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Introdiction. The article highlights the importance of optimizing the treatment of chronic heart failure (CHF) in patients with comorbid cardiopulmonary pathology, namely ischemic heart disease (CHD) in combination with chronic obstructive pulmonary disease (COPD). The results of our own research on the evaluation of the clinical efficacy of trimetazidine inclusion in the complex therapy of comorbid pathology are presented.Objective. To study the clinical efficacy of trimetazidine as part of the complex therapy of patients with ischemic heart failure in combination with COPD.Materials and methods. 60 patients with CHF II-III FC, left ventricular ejection fraction (LVEF) <45% were studied against the background of postinfarction cardiosclerosis and COPD of 2–3 degrees of airflow restriction. The patients were divided into 2 groups: 1st (30 patients) took trimetazidine; 2nd (30 patients) received therapy without the addition of trimetazidine. The dynamics of: clinical condition with the use of SHOCK, FC CHF, test with 6-min. walking, quality of life (MLHFQ, SGRQ), indicators of 24-bifunctional monitoring, TTE, spirometry, platelet aggregation and blood viscosity.Results and conclusion. The use of trimetazidine as part of therapy led to an improvement in the clinical course of the disease, significantly increased exercise tolerance. The number and duration of ischemia episodes decreased by 34 and 39% (p < 0.05). The number of angina attacks per week and the need for nitroglycerin decreased by 65% and 42% (p < 0.05), respectively. There was an improvement in intracardiac and peripheral hemodynamics. Thus, LV LV increased by 21%, pulmonary artery pressure decreased by 18%, the indicators of LVD, platelet aggregation and blood rheology improved. There was a more positive dynamics of lipid peroxidation and antioxidant system indicators compared to the control group.
Introdiction. The article highlights the importance of optimizing the treatment of chronic heart failure (CHF) in patients with comorbid cardiopulmonary pathology, namely ischemic heart disease (CHD) in combination with chronic obstructive pulmonary disease (COPD). The results of our own research on the evaluation of the clinical efficacy of trimetazidine inclusion in the complex therapy of comorbid pathology are presented.Objective. To study the clinical efficacy of trimetazidine as part of the complex therapy of patients with ischemic heart failure in combination with COPD.Materials and methods. 60 patients with CHF II-III FC, left ventricular ejection fraction (LVEF) <45% were studied against the background of postinfarction cardiosclerosis and COPD of 2–3 degrees of airflow restriction. The patients were divided into 2 groups: 1st (30 patients) took trimetazidine; 2nd (30 patients) received therapy without the addition of trimetazidine. The dynamics of: clinical condition with the use of SHOCK, FC CHF, test with 6-min. walking, quality of life (MLHFQ, SGRQ), indicators of 24-bifunctional monitoring, TTE, spirometry, platelet aggregation and blood viscosity.Results and conclusion. The use of trimetazidine as part of therapy led to an improvement in the clinical course of the disease, significantly increased exercise tolerance. The number and duration of ischemia episodes decreased by 34 and 39% (p < 0.05). The number of angina attacks per week and the need for nitroglycerin decreased by 65% and 42% (p < 0.05), respectively. There was an improvement in intracardiac and peripheral hemodynamics. Thus, LV LV increased by 21%, pulmonary artery pressure decreased by 18%, the indicators of LVD, platelet aggregation and blood rheology improved. There was a more positive dynamics of lipid peroxidation and antioxidant system indicators compared to the control group.
The aim of this study was to determine the possibility of studying the nature of the influence of cardiocytoprotectors on energy metabolism in cardiomyocytes using a model of human peripheral blood leukocytes.Materials and methods. Sixty Wistar rats were divided into groups: 1) intact rats; 2) rats with experimental myocardial ischemia; 3) rats with myocardial ischemia, which were injected with cardiocytoprotector – trimetazidine, 4) meldonium, 5) cytoflavin and 6) ethoxydol. Animals were taken out of the experiment 10 days after the administration of drugs by decapitation. The activities of pyruvate dehydrogenase and citrate synthase were determined in mitochondria of myocardial homogenates and in mitochondria of leukocytes by spectrophotometric methods.Results. The decrease in pyruvate dehydrogenase and citrate synthase activity in cardiomyocytes and in leukocytes were revealed in case of myocardial ischemia modeling. The introduction of cardiocytoprotectors led to the activation of these enzymes both in heart cells and in blood leukocytes. Direct positive correlations were obtained between the activity of pyruvate dehydrogenase in the mitochondria of cardiomyocytes and in the mitochondria of leukocytes (r = 0.811; p < 0.0001); between citrate synthase activity in the mitochondria of cardiomyocytes and in the mitochondria of leukocytes (r = 0.909; p < 0.0001).Conclusion. Changes in energy metabolism in blood leukocytes under the influence of cytoprotectors reflect similar changes occurring in heart cells.
The purpose of the study: to develop a general concept of a patient-oriented approach to the use of drugs with cytoprotective activity in patients with coronary heart disease (CHD). Materials and methods. Examination of 60 patients with CHD: stable angina pectoris of I-III functional classes was performed. According to the standard general clinical methods for verifying the diagnosis were used: ECG, Doppler echocardiography, coronary angiography, lipid profile, complete blood count, coagulogram, renal, hepatic complex. Also the condition of stress-realizing and stress-limiting systems of the functional system of adaptation was deeply examined in patients: determination of the level of personal anxiety by the method of questioning, determination of the concentration of cortisol, insulin, cAMP and cGMP in blood serum by the method of enzyme immunoassay; determination of the endothelial and inducible nitric oxide synthase levels in erythrocyte lysate by the method of enzyme immunoassay; the study of ATP and ADP concentrations in blood serum and erythrocytes, also the study of 2,3-DFG concentration in erythrocytes by spectrophotometric methods. The individual reactivity of blood leukocytes’ mitochondria of patients was estimated in vitro under the influence of metabolic drugs (trimetazidine, meldonium, cytoflavin) by confocal microscopy according to the technique developed and patented by us (mitochondria were stained with pyrene). The materials were processed statistically. Results. Two variants of the leukocyte mitochondrial response in patients with CHD to the introduction of metabolic correctors in vitro were found — in the form of their activation or inhibition, depending on numerous parameters of the initial state of patients, which served as the basis for the development of a general concept of a patient-oriented approach to the use of drugs with cytoprotective activity in patients with coronary heart disease. According to this concept, the individual reactivity of a patient with CHD to the administration of a metabolic drug depends on the initial state of the functional adaptation system, which can be determined by the activity of stress-realizing and stress-limiting systems (cortisol/insulin ratio, serum cAMP/cGMP, eNOS, iNOS of erythrocyte lysate) and by the degree of preservation of the structure and function of effector organs. It is appropriate to prescribe drugs that stimulate energy metabolism in cells only to patients with initial hypoergosis, reduced mitochondrial activity at the phases of activation or resistance of the general adaptation syndrome, while maintaining reserves for energy adaptation, by short courses. Conclusion. A general concept of a patient-oriented approach to the use of drugs with cytoprotective activity in patients with coronary artery disease has been developed, according to which metabolic correctors should be prescribed in short courses, provided that individual reserves for energy adaptation are preserved in patients with initial mitochondrial hypoergosis in the activation or resistance phase of the general adaptation syndrome.
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