Decrease In Myocardial Contractility Research Articles

Анализ функций миокарда по данным Стресс-эхокардиографии при безболевой ишемии миокарда

The purpose — to analyze the results of stress-EchoCG in patients with and without silent myocardial ischemia (SMI). Material and methods. Results of stress-EchoCG of 202 patients during exercise test (ET) on treadmill according to Bruce protocol were analyzed. Results. Patients with SMI were 2.5 times more likely to achieve submaximal heart rate (p = 0.015) compared with the control group (CG). With the same exercise load, the maximum heart rate was higher in SMI group (p = 0.04). Maximum depression of ST segment was greater in SMI than in CG (p = 0.04). Dynamic of ST segment during ET was found in 75.6% subjects in SMI group and in 36.6% subjects in CG (p = 0.0001). Decrease in myocardial contractility during ET was 80.5% in SMI and 34.1% in CG (p = 0.0001). Combination of ST segment depression and contractility decrease was 56% in SMI and 9.2% in CG (p = 0.0001). In SMI, contractility decrease was found in 84.2% of segments. Conclusions. Decrease in contractility is higher in SMI than in CG. Positive ET with ST segment depression is more common in SMI. Depression of ST segment on positive ET was deeper in SMI than in CG. Negative test happens more often at SMI. Duration of ET in SMI was shorter due to rapid achievement of submaximal heart rate or ST segment depression. In SMI, ischemic manifestations occurred earlier and were more severe than in CG. Combination of segmental contractility disorders and ST segment depression in ET is a feature of myocardium in SMI.

ВОПРОСЫ ДОГОСПИТАЛЬНОЙ ДИАГНОСТИКИ ОСТРОЙ РЕАКЦИИ ОТТОРЖЕНИЯ У ПАЦИЕНТА, ПЕРЕНЕСШЕГО ОРТОТОПИЧЕСКУЮ ТРАНСПЛАНТАЦИЮ СЕРДЦА

An acute cardiac transplant rejection is a reaction of the recipient’s immune system, which includes the cellular and/or humoral pathway of the immune response. This reaction is directed against the tissues of the “alien” donor organ. The alertness of clinicians regarding the possible development of an acute rejection reaction during the first year after heart transplantation is due to the extremely high risk of developing life-threatening conditions mediated by graft dysfunction. These include various cardiac arrhythmias and a progressive decrease in myocardial contractility. In case of untimely diagnosis of this serious complication, the risk of mortality of the patient who underwent orthotopic heart transplantation is extremely high. What changes in clinical, laboratory and instrumental examination parameters at the outpatient stage can help a practicing cardiologist to suspect the presence of an acute rejection reaction of a heart transplant in a patient who has undergone orthotopic heart transplantation? At present, there is no unambiguous answer to this question, and the topic of early detection and prediction of the development of an acute heart transplant rejection reaction is extremely relevant for modern scientific research and is of great practical interest in the field of transplantology and cardiology, in particular.

TRPC5 channel participates in myocardial injury in chronic intermittent hypoxia

ObjectiveThe purpose of this study is to develop an animal model of Chronic Intermittent Hypoxia (CIH) and investigate the role of the TRPC5 channel in cardiac damage in OSAHS rats. MethodsTwelve male Sprague Dawley rats were randomly divided into the CIH group and the Normoxic Control (NC) group. Changes in structure, function, and pathology of heart tissue were observed through echocardiography, transmission electron microscopy, HE-staining, and TUNEL staining. ResultsThe Interventricular Septum thickness at diastole (IVSd) and End-Diastolic Volume (EDV) of rats in the CIH group significantly increased, whereas the LV ejection fraction and LV fraction shortening significantly decreased. TEM showed that the myofilaments in the CIH group were loosely arranged, the sarcomere length varied, the cell matrix dissolved, the mitochondrial cristae were partly flocculent, the mitochondrial outer membrane dissolved and disappeared, and some mitochondria were swollen and vacuolated. The histopathological examination showed that the cardiomyocytes in the CIH group were swollen with granular degeneration, some of the myocardial fibers were broken and disorganized, and most of the nuclei were vacuolar and hypochromic. ConclusionCIH promoted oxidative stress, the influx of Ca2+, and the activation of the CaN/NFATc signaling pathway, which led to pathological changes in the morphology and ultrastructure of cardiomyocytes, the increase of myocardial apoptosis, and the decrease of myocardial contractility. These changes may be associated with the upregulation of TRPC5.

Relationship between free circulating DNA levels, ejection fraction and brain natriuretic peptide levels in patients with chronic heart failure: prospective observational study

BACKGROUND: Chronic heart failure (CHF) is one of the most serious problems in cardiovascular diseases, requiring accurate diagnosis and treatment. The search for new laboratory markers of CHF can improve the accuracy of diagnosis and identify the severity of the patients condition.
 AIM: Our aim was to study the relationship between the levels of free-circulating DNA (cfDNA) and brain natriuretic peptide (NT-proBNP) in the blood plasma of patients suffering from CHF with ejection fraction (EF), to investigate the relationship between these laboratory markers, and to evaluate the dynamics of changes in the studied parameters against the background of drug therapy.
 MATERIALS AND METHODS: The study involved 67 patients of both sexes with a diagnosis of CHF, verified by clinical and functional methods. 23 people without established chronic diseases formed the control group. At the stage of inclusion in the study, all patients underwent: physical examination, general blood test, biochemical blood test with determination of lipid profile, glucose, creatinine, NT-proBNP and cfDNA levels, as well as electrocardiography (ECG), electrocardiography (ECHO-CG), radiography of organs chest, ultrasound of the abdominal organs, 6-minute walk test. The level of cfDNA was determined using the method of P.P. Laktionov, S.N. Tamkovich, E.Yu. Rykova (2005). Repeated blood sampling with assessment of cfDNA and NT-proBNP levels was carried out in the group of patients with reduced ejection fraction 57 months from the start of treatment/correction of previous therapy.
 RESULTS: The study revealed significant differences in the levels of cfDNA in the blood plasma in patients with different EF (less than 40%, 4049%, 50% or more). At the same time, an inverse relationship was established between cfDNA indicators and EF, as well as between the level of NT-proBNP and EF, that is, a progressive decrease in myocardial contractility is accompanied by a combined increase in the levels of the studied markers in the blood, reflecting the severity of the patients condition. In addition, the positive effect of drug therapy on cfDNA and NT-proBNP levels in the group of patients with EF 40% has been proven.
 CONCLUSION: The identified patterns make it possible to consider the level of cfDNA in blood plasma as a potential biomarker of CHF, and also to use it for dynamic monitoring of patients.

Total Glucosides of Paeony Ameliorate Myocardial Injury in Chronic Heart Failure Rats by Suppressing PARP-1.

Total glucosides of paeony (TGP) have a potential protective effect on chronic heart failure (CHF) rats, but the mechanism remains unclear. PARP inhibition prevents the decrease in myocardial contractility. Therefore, we aim to investigate the effects and mechanisms of TGP on CHF and the role of PARP-1 in CHF. Left anterior descending ligation rats and adriamycin-treated H9C9 cells were used as CHF models, and captopril as a positive control for in vivo experiments. We found that TGP alleviated myocardial remodeling and improved cardiac morphology and function. TGP also reduced myocardial apoptosis and autophagy, decreased inflammatory factor release, and inhibited the PARP-1 and NF-κB proteins. Through cell transfection, we found that PAPR-1 knockdown inhibited NF-κB nuclear translocation. Additionally, TGP inhibited apoptosis, autophagy, and inflammation in CHF cells, while PARP-1 overexpression partially antagonized them. In conclusion, TGP has the potential to improve CHF and PARP-1 may be a potential target.

Determining the Association between 24-Hour Blood Pressure Variability and Major Adverse Cardiac Events (MACE) in Hospitalized Patients with Acute Myocardial Infarction: A Prospective Study

Acute myocardial infarction (AMI) is a challenging cardiovascular disease leading to a high rate of mortality. Some cardiomyocytes in AMI were affected by ischemia and necrosis, resulting in a decrease in myocardial contractility, an acute proinflammatory response, and an increase in sympathetic tone. In the meantime, proinflammation and endothelial dysfunction are induced by high blood pressure variability (BPV), which increases left ventricular workload, heart rate, and myocardial oxygen demand. As a result, a high BPV and the pathological effects it causes are likely to affect the onset of acute cardiac complications in AMI and the physiological function of the heart [1]. Patients Pulse changeability (BPV) has been fundamentally concentrated on through the crystal of congestive cardiovascular breakdown (CHF) and hypertension, yet not in that frame of mind of an intense coronary condition (ACS). This study means to explore the relationship between transient BPV and major unfavorable heart occasions (MACE) in AMI patients. The following order can be used to define MACEs: Death > shock > cerebrovascular stroke > heart failure > hypertensive crisis > life-threatening arrhythmias .This prospective study used the weighted standard deviation of 24-hour ambulatory blood pressure monitoring readings to include 74 patients who were hospitalized in the cardiology department at ARRAZI hospital MOHAMED VI, MARRAKECH between September 2022 and February 2023.
 Results: The average systolic BPV value which was estimated as standard deviation (SD) and average real variability (ARV) was more significant in the MACE group than in the non-MACE group. Systolic SD and systolic ARV in the MACE group were 12,78 mmHg and 11,61 mmHg respectively. In the non-MACE group, systolic SD and systolic ARV were 10.45 mmHg and 7,23 mmHg respectively. There was no significant association between BPV and MACE. However, there were significant differences between systolic ARV in patients with hypertension who experienced MACE and patients without hypertension who experienced MACE, unlike patients who didn’t experienced MACE for whom the ARV was nearly the same for patient with and without HBP.
 Conclusion: MACE was higher in the group BPV of AMI patients than that of non-MACE AMI patients. There was no significant association between BPV ​​and MACE during the acute phase of AMI, however the BPV was significantly more important for HBP patient who experienced MACE, which leads us to think that the screening of BPV in HBP patient may by a predictive factor for the development of MACEs.

Preclinical Large Animal Porcine Models for Cardiac Regeneration and Its Clinical Translation: Role of hiPSC-Derived Cardiomyocytes.

Myocardial Infarction (MI) occurs due to a blockage in the coronary artery resulting in ischemia and necrosis of cardiomyocytes in the left ventricular heart muscle. The dying cardiac tissue is replaced with fibrous scar tissue, causing a decrease in myocardial contractility and thus affecting the functional capacity of the myocardium. Treatments, such as stent placements, cardiac bypasses, or transplants are beneficial but with many limitations, and may decrease the overall life expectancy due to related complications. In recent years, with the advent of human induced pluripotent stem cells (hiPSCs), newer avenues using cell-based approaches for the treatment of MI have emerged as a potential for cardiac regeneration. While hiPSCs and their derived differentiated cells are promising candidates, their translatability for clinical applications has been hindered due to poor preclinical reproducibility. Various preclinical animal models for MI, ranging from mice to non-human primates, have been adopted in cardiovascular research to mimic MI in humans. Therefore, a comprehensive literature review was essential to elucidate the factors affecting the reproducibility and translatability of large animal models. In this review article, we have discussed different animal models available for studying stem-cell transplantation in cardiovascular applications, mainly focusing on the highly translatable porcine MI model.

Effects of Sulfur Amino Acids on Cardiodynamic Parameters of Isolated Rat Heart

Abstract Sulfur-containing amino acids are integral part of molecular mechanisms which underlie many aspects of cellular function and homeostasis, facilitated by reversible changes in oxidation states of sulfur atoms. Dysregulation of these pathways is associated with diverse pathologies, notably of the cardiovascular system, which are typically characterized by inappropriate plasma levels of sulfur-containing amino acids. The aim of this study was to assess the acute, direct effects of sulfur-containing amino acids and inorganic NaHS, as H2S donor, on cardiodynamic parameters in homocysteine treated rats. Moderate hyperhomocysteinemia did not cause significant decrease in myocardial contractility, but our findings suggest that NaHS and L-methionine cause negative effects on cardiac function in hearts of the rats treated with homocysteine, even in a single administration. Further investigations need to be carried out with purpose of better understanding and highlightening the impact of Hcy and sulphur amino acids on cardiac function.

ОПЫТ НАБЛЮДЕНИЯ ДЕТЕЙ С КАВАСАКИ-ПОДОБНЫМ (МУЛЬТИСИСТЕМНЫМ ВОСПАЛИТЕЛЬНЫМ) СИНДРОМОМ В ВОСТОЧНО-СИБИРСКОМ РЕГИОНЕ РОССИИ

The pathogenetic basis for Pediatric Multisystem Inflammatory Syndrome (PMIS) associated with SARS-CoV-2 is systemic vasculitis resulting from hyperproduction of pro-inflammatory cytokines associated with dysregulation of the immune response. Clinical manifestations of PMIS include fever with features of Kawasaki Syndrome (KS) and multi-organ dysfunction coupled with frequent unusual heart involvement, ranging from mild with minimal ECG changes or elevated troponin to fulminant myocarditis or Takotsubo syndrome (TTS). The purpose of the research was to study the characteristics of cardiovascular disorders in Kawasaki-like multisystem inflammatory syndrome associated with COVID-19 in children observed in the East Siberian area of Russia. A single-center retrospective cohort study was carried out on the basis of the Irkutsk Oblast Regional Children's Clinical Hospital (Irkutsk, Russia): 36 patients with PMIS associated with COVID-19 in Nov. 18, 2020 - Dec. 31, 2021, including 21 boys (M/F ratio 1.4:1) at the average age of 7.5 years old (1.5 months to 17 years old). The diagnostic signs of KS were observed in 34 (94%) children, including the complete set of diagnostic signs in 21 (58%). Refractory fever and a sharp increase in inflammatory biomarkers were detected in all 36 (100%) children; multiorgan dysfunction in 31 (86%); thrombocytopenia in 24 (67%); gastrointestinal syndrome in 25 (69%); cerebral dysfunction in 24 (66)%; various cardiovascular disorders in 30 (83%), including: dilatation of the left ventricle (LV) and a decrease in myocardial contractility in 3 (8%); moderate coronary dilatation in 5 (14%); thickening of the posterior LV walls in diastole in 5 (13%); thickening of the interventricular septum in diastole in 6 (16%). According to the MRI results performed in 15 children the signs of myocardial damage were found in 6 (40%). LV dilatation and decreased myocardial contractility were noted in 3 (8%) children, clinically apparent thrombotic complications in 3 (8%) children as well, and severe neurological deficit in one patient (3%). An increase in the level of D-dimer was observed in 26 (72%) patients, thrombocytopenia in 24 (67%), a statistically significant correlation between thrombocytopenia and myocardial damage was found (R=-0.506, p=0.001). The treatment measures were given as follows: inotropic support (dobutrex/dobutamine) was received by 8 (22%), artificial lung ventilation - by 8 (22%), intravenous human immunoglobulin 1.5-2.0 g/kg/course - by 28 (77%), dexamethasone - by 24 (67%), tocilizumab - by 2 (5%) patients. All 36 (100%) patients have survived. Conclusion: the Kawasaki-like multisystem inflammatory syndrome associated with COVID-19 was accompanied by the cardiovascular disorders (pericarditis, arrhythmias, abnormal ECG changes, elevated troponin and/or natriuretic peptide, LV thickening on echocardiography, coronary dilatation) in most patients, although LV dilatation and decreased myocardial contractility were observed in a few cases only. A negative correlation between thrombocytopenia and myocardial damage was found, which may indicate the involvement of thrombotic microvascular inflammation in the genesis of myocardial disorders.

Clinical and diagnostic characteristics of the development of hepatocardial syndrome in black and white cows in the early lactation period.

It is known that during the early postpartum and lactation periods in dairy cows, metabolic disorders develop, that is, ketosis, which can lead to secondary damage to internal organs. Therefore, it is important to address the issues of changing the lactating cows' clinical, laboratory, and physiological parameters regarding the development of hepatocardial syndrome. This study aimed to provide clinical and diagnostic justification for developing hepatocardial syndrome in highly productive dairy cows. The study was conducted on 20 black and white cows in the early postpartum period (7-10 days after birth), with a milk production level of >4500 kg of milk during the previous lactation period, a positive result in the formol colloid sedimentary test, the presence of deafness and splitting of heart sounds, changes in the size, or increased pain sensitivity of the percussion field of the liver. Clinically healthy dairy cows in the early postpartum period were used as controls (n = 24). Clinical, electrocardiographic, echocardiographic, and biochemical parameters were also evaluated. Dairy cows with hepatocardial syndrome developed arterial hypertension and sinus tachycardia, which led to a significant decrease in PQ and QT intervals at ECG. A significant increase in the diastolic size of the interventricular septum, systolic size of the free wall of the left ventricle, and diastolic and systolic sizes of the left ventricle and a significant decrease in the shortening fraction of the left ventricular myocardium were observed in the cows due to the development of hepatocardial syndrome. The affected cows demonstrated a significant increase in serum activity of gamma-glutamyl transferase, alanine aminotransferase, lactate dehydrogenase, creatine phosphokinase, alkaline phosphatase, troponin, malondialdehyde, diene conjugates, and ceruloplasmin and a decrease in glucose concentration. In addition, they demonstrated decreased activity of superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase. Hepatocardial syndrome in dairy cows occurs due to ketosis, characterized by arterial hypertension, sinus tachycardia, a moderate decrease in myocardial contractility, oxidative stress, and cytolysis of cardiomyocytes and hepatocytes. Therefore, the control and prevention of the development of hepatocardial syndrome will make it possible to maintain the productive health and longevity of dairy cows.

Dynamics of structural and functional characteristics of the heart in patients after myocardial infarction with ST segment elevation as a marker of progression of chronic heart failure

Objective. To identify the association of a number of clinical features and structural and functional characteristics of the heart with the progression of chronic heart failure (CHF) in patients one year after ST-segment elevation myocardial infarction (MI) (STEMI) with preserved and reduced left ventricular ejection fraction (EF) (LVEF).Design and methods. 120 patients with STEMI were included in a prospective study. During the study, all patients underwent an echocardiographic study using a Sonos 2500 device (Hewlett Packard, USA) on the 1st day (point I), on the 12th day (point II) of hospitalization, and also after 1 year (point III). Depending on the parameters of EF on the 1st day of the disease, the total sample of patients was divided into two: the 1st group — with preserved LVEF was represented by 86 (71,7 %), the 2nd group — with a reduced LVEF was represented by 34 (28,3 %) patients.Results. A total of 19 (15,8 %) adverse events were registered. In two cases, a fatal outcome (1,7 %) was recorded, the cause of which was repeated MI, in five (4,2 %) patients decompensation of СHF was noted, in eight (6,7 %) patients a clinic of progressive angina was traced, in four (3, 3 %) of patients were diagnosed recurrent MI. Deterioration of systolic and diastolic function was established one year after STEMI with preserved (≥ 50 %) LVEF: 17,6 % of patients began to correspond to the intermediate range of EF (40-49 %), the number of patients with diastolic dysfunction increased by 10 % compared to with acute study.Conclusions. Within a year after a STEMI with initially preserved LVEF, there is a deterioration in myocardial function in the form of a decrease in myocardial contractility and an increase in the number of patients with diastolic dysfunction.

The influence of non-steroidal anti-inflammatory drugs with different mechanisms of action on the course of stress reaction, the functional state of kidneys, liver, and heart on the model of acute general cooling

Inhibitors of the arachidonic acid cascade have significant potential as the agents for the prevention of severe cold injuries. The results of the previous studies have demonstrated the pronounced frigoprotective properties of certain non-steroidal anti-inflammatory drugs, primarily diclofenac sodium, etoricoxib, darbufelone mesylate, under the conditions of acute general cooling.
 The aim of the study: to investigate the effect of non-steroidal anti-inflammatory drugs with various mechanisms of action on the course of the stress reaction, the functional state of the kidneys, liver, and heart using the model of acute general cooling.
 Materials and Methods: The experiment was carried out using 35 outbreed male rats weighing 256±5 g. The studied drugs were administered intragastrically 30 minutes before cold injury modelling: diclofenac sodium at a dose of 7 mg/kg, etoricoxib at a dose of 5 mg/kg, darbufelone mesylate at a dose of 20 mg/kg. Acute general cooling was induced by exposure at –18 °C for 2 hours. The efficacy of the studied drugs was evaluated by the values as follows: the body temperature (measured rectally), the course of a stress reaction according to the criteria of “the stress triad”, the functional state of the kidney and liver according to the changes in the blood serum biochemical parameters, the functional state of the heart according to the electrocardiogram.
 Results: It was found that etoricoxib and darbufelone mesylate, and especially diclofenac sodium, demonstrate frigoprotective properties, reducing the severity of hypothermia, have stress-protective activity and a beneficial effect on the functional state of the kidneys. All investigated non-steroidal anti-inflammatory drugs prevent a decrease in myocardial contractility (by the effect on the systolic index) and lengthening of the QT interval caused by acute cold injury. Diclofenac sodium, unlike etoricoxib and darbufelone mesylate, does not enhance the effect of acute general cooling on intraventricular conduction. Under acute exposure to cold, no significant changes in the functional state of the liver were observed, including the groups receiving the nonsteroidal anti-inflammatory medicines.
 Conclusions: The prophylactic administration of the arachidonic acid cascade inhibitors, especially the non-selective COX-2 inhibitor diclofenac sodium, reduces the severity of the stress response, contributes to the maintenance of the renal and cardiac function. There are no significant changes in the functional state of the liver under conditions of the experiment

Функціональний стан кардіореспіраторної системи борців греко-римського стилю на етапі попередньої базової підготовки.

Greco-Roman wrestling places high demands on functional training, which determines the further success of tech-nical and tactical training of athletes. The aim is to determine the features of the functional state of the cardiorespiratory system of Greco-Roman wrestlers at the stage of preliminary basic training in the preparatory period. The study used theoretical research methods (theoretical analysis of scientific and methodological literature) and empirical: computer rheography (this device is intended to determine the functional state of the cardiovascular system), computer spirography (this device is intended to determine the functional state of the respiratory system), and mathematical methods statistics. The mean value of vital capacity in the group of wrestlers at the beginning of the study was 2.40 ± 0.04 l, which was 80.78 ± 1.85% of the appropriate values and showed reduced ability to external respiration and chest rigidity. The detailed distribution of Greco-Roman wrestling according to the forced vital lung capacity in relation to the normative values showed that this indicator in the norm was in 26% of subjects, in the conditional norm – in 41%, in 36% of subjects – in a slight decrease. Reduced ones compared to normal stroke volume (45.70 ± 1.41 ml) indicated a decrease in myocardial contractility, and proper values of minute volume of blood circulation were achieved due to increased heart rate, which is not a rational adaptive response in the state peace of mind. Functional training is an im-portant component of the preliminary basic training; the program of its improvement in Greco-Roman wrestling in the preparatory period is an urgent scientific and practical task of modern sport, and the indicators of physical fitness are a prerequisite for developing a program of improvement.

WHAT DRUGS YOU CAN PREFER IN CARDIOGENIC SHOCK?

Abstract: Relevance. The use of nitroglycerin (NG) in cardiogenic shock (СS) helps to normalize blood pressure, reduce the risk of death and improve prognosis. Aim. To study the effect of vasopressors, inotropic drugs and nitroglycerin on hemodynamics and reducing the risk of death in patients with cardiogenic shock. Material and methods. A comparative assessment of the effectiveness of treatment of СS in myocardial infarction with nitroglycerin and traditional approaches to therapy was carried out. In the control group of patients with СS (17 people), dopamine or norepinephrine was administered in the traditional way. In the main group of patients with СS (22 people), large doses of nitroglycerin were administered. After the stabilization of the state of health, the drip injection of NG continued in the usual doses. Results. In 20 of 22 patients of the main group, immediately after the jet injection of nitroglycerin, blood pressure began to be determined or significantly increased, 14 of them survived (63.6%). In 9 cases, blood pressure did not decrease anymore, vasopressors were not administered, nitroglycerin was administered by drop for another 2-3 days, the treatment ended with discharge in a satisfactory state. In another 2 cases, it was necessary to administer vasopressors in parallel with the drip administration of nitroglycerin, after its jet administration. In the control group, the only patient survived (5.9%). Conclusions. Analysis of literature data indicates that in conditions of maximum depletion of reserves and a decrease in myocardial contractility in patients with cardiogenic shock, the use of vasopressors and inotropic drugs accelerates the decompensation of insufficient blood supply and increases the risk of death. The main way to combat СS is still urgent myocardial revascularization, however, the restoration of the functional activity of hibernated cardiomyocytes will be more successful and safer with their gradual activation. This problem can be successfully solved using the methods of mechanical support of blood circulation or with the help of nitroglycerin. It will be possible to verify the validity of this assumption only on the basis of the results of randomized clinical trials.

Особенности клинических проявлений ишемической болезни сердца у больных с амиодаронассоциированным гипотиреозом

Coronary heart disease (CHD) is an acute problem of modern medicine. Primarily, it is determined by the high prevalence of the disease among the working-age population, as well as by the considerable mortality and disability associated with it. Amiodarone (Am) is the drug of choice in the treatment of cardiac arrhythmias (CA), one of the frequent and threatening manifestations of CHD. Long-term use of the drug can lead to the development of primary hypothyroidism (HT), which significantly aggravates the course of cardiovascular diseases. Objective. To assess the cardiovascular system (CVS) of CHD patients with the development of amiodarone-associated hypothyroidism (AmHT). Material and methods. Analysis of case histories of 810 patients with CHD and various CA who were taking Am for sinus rhythm control was performed. The case histories were examined and a retrospective analysis was performed on the clinical course of CHD in 28 patients with AmHT before and after the development of thyreopathy. To evaluate the state of cardiovascular system the patients' complaints, objective examination data, electrocardiography (ECG) and echocardiography (EchoCG) were assessed. Results. Long-term intake of Am by patients with CHD results in primary HT in 3.4% of cases. The formation of thyreopathy significantly affects the course of the disease. Patients show a 19.6% increase in myocardial volume indices and a 22.7% decrease in myocardial contractility, with a 30.2% increase in left ventricular myocardial mass (LVMM). Conclusion. Amiodarone-associated hypothyroidism is one of the significant complications developing in patients taking the drug for a long period of time. The formation of thyreopathy in patients with CHD significantly aggravates the course of the underlying disease, which should be taken into account when prescribing treatment and dynamic monitoring

The association between 24-h blood pressure variability and major adverse cardiac events (MACE) in hospitalized patients with acute myocardial infarction: a retrospective cohort study

BackgroundAcute myocardial infarction (AMI) is major cardiovascular disease that causes high morbidity and mortality. In AMI, ischemia and necrosis affected some cardiomyocytes leading to a decrease in myocardial contractility which is followed by an acute proinflammation reaction and increased sympathetic tone. Meanwhile, high blood pressure variability (BPV) causing an increased left ventricular workload, heart rate, myocardial oxygen demand and induces proinflamations and endothelial dysfunction. Therefore a high BPV and its associated pathological effects are likely to aggravate the physiological function of the heart and affect the emergence of acute cardiac complications in AMI patients. This study aims to investigate the association’s between short-term BPV and major adverse cardiac events (MACE) in AMI patients. This retrospective cohort study used simple random sampling to identify AMI patients who were hospitalized at Cipto Mangunkusumo National Hospital between January 2018 and December 2019. Mann Withney was performed to investigate the association between BPV and MACE.ResultsThe average systolic BPV value which was calculated as standard deviation (SD) and average real variability (ARV) was higher in the MACE group than in the non-MACE group. Systolic SD and systolic ARV in the MACE group were 13.28 ± 5.41 mmHg and 9.88 ± 3.81 mmHg respectively. In the non-MACE group, systolic SD and systolic ARV were 10.76 (4.59–26.17) mmHg and 8.65 (3.22–19.35) mmHg respectively. There was no significant association between BPV and MACE. However, there were significant differences between systolic SD and systolic ARV in patients with hypertension who experienced MACE and patients without hypertension who experienced MACE.ConclusionsThe BPV of AMI patients who experience MACE was higher than that of non-MACE AMI patients. There was no significant association between BPV ​​and MACE during the acute phase of AMI.

Миокардиальный станнинг в медицине неотложных и критических состояний, ассоциированных с системной гипоксией

Актуальность. Миокардиальный станнинг — феномен, заключающийся в продолжительном снижении сократительной способности миокарда после краткого периода ишемии/реперфузии, при котором не происходит омертвения ткани сердечной мышцы. Если изначально феномен станнинга ассоциировали исключительно с проявлениями ишемической болезни сердца, то в настоящее время имеется все больше свидетельств о том, что миокардиальный станнинг может осложнять совсем другую патологию. Цель: изучение результатов работ оте-чественных и зарубежных ученых, посвященных наблюдению феномена станнинга в медицине неотложных состояний, и систематизация накопленного клинического материала. Материалы и методы. Детальное изучение результатов современных клинических исследований, посвященных диагностике снижения сократительной способности миокарда у пациентов, находящихся в критических состояниях, которые развились не вследствие манифестации острого коронарного синдрома, обсуждению механизмов патогенеза миокардиальной дисфункции при этих состояниях и принципам оказания таким больным экстренной и специализированной медицинской помощи. Результаты. Для феномена миокардиального станнинга характерны следующие отличительные признаки: 1. Коронарный кровоток после перенесенного эпизода ишемии практически полностью восстанавливается. После ишемии очень часто регистрируется кратковременный период гиперперфузии. 2. Несмотря на восстановление коронарного кровотока, имеет место продолжительное снижение сократимости миокарда. 3. Необратимого повреждения кардиомиоцитов в период ишемии не происходит. 4. Снижение сократительной способности сердца, наблюдающееся после ишемии и последующей реперфузии, является полностью обратимым. Основными механизмами развития миокардиального станнинга являются: усиленная генерация активных форм кислорода в период реперфузии; перегрузка кардиомиоцитов кальцием; снижение сопряженности между процессами электрического возбуждения миокарда и его сократимостью. Продукция простациклина, активность ангиотензина I, II и ангиотензинпревращающего фермента, продукция брадикинина моделируют тяжесть мио-кардиальной дисфункции при станнинге. Причиной станнинга может быть индуцированная катехоламинами кардиотоксичность. Миокардиальный станнинг можно наблюдать у пациентов с геморрагическим, септическим шоком, субарахноидальными кровоизлияниями, на фоне проведения гемодиализа, после криза при феохромоцитоме, после реанимационной акции. Выводы. Миокардиальный станнинг требует своевременной диагностики, поскольку проведение гемодинамической коррекции не с помощью инотропной поддержки, а по другим направлениям, а именно за счет увеличения скорости объемной нагрузки (агрессивная инфузионная терапия) или применения вазопрессоров, может резко ухудшить состояние пациента вследствие увеличения нагрузки на ослабленное сердце.

Heart failure in children and adolescents (high yield topics for primary care pediatrician)

HF in children is a life-threatening polyethiological state with a tendency to progression. There are acute and chronic heart failure, the causes of which are largely determined by age. Depending on the causes and features of hemodynamics, HF can occur with a stored (and borderline) and with a reduced ejection fraction. In early and young childhood, HF is manifested primarily by a decrease in appetite, sweating, decreased physical activity and a slowdown in physical development. At an older age, shortness of breath, edema, and enlargement of the liver are highlighted. The determination of biochemical markers of myocardial insufficiency (natriuretic peptide, troponin) is important for assessing the degree of HF, although the standards for their concentration for different age groups require further refinement. An instrumental study noted a decrease in myocardial contractility. Initially, myocardial oxygen consumption is increasing, which indicates its irrational use and corresponds to increased peroxidation. Subsequently, myocardial oxygen consumption decreases even without signs of coronary pathology. Treatment should include mandatory sufficient calorie intake, sparing regimen, complex drug therapy.

Current understanding of pathophysiological mechanisms of peripartal cardiomyopathy

The aim of the study. To analyze literature data in order to study the pathophysiological mechanisms of development of peripartum cardiomyopathy. Research methods and materials. A review of modern Russian and foreign, mainly English-speaking, literature on the pathogenetic mechanisms of IPAH development was carried out. We took into account publications not older than 6 years, published in specialized medical journals and guidelines. Results. According to the data of modern studies devoted to the peculiarities of the development of peripartum cardiomyopathy, much attention is paid to the risk factors of the disease, in particular the age-related obstetric history, pregnancy with twins or more, and arterial hypertension. In addition, the significance of genetic predisposition, inflammatory syndrome has been proven, and the vasculo-hormonal theory is being studied. Difficult issues of the etiopathogenesis of the disease, including myocarditis, the role of the prolactin-cathepsin-prolactin 16 kDa system, and malnutrition are discussed.Conclusion. Pathophysiological mechanism of development of peripartum cardiomyopathy. appears as a complex combination of inflammatory changes in the myocardium with the participation of a cardiotoxic subfragment – prolactin 16 kDa, which causes damage and dysfunction of the endothelium under hemodynamic stress against the background of possible genetic changes, which leads to damage to cardiomyocytes and a decrease in myocardial contractility.

Silent myocardial ischemia in patients with type 2 diabetes mellitus: a clinical case

Background. Type 2 diabetes mellitus (DM) is an important medical, social, and economic problem due to the high prevalence of the disease, which often leads to disability and significantly increases mortality in elderly people. One of the causes of coronary heart disease (CHD) in patients with type 2 DM is autonomic cardiovascular neuropathy, which is characterized by damage to the autonomic nervous system and manifests itself in a varying clinical picture, including silent myocardial ischemia (SMI). The prevalence of SMI among patients with type 2 DM is much higher than in people without it. The purpose was to study the clinical case of a patient with type 2 DM and CHD, raise awareness of the prevalence and influence of type 2 DM on CHD progression by focusing on diagnostic research and treatment strategies. Materials and methods. The clinical case of the detected silent ischemia in a patient with type 2 DM was analyzed. The complaints were as following: high blood pressure, moderate shortness of breath during walking, pain, and numbness of the lower extremities. Anamnesis: type 2 DM over 20 years; endovascular stenting of the right common iliac artery due to obliterating atherosclerosis of the arteries of the lower extremities; hypertension over 10 years; obesity. Based on this data, CHD was suspected. Results. The Holter monitoring revealed rare episodes of reversible ischemic repolarization. ECG demonstrated the deviation of the electrical axis to the left, hypertrophy of the left ventricular myocardium, diffuse violation of repolarization processes. Ultrasound of the heart found aortic atherosclerosis, left ventricular myocardial hypertrophy, a moderate decrease in myocardial contractility. Ultrasound of vessels of the lower extremities showed the signs of obliterating atherosclerosis with decompensation of peripheral blood flow. Coronary angiography demonstrated left coronary artery with critical subocclusions (90 %), right coronary artery with chronic occlusion in the middle segment (100 %). There was established the diagnosis: coronary heart disease (silent ischemia); diffuse stenotic atherosclerosis of the coronary artery (coronary angiography May 2019); arterial hypertension II stage, degree 2; HF II stage; II NYHA; type 2 diabetes mellitus, insulin-dependent, decompensated; obesity I stage; obliterating atherosclerosis of the arteries of the lower extremities (condition after endovascular stenting of the right common iliac artery on January 2018); chronic pancreatitis in remission, peptic ulcer of the duodenum (operated in 1981); chronic cholecystitis in remission. The treatment was prescribed: insulin therapy, nebivolol, eplerenone, candesartan, clopidogrel, rosuvastatin. Coronary artery bypass grafting is recommended. Conclusions. Thereby, timely diagnosis and adequate treatment can avoid complications of type 2 DM and improve quality and lifetime. With type 2 DM, CHD is often masked and remains undiagnosed, leading to complications and death, therefore more attention to such patients is needed.