scholarly journals The role of circulating autoantibodies in relation to proteins in structural cardiomyocytes and functional changes of the heart in patients with chronic myocarditis

2013 ◽  
Vol 4 (4) ◽  
pp. 40-44
Author(s):  
E. V Gladysheva ◽  
S. L Grishaev ◽  
V. S Nikiforov ◽  
A. S Svistov ◽  
V. N Solntsev
Keyword(s):  
Heart Failure ◽  
Cardiac Dysfunction ◽  
Structural Changes ◽  
Myocardial Inflammation ◽  
Cardiac Myosin ◽  
Functional Changes ◽  
Chronic Myocarditis ◽  
Examination Methods ◽  
Circulating Autoantibodies

Evidence that has been progressively gathered implicates an important role of the immune system in the course of heart failure. In the majority of heart disease patients, disturbances of humoral immunity with production of cardiodepressant antibodies may play a functional role in cardiac dysfunction. This study evaluates the role of autoantibodies to the cardiac myosin. We examined 52 patients (from 14 till 61 years) with chronic myocarditis. The main examination methods were clinical and biochemical blood tests, ECG, ambulatory Holter ECG monitoring, echocardiography. Autoantibodies to the cardiac myosin were determined by ELISA. These autoantibodies correlate with myocardial inflammation. Also they are associated with structural changes of the heart (hypertrophy, dilation) and cardiac dysfunction (contractility, rhythm and conduction). The degree of expression of these disorders is related to the severity of chronic heart failure.

scholarly journals Cardiac Electrical and Structural Changes During Bacterial Infection: An Instructive Model to Study Cardiac Dysfunction in Sepsis

2016 ◽  
Vol 5 (9) ◽  
Author(s):  
Michael A. Makara ◽  
Ky V. Hoang ◽  
Latha P. Ganesan ◽  
Elliot D. Crouser ◽  
Mahmood Khan ◽  
...  
Keyword(s):  
Cardiac Dysfunction ◽  
Structural Changes ◽  
Immune Cell ◽  
Left Ventricular ◽  
Infection Model ◽  
Myocardial Inflammation ◽  
Multiple Time ◽  
Heat Shock Factor 1 ◽  
Cardiac Damage

Background Sepsis patients with cardiac dysfunction have significantly higher mortality. Although several pathways are associated with myocardial damage in sepsis, the precise cause(s) remains unclear and treatment options are limited. This study was designed to develop a new model to investigate the early events of cardiac damage during sepsis progression. Methods and Results Francisella tularensis subspecies novicida ( Ft.n ) is a Gram‐negative intracellular pathogen causing severe sepsis syndrome in mice. BALB /c mice (N=12) were sham treated or infected with Ft.n through the intranasal route. Serial electrocardiograms were recorded at multiple time points until 96 hours. Hearts were then harvested for histology and gene expression studies. Similar to septic patients, we illustrate both cardiac electrical and structural phenotypes in our murine Ft.n infection model, including prominent R' wave formation, prolonged QRS intervals, and significant left ventricular dysfunction. Notably, in infected animals, we detected numerous microlesions in the myocardium, previously observed following nosocomial Streptococcu s infection and in sepsis patients. We show that Ft.n ‐mediated microlesions are attributed to cardiomyocyte apoptosis, increased immune cell infiltration, and expression of inflammatory mediators (tumor necrosis factor, interleukin [ IL] ‐1β, IL ‐8, and superoxide dismutase 2). Finally, we identify increased expression of microRNA‐155 and rapid degradation of heat shock factor 1 following cardiac Ft.n infection as a primary cause of myocardial inflammation and apoptosis. Conclusions We have developed and characterized an Ft.n infection model to understand the pathogenesis of cardiac dysregulation in sepsis. Our findings illustrate novel in vivo phenotypes underlying cardiac dysfunction during Ft.n infection with significant translational impact on our understanding of sepsis pathophysiology.

scholarly journals Metabolic syndrome and chronic heart failure: a modern aspect of the problem

2022 ◽  
Vol 21 (1) ◽  
pp. 105-113
Author(s):  
Tatiana Fedorova ◽  
Natalya Semenenko ◽  
Serafima Tazina ◽  
Alexander Mamonov ◽  
Tatiana Sotnikova
Keyword(s):  
Heart Failure ◽  
Metabolic Syndrome ◽  
Chronic Heart Failure ◽  
Clinical Course ◽  
Rapid Development ◽  
Medical Science ◽  
Left Ventricular ◽  
Modern Aspect ◽  
Functional Changes

Objective: The increase of morbidity results from both an increase of life expectancy of the population, and influence of various risk factors contributing to development and increase of chronic heart failure (CHF). The combination of several atherogenic mechanisms (abdominal obesity (AO), insulin resistance (IR), arterial hypertension (AH), hyperglycemia, dyslipidemia), combined as “metabolic syndrome” (MS), causes a more rapid development of CHF. Materials and methods: The research finding of 74 patients with class II-III of CHF, including 37 patients (50%) with MS, are presented. The age structure of the pathology, severity of clinical course, data of laboratory and instrumental examination in various groups of patients were evaluated. A special program included an echocardiographic test with an assessment of various myocardial parameters. Results and Discussion: Research materials find out a number of characteristics of CHF clinical course (its earlier development and severe course) in patients with MS. Echocardiographic tests reveal an increase of heart chambers sizes, thickness of left and right ventricle, pulmonary hypertension. Myocardium morpho-functional changes are more significant in patients with CHF and MS than in those without MS. An increase in leptin levels, a marker of obesity, fibrosis and inflammation, has been found. Leptin, C-reactive peptide (CRP) and high-sensitive troponin in patients with MS significantly exceeded those in patientswithout MS. Correlations of leptin levels, adiponectin, CRP and left ventricular mass, thickness of epicardial fat (TEF), ejection fraction were established. Conclusion: Materials of the research indicate the important role of inflammatory and dysmetabolic processes in development and progression of CHF in patients with MS. Bangladesh Journal of Medical Science Vol. 21(1) 2022 Page : 105-113

Abstract 519: Talin is Required for Normal Adult Heart Function

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Yoshitake Cho ◽  
Ruixia Li ◽  
Ana M Manso ◽  
Robert S Ross
Keyword(s):  
Heart Failure ◽  
Cardiac Function ◽  
Cardiac Dysfunction ◽  
Cardiac Development ◽  
Heart Function ◽  
Left Ventricular ◽  
Mass Spectrometry Analysis ◽  
Adult Heart ◽  
Spectrometry Analysis ◽  
Functional Changes

Talin (Tln) is a component of muscle costameres that links integrins to other components of the cellular cytoskeleton and plays an important role in maintaining the cellular integrity of cardiac myocytes (CM). There are two talin genes, Tln1 and Tln2, expressed in the heart. Tln1 is ubiquitously expressed, and Tln2 is dominantly expressed in CM. In our previous study, we show that the global deletion of Tln2 in mice (T2KO) caused no structural or functional changes in the heart, presumably because CM Tln1 became up-regulated. However, we found that mice lacking both CM Tln1 and Tln2 exhibit cardiac dysfunction by 4 weeks (w) of age with 100% mortality by 6 months (m), showing Tln plays an essential role in cardiac development and in maintaining cardiac function. In this study, we produced a tamoxifen (Tamo)-inducible mouse model in which Tln1 could be explicitly reduced in the adult CM (T1icKO), and then generate T1icKO:T2KO (T1/2dKO), so that the function of Tln could be assessed in the postnatal heart. T2KO and Tln1/2dKO mice were injected with Tamo at 8w. Echocardiograms were performed to evaluate cardiac function up to 8w post-Tamo injection. While T2KO mice showed normal cardiac function, T1/2dKO exhibited a gradual decrease in function post-Tamo injection. At 8w post-Tamo injection, T1/2dKO mice showed cardiac hypertrophy, fibrosis, and heart failure. To understand the mechanism by which deletion CM talin leads to cardiac dysfunction, left ventricular tissue protein lysates from T2KO and T1/2dKO mice at 4w post-Tamo when cardiac function (echo) and structure were preserved in dKO. The protein lysates were subjected to quantitative mass spectrometry analysis. We found there are 1,100 proteins differentially expressed in T2KO and T1/2dKO hearts. Pathway analysis was performed, and the results showed that proteins involved in vesicle transport, protein folding, and innate immunity are most up-regulated in the T1/2dKO heart. Taken together, our results show that Tln is required for maintaining proper cardiac function in the adult heart. The deletion of Tln in CM results in the up-regulation of multiple intracellular pathways, and we are currently studying the role of each pathway in the pathogenesis of heart failure induced by CM Tln deletion.

scholarly journals Diagnostic, clinical and prognostic aspects determine the concentration of C-reactive protein in chronic heart failure.

2018 ◽  
Vol 96 (3) ◽  
pp. 197-207
Author(s):  
Andrey A. Bobylev ◽  
S. A. Rachina ◽  
S. N. Avdeev ◽  
A. A. Petrov
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Disease Severity ◽  
Cardiac Dysfunction ◽  
Inflammatory Marker ◽  
High Sensitivity ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Incident Heart Failure

A lot of mechanisms in development and progression of cardiac dysfunction are associated with changes of multiple markers and high-sensitivity C-reactive protein is one of them. The role of this inflammatory marker in heart failure pathogenesis requires further study. However, various recent reports have suggested that C-reactive protein assessment may be used for prediction of incident heart failure, its prognosis and estimation of the disease severity.

scholarly journals ECONOMIC REFORM AND FUNCTIONAL CHANGES OF THE AUTHORITIES OF BURYATIA IN THE LATE 1960S – 1970S

2017 ◽  
pp. 78-83
Author(s):  
E. T. Protasov
Keyword(s):  
Structural Changes ◽  
Soviet Period ◽  
Institutional Research ◽  
Economic Management ◽  
Functional Changes ◽  
Power And Control ◽  
Formation And Evolution ◽  
The Subject ◽  
And Control

The subject of the research is the analysis of economic and structural changes  in  the  country  and  the  autonomous  republic  in  the  examined  period with the use of the systemic and comparative approaches, as well as institutional research method. When planning the economic reforms, the USSR and the Buryat ASSR bodies of state power and control did an active and purposeful job to implement them and carried out an effective personnel policy. In 1965 – 1966 the territorial management system was abolished in industrial production. Branch management was passed on to newly created ministries, the role of state committees increased. These facts created auspicious conditions for scientific and technical progress development. Moreover, the main purpose of the production was the course on development and inculcation of economic management methods, independence of enterprises, and reduction of administrative regulation of their activity. The results of economic development during the 8th five-year plan were the best for the whole Soviet period. At the same time, macroeconomics still maintained an extensive character. The provided materials interpreted in a modern light can be used for reconsideration of state governing bodies’ formation and evolution. 

Advancement of Mechanisms of Coxsackie Virus B3-Induced Myocarditis Pathogenesis and the Potential Therapeutic Targets

2019 ◽  
Vol 20 (14) ◽  
pp. 1461-1473 ◽  
Author(s):  
Tolessa Muleta Daba ◽  
Yue Zhao ◽  
Zhenwei Pan
Keyword(s):  
Heart Failure ◽  
Dilated Cardiomyopathy ◽  
Treatment Options ◽  
Viral Myocarditis ◽  
Micro Rna ◽  
Biological Molecules ◽  
Coxsackie Virus ◽  
Chronic Myocarditis ◽  
Coxsackie Virus B3

Viral myocarditis is a cardiac disease caused by Group B Coxsackie virus of Enterovirus genus in the Picorna viridae family. It causes heart failure in children, young and adults. Ten Percent (10%) of acute heart failure and 12% of sudden deaths in young and adults who are less than 40 years is due to this viral myocarditis. If treatment action is not taken earlier, the viral disease can develop into chronic myocarditis and Dilated Cardiomyopathy which lead to congestive heart failure. And these eventually result in a reduced cardiac function which finally brings the victim to death. The only treatment option of the disease is heart transplantation once the acute stage of disease develops to chronic and Dilated Cardiomyopathy. Currently, there is a limitation in daily clinical treatments and even some available treatment options are ineffective. Therefore, focusing on search for treatment options through investigation is imperative. Recent studies have reported that biological molecules show a promising role. But their mechanism of pathogenesis is still unclear. A detailed study on identifying the role of biological molecules involved in Coxsackie B3 virus induced myocarditis and their mechanisms of pathogenesis; compiling and disseminating the findings of the investigation to the scientific communities contribute one step forward to the solution. Therefore, this review is aimed at compiling information from findings of current studies on the potential therapeutic role of micro RNA, cytokines and chemokines on the mechanism of pathogenesis of Coxsackie virus B3- induced myocarditis to give brief information for scholars to conduct a detailed study in the area.

scholarly journals Cardiac Dysfunction in Rheumatoid Arthritis: The Role of Inflammation

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 881
Author(s):  
Jianmin Chen ◽  
Lucy V. Norling ◽  
Dianne Cooper
Keyword(s):  
Rheumatoid Arthritis ◽  
Heart Failure ◽  
Cardiovascular Disease ◽  
Heart Disease ◽  
Cardiac Dysfunction ◽  
Preserved Ejection Fraction ◽  
Risk Of Mortality ◽  
Increased Risk ◽  
Systemic Inflammatory Disease

Rheumatoid arthritis is a chronic, systemic inflammatory disease that carries an increased risk of mortality due to cardiovascular disease. The link between inflammation and atherosclerotic disease is clear; however, recent evidence suggests that inflammation may also play a role in the development of nonischemic heart disease in rheumatoid arthritis (RA) patients. We consider here the link between inflammation and cardiovascular disease in the RA community with a focus on heart failure with preserved ejection fraction. The effect of current anti-inflammatory therapeutics, used to treat RA patients, on cardiovascular disease are discussed as well as whether targeting resolution of inflammation might offer an alternative strategy for tempering inflammation and subsequent inflammation-driven comorbidities in RA.

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