomerular hemodynamics, as well as stimulation of erythropoiesis as a result of simulating systemic hypoxia. The described processes may serve as the basis for the cardioprotective and nephroprotective effects of SGLT2 inhibitors.
In recent years, it has been shown that sodium-g lucose co-transporter type 2 inhibitors (SGLT2), drugs for type 2 diabetes mellitus treatment, significantly improve metabolic parameters and have protective effect on the kidneys and heart not only in patients with type 2 diabetes mellitus. New research indicates that the progression of chronic heart failure (CHF) and chronic kidney disease (CKD) involves metabolic reprogramming, which consists of a deterioration in energy metabolism in the heart as a result of a mismatch between glucose uptake and its oxidation, leading to the accumulation of glucose-6-phosphate (G6P), glycogen and activation of the pentose phosphate pathway. This nutrient excess activates the mammalian target of rapamycin (mTOR), thereby promoting pathological myocardial remodeling, and at the same time suppresses the nutrient deficiency sensors SIRT1, AMPK and PGC-1α, which is accompanied by mitochondrial dysfunction, increased oxidative stress and decreased fatty acid oxidation. Similar processes occur in the proximal convoluted tubules of the kidneys in CKD, leading to renal dysfunction, albuminuria, and interstitial fibrosis. SGLT2 inhibitors inhibit the reabsorption of sodium and glucose in the proximal tubule, which leads to increased urinary glucose excretion and moderate osmotic diuresis and natriuresis. Nutrient deficiency resulting from glucose excretion promotes the activation of AMPK, which is involved in the regulation of mitochondrial biogenesis by stimulating PGC-1α, stimulates catabolic metabolism and activates autophagy by inhibiting mTORC1, which is accompanied by antiinflammatory effects, reduced oxidative stress and apoptosis and increased autophagy. These processes are accompanied by a decrease in blood pressure and a decrease in the load on the myocardium, with a simultaneous decrease in the tone of the sympathetic nervous system. Taking SGLT2 inhibitors is accompanied by normalization of tubuloglomerular feedback and a decrease in hyperfiltration, which has a beneficial effect on glomerular hemodynamics, as well as stimulation of erythropoiesis as a result of simulating systemic hypoxia. The described processes may serve as the basis for the cardioprotective and nephroprotective effects of SGLT2 inhibitors.
Target. To identify predictors of the risk of adverse events over a three-year period in patients with chronic heart failure (CHF). Materials and methods. A retrospective study was conducted on 278 people diagnosed with CHF in patients with coronary heart disease (CHD). Statistical data processing was carried out using Excel and XLSTAT programs with linear regression calculations. Results. In the study group, there were 181 male patients and 97 female patients. Among the concomitant diseases, the most common diseases were endocrine system diseases, obesity and gastrointestinal pathology. According to Charlson comorbidity index calculations, 121 patients had an index of 6 or higher, which corresponds to a possible 10-year survival rate of less than 21%. When analyzing the data, patients with CHF had a three-year survival rate of 67.3% of the study group, 32.7% of patients died. A statistically significant direct relationship between three-year survival was identified with the following indicators: age over 66 years, stage IIB-III CHF, Echo-CG data (low LVEF, left ventricular diameter, systolic pressure in the pulmonary artery (SPAP), the presence of hypertension (HBP) and atrial fibrillation (AF), Charlson comorbidity index more than 5 points, glomerular filtration rate (GFR) less than 60 ml/min, complete blood count (CBC) data - a decrease in hemoglobin level below 131 g/l and an increase in ESR level above 14 mm/h Surgical interventions such as coronary artery bypass grafting (CABG) and percutaneous coronary intervention (PCI) were associated with better patient survival. Conclusion. The identified predictors of unfavorable outcome will improve the prediction of outcomes in patients with CHF. Performing coronary revascularization in patients with coronary artery disease complicated by CHF was associated with better patient survival. In order to ensure qualified monitoring of patients with CHF and ensure continuity of management of these patients, it seems relevant to create a specialized office for the management of patients with CHF on the basis of the State Institution of the Republic of Kazakhstan “Clinical Cardiology Dispensary”.
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