Cause Of Congestive Heart Failure Research Articles

Exploring the Regulation and Function of Rpl3l in the Development of Early-Onset Dilated Cardiomyopathy and Congestive Heart Failure Using Systems Genetics Approach.

Cardiomyopathies, diseases affecting the myocardium, are common causes of congestive heart failure (CHF) and sudden cardiac death. Recently, biallelic variants in ribosomal protein L3-like (RPL3L) have been reported to be associated with severe neonatal dilated cardiomyopathy (DCM) and CHF. This study employs a systems genetics approach to gain understanding of the regulatory mechanisms underlying the role of RPL3L in DCM. Genetic correlation, expression quantitative trait loci (eQTL) mapping, differential expression analysis and comparative functional analysis were performed using cardiac gene expression data from the patients and murine genetic reference populations (GRPs) of BXD mice (recombinant inbred strains from a cross of C57BL/6J and DBA/2J mice). Additionally, immune infiltration analysis was performed to understand the relationship between DCM, immune cells and RPL3L expression. Systems genetics analysis identified high expression of Rpl3l mRNA, which ranged from 11.31 to 12.16 across murine GRPs of BXD mice, with an ~1.8-fold difference. Pathways such as "diabetic cardiomyopathy", "focal adhesion", "oxidative phosphorylation" and "DCM" were significantly associated with Rpl3l. eQTL mapping suggested Myl4 (Chr 11) and Sdha (Chr 13) as the upstream regulators of Rpl3l. The mRNA expression of Rpl3l, Myl4 and Sdha was significantly correlated with multiple echocardiography traits in BXD mice. Immune infiltration analysis revealed a significant association of RPL3L and SDHA with seven immune cells (CD4, CD8-naive T cell, CD8 T cell, macrophages, cytotoxic T cell, gamma delta T cell and exhausted T cell) that were also differentially infiltrated between heart samples obtained from DCM patients and normal individuals. RPL3L is highly expressed in the heart tissue of humans and mice. Expression of Rpl3l and its upstream regulators, Myl4 and Sdha, correlate with multiple cardiac function traits in murine GRPs of BXD mice, while RPL3L and SDHA correlate with immune cell infiltration in DCM patient hearts, suggesting important roles for RPL3L in DCM and CHF pathogenesis via immune inflammation, necessitating experimental validations of Myl4 and Sdha in Rpl3l regulation.

Transgenic Mice Expressing Functional TCRs Specific to Cardiac Myhc-α 334-352 on Both CD4 and CD8 T Cells Are Resistant to the Development of Myocarditis on C57BL/6 Genetic Background.

Myocarditis is a predominant cause of congestive heart failure and sudden death in children and young adolescents that can lead to dilated cardiomyopathy. Lymphocytic myocarditis mediated by T cells can result from the recognition of cardiac antigens that may involve CD4 or CD8 T cells or both. In this report, we describe the generation of T cell receptor (TCR) transgenic mice on a C57BL/6 genetic background specific to cardiac myosin heavy chain (Myhc)-α 334-352 and make the following observations: First, we verified that Myhc-α 334-352 was immunogenic in wild-type C57BL/6 mice and induced antigen-specific CD4 T cell responses despite being a poor binder of IAb; however, the immunized animals developed only mild myocarditis. Second, TCRs specific to Myhc-α 334-352 in transgenic mice were expressed in both CD4 and CD8 T cells, suggesting that the expression of epitope-specific TCR is common to both cell types. Third, although T cells from naïve transgenic mice did not respond to Myhc-α 334-352, both CD4 and CD8 T cells from animals immunized with Myhc-α 334-352 responded to the peptide, indicating that antigen priming is necessary to break tolerance. Fourth, although the transgenic T cells could produce significant amounts of interferon-γ and interleukin-17, the immunized animals developed only mild disease, indicating that other soluble factors might be necessary for developing severe myocarditis. Alternatively, the C57BL/6 genetic background might be a major contributing factor for resistance to the development of myocarditis. Taken together, our model permits the determination of the roles of both CD4 and CD8 T cells to understand the disease-resistance mechanisms of myocarditis in a single transgenic system antigen-specifically.

A VEIN OF GALEN MALFORMATION - A RARE CAUSE OF CONGESTIVE CARDIAC FAILURE IN NEONATE

Vein of Galen aneurysmal malformation (VGAM) is a rare congenital vascular malformation caused by the maldevelopment of its embryonic precursor, the median prosencephalic vein of Markowski. Vein of Galen aneurysmal malformation (VGAM) is a rare cause of congestive heart failure in the neonatal period and carries a high mortality rate. It is a difcult diagnosis because the clinical picture often presents with symptoms suggesting that the patient has a congenital cardiac malformation.1,2 Patients are subjected to high-risk procedures such as cardiac catheterization to establish a diagnosis. These investigations often have negative ndings and can delay correct diagnosis. Here we report a case of Four days old neonate with c/o Increased respiratory activity since 2 days with tachycardia, tachypnea and oliguria. Continuous murmur was noted with features suggestive of Congestive cardiac failure i.e. Tachycardia, tachypnoea, hepatomegaly. Bruit + over Anterior Fontanelle. USG skull revealed the presence of Vein of Gallen Aneurysmal Malformation. 2D ECHO was done which suggestive of Congenital Heart Disease; moderate OS ASD with left to right shunt Dilated cardiac chambers; No PAH; Normal biventricular function .CECT Brain showed the presence of Aneurysmal deep venous structure measuring 20 x 25 mm noted in the supratentorial region of posterior fossa (in quadrigeminal cistern) which drained to vein of galen (VGAM) and the vessel feeding the aneurysm was arising from basilar artery.Hence diagnosis was made.Child initially treated symptomatically for cardiac failure then Endovascular treatment i.e. embolization was performed on 30th day of life.The VGAM was partially occluded.Then symptoms got relieved after Embolization

Identification of BMP10 as a Novel Gene Contributing to Dilated Cardiomyopathy.

Dilated cardiomyopathy (DCM), characterized by left ventricular or biventricular enlargement with systolic dysfunction, is the most common type of cardiac muscle disease. It is a major cause of congestive heart failure and the most frequent indication for heart transplantation. Aggregating evidence has convincingly demonstrated that DCM has an underlying genetic basis, though the genetic defects responsible for DCM in a larger proportion of cases remain elusive, motivating the ongoing research for new DCM-causative genes. In the current investigation, a multigenerational family affected with autosomal-dominant DCM was recruited from the Chinese Han population. By whole-exome sequencing and Sanger sequencing analyses of the DNAs from the family members, a new BMP10 variation, NM_014482.3:c.166C > T;p.(Gln56*), was discovered and verified to be in co-segregation with the DCM phenotype in the entire family. The heterozygous BMP10 variant was not detected in 268 healthy volunteers enrolled as control subjects. The functional measurement via dual-luciferase reporter assay revealed that Gln56*-mutant BMP10 lost the ability to transactivate its target genes NKX2.5 and TBX20, two genes that had been causally linked to DCM. The findings strongly indicate BMP10 as a new gene contributing to DCM in humans and support BMP10 haploinsufficiency as an alternative pathogenic mechanism underpinning DCM, implying potential implications for the early genetic diagnosis and precision prophylaxis of DCM.

Abstract 13256: Prognosis of Congestive Heart Failure Due to Chagas Disease in Women and Men

Introduction: Chronic Chagas cardiomyopathy (CCC) is one of the leading causes of congestive heart failure (CHF) in Latin America and carries a high morbidity and mortality burden. Previously, it was believed that there was no epidemiological and clinical evidence of a gender-associated risk of death in patients with CCC. Hypothesis: to analyze the mortality of congestive heart failure due to CCC in women and men. Methods: From February 2017 to September 2020, we followed a cohort of patients with CHF due to CCC in a single-center outpatient clinic. Serologic tests defined Chagas disease. Baseline data included clinical characteristics and echocardiographic findings. Statistical analyses were performed with the Kaplan-Meier method and Cox proportional hazards methods. Results: We studied 733 patients, mean of 61.4 ± 12.3 years, and 381 (52%) males. At baseline, women were older (63.0±11.9 vs. 60±12.4 years; p=0.01), had a higher prevalence of CKD (9.7 vs. 5.1%; p=0.002), higher mean left ventricular ejection fraction (LVEF) (44.5±14.6% vs. 37.3±14.8%; p<0.001), and a lower left ventricular diastolic diameter (LVDD) (56.7±8.9 vs. 62.4±9.4 mm; p<0.001). Over a 3-years follow-up period, 294 patients died being 168 (57%) men and 126 (43%) women (log-rank; p=0.002). Women had more implantable pacemakers (26.1% vs. 16.5%; p=0.002) and men more implantable cardioverter-defibrillators (20.7% vs. 12.5%; p=0.003). Heart transplants occurred in 10.8% of men and 7.4% of women (p=NS). Cox regression for death adjusted for age, sex, previous myocardial infarction, diabetes, previous stroke, chronic kidney disease (CKD), atrial fibrillation, and LVEF showed men (HR=1.4; 95%CL:1.1-1.8), previous stroke (HR=2.4; 95%CL:1.5-3.6), diabetes (HR=2.0; 95%CL: 1.3-3.1), and CKD (HR=1.8; 95%CL:1.3-2.6) as the main predictors of death. Conclusions: women had a better prognosis than men. Treatment of comorbidities will significantly reduce the death rate in CHF due to CCC.

Complement factor D derived from epicardial adipose tissue participates in cardiomyocyte apoptosis after myocardial infarction by mediating PARP-1 activity

BackgroundAcute myocardial infarction (MI) is considered to be the main cause of congestive heart failure. The aim of this study was to provide an in-depth analysis of athophysiological processes and provide key targets for intervention in the occurrence of acute MI. MethodsA rat model of MI was established by ligation of left anterior descending branch. Heart tissue, epicardial adipose tissue (EAT) and subcutaneous adipose tissue (SAT) were collected. H9c2 cells were used to explore the mechanism of complement factor D (CFD) regulating cardiomyocyte apoptosis. ResultsMyocardial apoptosis were observed in MI rat, and more EAT was found in the MI group in vivo. The conditioned medium prepared by EAT (EAT-CM) significantly reduced the activity of H9c2 cells. The content of CFD in EAT was significantly increased, and CFD promoted cardiomyocyte apoptosis in vitro and CFD-IN1 (a selective inhibitor of CFD) could revised this effect. CFD induced poly ADP-ribosepolymerase-1 (PARP-1) overactivation. Furthermore, the addition of pan-caspase inhibitor Z-VAD in the SAT-CM + CFD group couldn't affect H9c2 cell apoptosis. CFD induced cell apoptosis via PARP-1 activation and PARP-1 inhibitor 3-Aminobenzamide could revise this effect. The injection of CFD-IN1 in MI rat model confirmed that inhibition of CFD activity alleviated cardiomyocytes apoptosis. ConclusionOur findings indicate that EAT mediating cardiomyocyte apoptosis after MI through secretion of CFD and activation of PARP-1 activity.

Etiology of Congestive Heart Failure in Children

Objective: To determine the frequency of common causes of congestive heart failure among children in a tertiary care hospital. Study Design: Cross-sectional study Place and Duration of Study: Department of Paediatrics Medicine, Services Hospital, Lahore from 1st January 2018 to 30th June 2018. Methodology: Ninety children were enrolled. Demographic information like name, age, gender, weight of child was noted. Complete blood count, echocardiography and chest X-ray were done. Children underwent assessment for presence of causes of congestive heart failure. Results: Fifty six (62.22%) were between 2-30 months of age whereas 34 (37.78%) were between 31-60 months of age with mean age 29.4±12.47 months. There were 40 (44.44%) males and 50 (55.56%) females. The causes of CCF were acute myocarditis in 39 (43.33%), congenital heart disease in 31 (34.44%) and severe anemia in 20 (22.33%). Conclusion: Acute myocarditis is one of the common causes of congestive heart failure in children aftersevere anemiaand congenital heart disease. Keywords: Congestive heart failure, Common causes, Acute myocarditis, Congenital heart disease, Severe anemia

Principais fatores de risco em cães com insuficiência cardíaca congestiva diagnosticada por parâmetros ecocardiográficos

Nowadays, congestive heart failure is one of the major complications of heart disease in small animals, which is characterized by a clinical condition in which the heart is unable to eject the blood efficiently. At long term, some compensatory mechanisms it will eventually become detrimental and, mainly, due to the congestion caused by it. In dogs, the main cause of CHF is chronic mitral valve degeneration, it is responsible for the degeneration of collagen present in the mitral valve structure that will have detrimental consequences on the entire circulatory system. The aim of the present study was to perform a retrospective study of 498 echocardiographic reports collected at a veterinary cardiology service of the Bauru region, from January 2017 to June 2019. Two groups were formed according to the Doppler echocardiographic alterations found, one that included animals with characteristics of congestive heart failure (CHF), and the other formed by non-CHF patients. Of the total number of animals evaluated, 61 were classified as affected by congestive heart failure and after classification, it was considered the main epidemiological factors (race, sex and age) of animals belonging to this group. Small breed animals were overrepresented and also elderly animals, with no apparent sexual predisposition. In addition, animals with CHF presented higher values when compared to animals without CHF of LA/Ao ratio (2.31 ± 0.30 vs. 1.46 ± 0.35), E/IRTV ratio (2.96 ± 0.39 vs. 1.16 ± 0.43) and E-wave velocity (1.45 m/s ± 0.18 vs. 0.75 m/s ± 0.22) on echocardiographic examination.

Laboratory Grown Biofilms of Bacteria Associated with Human Atherosclerotic Carotid Arteries Release Collagenases and Gelatinases during Iron-Induced Dispersion.

ABSTRACTThe association of bacteria with arterial plaque lesions in patients with atherosclerosis has been widely reported. However, the role these bacteria play in the progression of atherosclerosis is still unclear. Previous work in our lab has demonstrated that bacteria exist in carotid artery plaques as biofilm deposits. Biofilms are communities of microorganisms enmeshed within a protective, self-produced extracellular matrix and have been shown to contribute to chronic infections in humans. Biofilm communities have the potential to impact surrounding tissues in an infection if they undergo a dispersion response, releasing bacteria into the surrounding environment by enzymatic degradation of the extracellular matrix. One concern relating to these enzymes is that they could cause collateral damage to host tissues. In this study, we present an in vitro multispecies biofilm culturing model used to investigate the potential role of bacterial biofilm dispersion in the progression of atherosclerosis. This work has demonstrated an increase in cell release from mixed-species biofilms formed by bacteria associated with human carotid arterial plaque deposits following treatment with iron or a combination of norepinephrine and transferrin. Greater extracellular lipase, protease, and collagenase/gelatinase activity was also associated with iron-treated biofilms. The results of this work suggest that bacteria in this model undergo iron-induced biofilm dispersion, as evidenced by the increased cell release and higher enzyme activity following treatment. This work demonstrates the potential for multispecies biofilm dispersion to contribute to arterial tissue degradation by bacteria and suggests that in atherosclerotic infections, biofilm dispersion may contribute to thrombogenesis, which can lead to heart attack or stroke.IMPORTANCE Atherosclerosis, or hardening of the arteries, is a leading cause of congestive heart failure, heart attack, and stroke in humans. Mounting evidence, in the literature and from our lab, points to the regular involvement of bacteria within arterial plaque deposits in patients with advanced atherosclerosis. Very little is known about the behavior of these bacteria and whether they may contribute to tissue damage in infected arteries. Tissue damage within the arterial plaque lesion can lead to rupture of the plaque contents into the bloodstream, where a clot may form, resulting in a potential heart attack or stroke. This study shows that plaque-associated bacteria, when cultured as mixed-species biofilms in the laboratory, can release degradative enzymes into their environment as the result of a dispersion response triggered by iron. These degradative enzymes can digest proteins and lipids which are associated with the tissues that separate the plaque lesion from the arterial lumen. Thus, this study demonstrates that if mixed species biofilms are induced to undergo dispersion in an infected atherosclerotic lesion when exposed to an elevated concentration of free iron, they have the potential to contribute to the weakening of arterial tissues, which may contribute to atherosclerotic plaque destabilization.

Comparison of Intestinal Microbiota Between Healthy and MMVD Chihuahuas Using 16S rRNA Gene Amplicon Sequencing.

Myxomatous mitral valve disease (MMVD) is the most common cause of congestive heart failure in dogs, and although complications of MMVD to the lungs and kidneys have been identified, complications to the gut are less well understood. The intestinal microbiota is an important factor in the gut, and although the association between heart disease and the intestinal microbiota has been shown in human medicine, it is unknown in dogs. The study aimed to evaluate the relationship between MMVD and gut microbiota. A total of 69 healthy Chihuahuas and Chihuahuas with MMVD were evaluated for cardiac health by echocardiography and chest radiography and grouped according to ACVIM guidelines. Fecal samples were collected from all cases and 16S rRNA sequencing was used to reveal the intestinal microbiota. There were significant differences in LA/Ao, LVIDd, E vel, VHS, and VLAS with the severity of ACVIM. On the other hand, there were no significant differences in the diversity and composition of gut microbiota among the groups. The present study did not identify the effects of MMVD on the gut microbiota.

Impaired Left Ventricular Ejection Fraction Induces “Very Early Pre-Diagnostic” Hemopoietic Modifications in Myeloid Leukemia Patients

Background: There is strong association between clonal hematopoiesis of undetermined prognosis (CHIP) and coronary artery disease (CAD) development. Indeed, ischemic heart disease is a leading cause of congestive heart failure (CHF) in western society. CH induces not only enhanced risk for myeloid malignancies, but also significant cardiovascular morbidity in elderly patients (pt). Pt with impaired ejection fraction (EF) and clinical manifestation of heart failure frequently initiates systemic pro-inflammatory state [SPS] characterized by interleukin-6 (IL6) and tumor necrosis factor alpha (TNF-α) upregulation. Previous studies suggest that such an inflammatory state is capable of sustaining and/or accelerating hemopoietic clonal selection/dominance. How these CHF induced inflammatory changes affect “peripheral blood cell count composition' in pt with suspected CHIP is unknown. However, modifications in peripheral blood count data ”months before hemopoietic malignancy diagnosis“ may inform association between clonal dynamics and hemopoietic output under CHF stress. The primary objective of our study was to investigate effect of heart failure in ”pre- AML diagnosis“ peripheral blood count data to detect ”early“ hemopoietic modifications induced by CHF. Methods: After IRB approval, AML pt diagnosed with and without CHF were selected for analysis. Given possible differential inflammatory effect between pt exhibiting CHF with and with low EF, we analyzed peripheral blood cell count in pt with ”echocardiographically confirmed“ EF <> 50% and those pt with and without clinically documented CHF [cdCHF]. Descriptive statistics was performed for categorical and continues variable with Chi-square and t-test. SAS software was used for analysis. Results: 27/152 (17.7%) and 125/152 (82.2%) pt developed or not EF <50%. Median age was 71.1 years (y) v 61.2 y, in pt with and without EF<50%, p=<0.0001. Aging was negatively correlated with EF, [R= -0.25, p=0.001]. Median age was 73 y v 61 y, for pt with and without cdCHF, p=0.001. 100% and 82% of pt were male among those with and without EF <50%. In pt who had or did not have EF <55% Favorable (fav), Intermediate (Int) and unfavorable (unfav) ELN-2017 subgroups were 3.23% vs 13.6%; 42% vs 46%; and 55% vs 40%, p=0.07. To address our main hypothesis that CHF induces ”early pre-diagnostic AML' hemopoietic modifications, CBC data at 6 and 12 months (m) before AML onset in pt with and without EF<50% v those with and without cdCHF was extracted. At 12 m prior AML diagnosis, EF<> 50% detected differential expression for WBC [p=0.07], Hemoglobin [p=0.002], platelets [p=0.05] and absolute lymphocyte count (ALC) [p=0.006] [Fig 1, panel A, C, I, K]. Similarly, EF <>50% at 6 m prior AML diagnosis detected differential expression for platelets [p=0.01], ALC [p=0.04] [Fig 1, panel D, J, L]. In contrast, cdCHF detected only differential hemoglobin at 12 m [p=0.01]. Conclusions: CHF induces quantitative count defects 6 and 12 m before AML diagnosis. Changes are characterized by WBC, hemoglobin, platelets and ALC decline that are directly correlated with objective left ventricular EF impairment, but not with only clinical CHF. Our study adds body of evidence to support the role of CHF with low EF as “hemopoietic cell extrinsic stressor'. CHF associated with low EF seems to be prerequisite for hemopoietic stress in hosts with already initiated clonal hematopoiesis. Our findings have important experimental implications, especially for studies that seek to understand how cell extrinsic stressors facilitate clonal progression. [Display omitted] DisclosuresNo relevant conflicts of interest to declare.

AN INTRA-OPERATIVE TRANSESOPHAGEAL ECHOCARDIOGRAPHIC STUDY TO COMPARE THE EFFECT OF SEVOFLURANE AND ISOFLURANE ON LEFT VENTRICULAR DYSFUNCTION IN PATIENTS WITH ISCHEMIC HEART DISEASE UNDERGOING CORONARY ARTERY BYPASS GRAFTING USING CARDIOPULMONARY BYPASS

An Intra-operative Transesophageal Echocardiographic Study to Compare The Effect of Sevourane and Isourane on Left Ventricular Dysfunction In Patients With Ischemic Heart Disease Undergoing Coronary Artery Bypass Grafting Using Cardiopulmonary Bypass Context : Diastolic dysfunction has been increasingly recognized as an important cause of congestive heart failure (CHF) and resultant morbidity. About 50% patients with CHF have 'diastolic heart failure' in spite of a normal systolic function with preserved ejection fraction. The widely used volatile anesthetic agents, Isourane and Sevourane, are considered important components of balanced anesthesia technique. However their effects on left ventricular (LV) systolic and diastolic function have not been precisely dened. This study was designed to quantify and compare their effects on left ventricular function by TEE before start of CPB. Aims : To compare the effects of Isourane and Sevourane on echocardiographic LVsystolic and diastolic parameters. Settings and design : After obtaining institutional ethics committee clearance and informed consent from 60 patients operated within my study period was included . Data were collected after induction and just before going on bypass. Materials and Methods : After inducing the patients with institutional protocol one group was given isourane(Group I) and another group was given sevourane(Group S), both at 1MAC. TEE parameters measuring LVsystolic and diastolic functions were done. Statistical analysis : Data were analysed by Epi Info (TM) 7.2.2.2. Result and conclusion :Isourane was better than sevourane in comparism of systolic and diastolic dysfunction.

Cardiac Magnetic Resonance Tissue Characterization in Ischemic Cardiomyopathy.

Ischemic cardiomyopathy (ICM) is one of the most common causes of congestive heart failure. In patients with ICM, tissue characterization with cardiac magnetic resonance imaging (CMR) allows for evaluation of myocardial abnormalities in acute and chronic settings. Myocardial edema, microvascular obstruction (MVO), intracardiac thrombus, intramyocardial hemorrhage, and late gadolinium enhancement of the myocardium are easily depicted using standard CMR sequences. In the acute setting, tissue characterization is mainly focused on assessment of ventricular thrombus and MVO, which are associated with poor prognosis. Conversely, in chronic ICM, it is important to depict late gadolinium enhancement and myocardial ischemia using stress perfusion sequences. Overall, with CMR's ability to accurately characterize myocardial tissue in acute and chronic ICM, it represents a valuable diagnostic and prognostic imaging method for treatment planning. In particular, tissue characterization abnormalities in the acute setting can provide information regarding the patients that may develop major adverse cardiac event and show the presence of ventricular thrombus; in the chronic setting, evaluation of viable myocardium can be fundamental for planning myocardial revascularization. In this review, the main findings on tissue characterization are illustrated in acute and chronic settings using qualitative and quantitative tissue characterization.

Clinico-Etiological profile of congestive heart failure (CHF) in children

Congestive heart failure (CHF) occurs when the heart doesn’t pump blood to meet the oxygen demand of the various organs. Usually congenital heart disease (CHD) like VSD, PDA, CoA, TGA physiology, ECD, Ebstein anomaly present with CHF before U5 age. In India most common cause of CHF from 5 to 15 yrs. age is due to Rheumatic Fever / RHD. We also get cases like pericardial effusion, constrictive pericarditis, DCM, AR in rheumatic disease, iron overload causing myocardial failure in Thalassemia and anemia presenting as CHF as in more than 5-year children. CHF cases contribute to about 10% of mortality in children.We conducted a Hospital based descriptive and cross-sectional study from November 2018 to October 2020 at Pediatric department of M.K.C.G Medical College Hospital, Berhampur. All pediatric patients with signs and symptoms of CHF as per clinical diagnosis in the age group of 1 month to 14 year were included in our study. The study population was 136. Out of the total cardiac cases, 57% were CHD, 43% were acquired. Among the total 105 cardiac cases of CHF, CHD were 60(57.2%). Out of the total CHD, acyanotic heart diseases were 46.7% and acquired heart diseases constituted 42.8%. Out of total 136 cases 87(63.2%) were discharged, 23(17.6%) died, 19 cases (14%) were referred to higher centre. After data collection detail analysis was made by SPSS software. An initiative regarding addressing the problematic Congestive heart failure along with its clinical management will definitely help the future generation and researchers.

Clinical, electrical and echocardiographic profile of the association of stroke and congestive heart failure: About 344 cases

Congestive heart failure (CHF) is a leading cause of death and a major health problem accross the world. The incidence is increasing with the aging og population. CHF and stroke share the same risk factors, particularly hypertension and atrial fibrillation. The objective of this study is to investigate the clinical, electrical and echocardiographic profile of CHF patients with stroke. It is a transversal retrospective study conducted between May 2006 and June 2019 including all patients beyond the age of 14 with CHF and diabetes followed-up in the therapeutic unit of heart failure of our department. The data were collected on Excel and analyzed using SPSS 2.0 software. We studied the profile of CHF patients with stroke. 344 patients were collected (10% of all CHF patients). Mean age was 68,85 ± 12,60 years, male predominance (66,9%). The main cardiovascular risk factor was hypertension (46,5%), smoking in 40,1% and diabetes in 32,8%. The leading cause of CHF was ischemic heart disease in 76,4%, valvular heart disease in 15,5%, dilated cardiomyopathy in 5,5%. Permanent atrial fibrillation was present in 17,3% of cases. Mean LVEF was 36,27 ± 10,61% with no statistical difference with CHF patients without stroke (P = 0.057). The left ventricle was dilated in 76,7%, 2% of patients had an intra-cavitary thrombus. 53,8% of patients were anticoagulated. CHF and stroke share the same risk factors. CHF with reduced LVEF is at risk of stroke. Secondary prevention may improve the prognosis and the benefit of anticoagulation is still controversial.

Etiological aspects of congestive heart failure in hospital university Ibn Rochd (about 3412 patients)

Congestive heart failure (CHF) is a major and growing health problem around the world. In Africa, heart failure seems to be attributable mostly to systolic dysfunction and occurs as a major complication of high blood pressure. As a contribution to decreasing mortality of acute myocardial infarction and better treatment of high blood pressure as well as congestive heart failure the number of patients in heart failure have increased substantially. In contrast to the Framingham Study, nowadays coronary artery disease is the most prevalent etiology of congestive heart failure followed by hypertensive heart disease. The main objective of the study is to relate the principle causes leading to heart failure in our department. It is a transversal retrospective study conducted between May 2006 and June 2019 including all patients beyond the age of 14 with congestive heart failure followed-up in the therapeutic unit of heart failure of our department. The data were collected on Excel and analyzed using SPSS 2.0 software. We studied cardiovascular risk factors prevalence and causes repartition among these patients. The mean age was 64,92 ± 12,95 years, sex ratio H/F was 1,7, the prevalence of hypertension was 38,9%, 30,4% were diabetic, 31,9% were smokers, 9,9% were dyslipidemic. The leading cause of CHF among our patients was ischemic heart disease (76,81%), 13,47% dilated cardiomyopathy, 4,83% valvular heart disease, 2,38% cardiac toxicity, 0,9% of heart failure with preserved ejection fraction, 0,4% peripartum cardiomyopathy, 0,3% arrhythmia–induced cardiomyopathy. Our data show a high incidence of ischemic heart disease. Despite advances in our therapies for ischemic heart disease and hypertension, CHF remains a common and highly lethal condition. There is accumulating evidence that treatment of hypertension and ischemic heart disease can decrease the incidence of clinical CHF, related morbidity and mortality.

SAT-470 When The Heart Can’t Clap To The Thyroid’s Beat

Hyperthyroidism is associated with multiple cardiac pathologies including dilated cardiomyopathy, isolated right ventricular heart failure, and atrial fibrillation (AF). Long standing untreated hyperthyroidism in conjunction with AF can cause severe dilated cardiomyopathy with reduced ejection fraction that is completely reversible with treatment. We present the case of a previously healthy male who presented with florid congestive heart failure (CHF) as an initial presentation for hyperthyroidism. A 37-year-old male presented to the emergency department with progressively worsening dyspnea on exertion and lower extremity edema for one month. His heart rate was noted to be 172 bpm and an EKG was done that showed AF. He was clinically noted to be in heart failure and was admitted for further management. He was started on metoprolol with good heart rate control and was started on furosemide for diuresis. A transthoracic echocardiogram was done and showed severe global hypokinesis with left ventricular ejection fraction reduced to 20% along with bi-atrial enlargement and dilated left ventricular cavity. Ischemic cardiomyopathy was ruled out with left heart catheterization. A TSH level was checked as a part of workup for non-ischemic cardiomyopathy and atrial fibrillation and was markedly reduced to <0.01mIU/L with free T4 of 1.49ng/dL and free T3 of 6.7ng/dL. A diagnosis of hyperthyroid cardiomyopathy with concomitant tachycardia induced cardiomyopathy was made. Autoimmune workup was negative for anti-thyroid-peroxidase and anti-thyroid-stimulating antibodies. Ultrasound of his thyroid gland revealed multiple thyroid nodules concerning for toxic multinodular goiter. He was started on methimazole and discharged after volume optimization with diuresis to closely follow up with endocrinology and cardiology for further management. CHF can be the primary presentation in about 6% of patients with hyperthyroidism. T3 is the main thyroid hormone that binds to cardiomyocytes. It increases the expression of beta-adrenergic receptors on cardiomyocytes and subsequently increases heart rate and contractility. T3 can also cause atrial arrhythmias such as AF by decreasing the parasympathetic tone. Concomitant AF and hyperthyroidism can cause reduced ejection fraction due to tachycardia induced cardiomyopathy and dilated cardiomyopathy. Treatment mainly is with beta-blockers that slow down the heart as well decrease serum T3 levels by blocking 5-monodeiodinase which converts T4 to T3. Our patient was started on beta-blocker and methimazole with good reduction in heart rate and improvement of symptoms. Recovery of cardiac function will be assessed with longitudinal follow up. As hyperthyroidism is one of the few causes of CHF that is completely reversible, clinicians must maintain low degree of suspicion in patients with new onset heart failure especially when associated with AF.

Exosomal lncRNA AK139128 Derived from Hypoxic Cardiomyocytes Promotes Apoptosis and Inhibits Cell Proliferation in Cardiac Fibroblasts.

IntroductionMyocardial infarction (MI) is the leading cause of congestive heart failure and mortality. Hypoxia is an important trigger in the cardiac remodeling of the myocardium in the development and progression of cardiac diseases.ObjectiveThus, we aimed to investigate the effect of hypoxia-induced exosomes on cardiac fibroblasts (CFs) and its related mechanisms.Materials and MethodsIn this study, we successfully isolated and identified the exosomes from hypoxic cardiomyocytes (CMs). Exosomes derived from hypoxic CMs promoted apoptosis and inhibited proliferation, migration, and invasion in CFs. RNA-Seq assay suggested that long noncoding RNA AK139128 (lncRNA AK139128) was found to overexpress in both hypoxic CMs and CMs-secreting exosomes. After coculturing with CFs, hypoxic exosomes increased the expression of AK139128 in recipient CFs. Moreover, exosomal AK139128 derived from hypoxic CMs stimulated CFs apoptosis and inhibited proliferation, migration, and invasion. Furthermore, the effect of exosomal AK139128 derived from hypoxic CMs could also exacerbate MI in the rat model.ConclusionTaken together, hypoxia upregulated the level of AK139128 in CMs and exosomes and exosomal AK139128 derived from hypoxic CMs modulated cellular activities of CFs in vitro and in vivo. This study provides a new understanding of the mechanism underlying hypoxia-related cardiac diseases and insight into developing new therapeutic strategies.

PENGUKURAN TEKANAN DARAH PADA PASIEN GAGAL JANTUNG KONGESTIF DI INSTALASI RAWAT INAP RUMAH SAKIT ST. ELISABETH SEMARANG

Congestive heart failure (CHF) is one of the top 10 diseases in the Inpatient of. St. Elisabeth Hospital Semarang. The main cause of CHF is hypertension. CHF patients receive antihypertensive therapy to control their blood pressure. This study aims to determine the decrease in blood pressure of CHF patients and the suitability of blood pressure of CHF patients with their treatment targets according to the Eighth Joint National Committee (JNC VIII) at the Inpatient Installation of St. Elisabeth Hospital Semarang. This research is an observational descriptive study, using retrospective data. Data was taken from medical records of CHF patients in inpatients who received antihypertensive therapy for the period October - December 2017, 40 years or older, with or without concomitant diseases. Based on the results of tracing of medical records it is known that the number of CHF patients who met the inclusion criteria was 60 people, consisting of 30 male patients and 30 female patients. A total of 35 patients (58.33%) were aged over 60 years. A total of 19 patients had concomitant diabetes mellitus type 2 and / or chronic kidney failure. A total of 51 patients (85%) during hospitalization experienced an average reduction in systolic BP of 21.65 mmHg and as many as 37 patients (61.67%) experienced an average reduction in diastolic BP of 13.38 mmHg. The suitability of the patient's blood pressure when leaving the hospital with the target blood pressure according to JNC VIII is 81.67%. Thus the progression of cardiac deterioration in most CHF patients can be inhibited.

Factors determining exercise capacity evaluated during cardiopulmonary exercise testing in 6-month follow-up after ST elevation myocardial infarction.

ST elevation myocardial infarction (STEMI) is one of the main causes of congestive heart failure (CHF). The main symptom of CHF is exercise tolerance impairment. The aim of the study was to evaluate the prevalence and risk factors for impaired exercise tolerance in patients after STEMI. A total of 84 patients with STEMI were analysed in the study. Cardiopulmonary exercise test (CPET) was performed 6months after STEMI. Impaired exercise tolerance defined as peak VO2<84% predicted for age and sex was present in 49 (58%) patients and was connected with lack of abciximab administration (91.4 versus 69%, P=0·02) and the presence of mitral regurgitation (47 versus 23%, P=0·02). In univariate analysis, the troponin I level at admission (OR 1·89, P=0·047), the use of abciximab (OR 0·21, P=0·03), the presence of mitral regurgitation (OR 2·98, P=0·03) and NT-proBNP concentration (OR 2·17, P=0·021) were related to impaired exercise tolerance. The best multivariate model for predicting impaired exercisetolerance included mitral regurgitation and lack of abciximab administration. Impaired exercise tolerance after STEMI is common. Mitral regurgitation and lack of abciximab administration are the best predicting factors of impaired exercise tolerance after STEMI.