Abstract 417: Cardiac Akap12 Signalosome Overexpression Exacerbation of Heart Failure and β-arrestin Signaling Pathway

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Hanan Qasim ◽  
Arfaxad Reyes Alcaraz ◽  
Bradley K McConnell
Keyword(s):  
Gene Expression ◽  
Heart Failure ◽  
Protein Expression ◽  
Signaling Pathway ◽  
Systolic Function ◽  
Left Ventricular ◽  
Control Groups ◽  
Expression Levels ◽  
Anchoring Protein ◽  
The Impact

Background: Heart failure (HF) is responsible for 1 out of 8 deaths per year in the U.S.A. andis the major cause of death globally. In HF, chronic β-adrenergic receptor (β-AR)stimulation leads to reduced cardiac function due in part to β-AR desensitization.β-arrestins are proteins that play a major role in desensitizing G protein-coupledreceptors (GPCRs) such as β-AR. Previously we reported enhanced cardiacfunction in mice lacking functional A Kinase Anchoring Protein 12 (AKAP12). Inthis study, we aim to investigate the impact of AKAP12 overexpression(oxAKAP12) on HF progression through assessing β-arrestins. Our central hypothesis is that cardiac AKAP12 overexpression potentiates HF developmentby influencing β-arrestin signaling downstream of the β-AR. Methods: HF was developed in WT and oxAKAP12-Tg mice (8-10) weeks old males andfemales, through chronic Isoproterenol (ISO) administration (60mg/kg/day for 14days). Left ventricular homogenates were used for gene expression analysis.Furthermore, AKAP12 was transiently overexpressed in AC16 cells (humancardiomyocytes cell line), to asses protein expression levels and Gαs pathwayactivity, upon treatment with 100 nM of ISO. Results: Cardiac oxAKAP12 in both males and females reduced left ventricular ejectionfraction (EF) by 14.5±2.5% and fractional shortening (FS) by 22.7±2% after 14-days of chronic ISO treatment when compared to control groups. β-arrestin-1gene expression levels were significantly lower (p=0.022) in oxAKAP12 malehomogenates treated with ISO (14 days) compared to control groups.Interestingly, female homogenates overexpressing AKAP12 showed significantlyhigher β-arrestin-1 gene expression levels (p<0.0001) with ISO treatment,compared to control groups. In AC16 cells overexpressing AKAP12 and treatedwith ISO, Gαs activity and β-arrestin-1 protein expression levels were bothreduced by 50% compared to AC16 ISO treated groups. Conclusion: Cardiac oxAKAP12 negatively influences systolic function in both male andfemale mice, potentially through affecting β-arrestin signaling pathway. Thus,designing novel drugs to inhibit AKAP12 is promising to ameliorate HF.

Long-term levosimendan treatment improves systolic function and myocardial relaxation in mice with cardiomyocyte-specific disruption of the Serca2 gene

2013 ◽  
Vol 115 (10) ◽  
pp. 1572-1580 ◽  
Author(s):  
Vigdis Hillestad ◽  
Frank Kramer ◽  
Stefan Golz ◽  
Andreas Knorr ◽  
Kristin B. Andersson ◽  
...  
Keyword(s):  
Gene Expression ◽  
Heart Failure ◽  
Cardiac Function ◽  
Diastolic Dysfunction ◽  
Systolic Function ◽  
Cytosolic Calcium ◽  
Left Ventricular ◽  
Pressure Measurements ◽  
Human Heart Failure

In human heart failure (HF), reduced cardiac function has, at least partly, been ascribed to altered calcium homeostasis in cardiomyocytes. The effects of the calcium sensitizer levosimendan on diastolic dysfunction caused by reduced removal of calcium from cytosol in early diastole are not well known. In this study, we investigated the effect of long-term levosimendan treatment in a murine model of HF where the sarco(endo)plasmatic reticulum ATPase ( Serca) gene is specifically disrupted in the cardiomyocytes, leading to reduced removal of cytosolic calcium. After induction of Serca2 gene disruption, these mice develop marked diastolic dysfunction as well as impaired contractility. SERCA2 knockout (SERCA2KO) mice were treated with levosimendan or vehicle from the time of KO induction. At the 7-wk end point, cardiac function was assessed by echocardiography and pressure measurements. Vehicle-treated SERCA2KO mice showed significantly diminished left-ventricular (LV) contractility, as shown by decreased ejection fraction, stroke volume, and cardiac output. LV pressure measurements revealed a marked increase in the time constant (τ) of isovolumetric pressure decay, showing impaired relaxation. Levosimendan treatment significantly improved all three systolic parameters. Moreover, a significant reduction in τ toward normalization indicated improved relaxation. Gene-expression analysis, however, revealed an increase in genes related to production of the ECM in animals treated with levosimendan. In conclusion, long-term levosimendan treatment improves both contractility and relaxation in a heart-failure model with marked diastolic dysfunction due to reduced calcium transients. However, altered gene expression related to fibrosis was observed.

Abstract 16485: The Nitroxyl Donor 1-Nitrosocyclohexyl Acetate Limits Cardiac Superoxide Upregulation and Diastolic Dysfunction in a Mouse Model of Diabetic Cardiomyopathy

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Rebecca H Ritchie ◽  
Nga Cao ◽  
Yung George Wong ◽  
Sarah Rosli ◽  
Helen Kiriazis ◽  
...  
Keyword(s):  
Heart Failure ◽  
Mouse Model ◽  
Diastolic Dysfunction ◽  
Diabetic Cardiomyopathy ◽  
Ex Vivo ◽  
Systolic Function ◽  
Left Ventricular ◽  
Cardiomyocyte Hypertrophy ◽  
Lv Diastolic Dysfunction ◽  
The Impact

Nitroxyl (HNO), a redox congener of NO•, is a novel regulator of cardiovascular function combining vasodilator and positive inotropic properties. Our previous studies have demonstrated these properties occur concomitantly in the intact heart; HNO moreover also exhibits antihypertrophic and superoxide-suppressing actions. HNO donors may thus offer favorable actions in heart failure. The impact of chronic HNO donor administration has however yet to be reported in this context. We tested the hypothesis that the HNO donor 1-nitrosocyclohexyl acetate (1-NCA) limits cardiomyocyte hypertrophy and left ventricular (LV) diastolic dysfunction in a mouse model of diabetic cardiomyopathy in vivo. Male 6 week-old FVB/N mice received either streptozotocin (55 mg/kg/day i.p. for 5 days, n=17), to induce type 1 diabetes, or citrate vehicle (n=16). After 4 weeks of hyperglycemia, mice were allocated to 1-NCA therapy (83mg/kg/day i.p.) or vehicle, and followed for a further 4 weeks. As shown in the table, blood glucose was unaffected by 1-NCA. LV diastolic dysfunction was evident in diabetic mice, measured as echocardiography-derived A wave velocity, deceleration time and E:A ratio; LV systolic function was preserved. Diabetes-induced diastolic dysfunction was accompanied by increased LV cardiomyocyte size, hypertrophic and pro-fibrotic gene expression, and upregulation of LV superoxide. These characteristics of diabetic cardiomyopathy were largely prevented by 1-NCA treatment. Selectivity of 1-NCA as a donor of HNO versus NO• was demonstrated by the sensitivity of the coronary vasodilation response of 1-NCA to the HNO scavenger L-cysteine (4mM), but not to the NO• scavenger hydroxocobalamin (50μM), in the normal rat heart ex vivo (n=3-7). Collectively, our studies provide the first evidence that HNO donors may represent a promising new strategy for the treatment of diabetic cardiomyopathy, and implies their therapeutic efficacy in settings of chronic heart failure.

P935 Association of intracellular iron status with left ventricular systolic function response to exercise in heart failure with preserved ejection fraction

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
M Przewlocka-Kosmala ◽  
E Jasic-Szpak ◽  
E A Jankowska ◽  
P Ponikowski ◽  
W Kosmala
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Systolic Function ◽  
Iron Status ◽  
Left Ventricular ◽  
Exercise Intolerance ◽  
Lv Function ◽  
Preserved Ejection Fraction ◽  
Intracellular Iron ◽  
The Impact

Abstract The intracellular iron depletion has been recognized to contribute to the dysregulation of cell energetics. The soluble transferrin receptor (sTfR) is regarded as a marker of cellular iron balance, and its elevated level reflects an insufficient iron delivery to target tissues. Despite the strong pathophysiological link, there is a scarcity of data on the impact of intracellular iron status on myocardial performance. Aim To investigate the association between the intracellular iron status, as assessed by sTfR, and left ventricular (LV) function in a well-characterized population with heart failure and preserved ejection fraction (HFpEF). Methods A complete echocardiogram including evaluation of LV global longitudinal deformation by speckle tracking (GLS) was performed at rest and immediately post-exercise in 83 pts (age 66 ± 8 yrs) with symptomatic HFpEF. Results Pts with the highest sTfR concentrations (from the 3rd sTfR tertile) demonstrated significantly lower exertional GLS than their peers from the other 2 tertiles and lower resting GLS vs. the 2nd tertile (Table). Exercise GLS was inversely correlated with sTfR (r=-0.27, p = 0.01), and this association remained significant after adjustment for age, sex, BMI, LV mass, exercise blood pressure, hemoglobin and serum galectin-3 – a marker of fibrosis (beta=-0.24, p = 0.04). Conclusions In HFpEF, higher sTfR reflecting a decreased global intracellular iron content is independently associated with reduced LV longitudinal contractility response to exertion. This might represent another mechanism of exercise intolerance and should be considered in management strategies in this condition. Abstract P935 Figure.

scholarly journals P791 Left atrial stiffness as a predictor of cardiac events in patients with heart failure and reduced ejection fraction: the impact of diabetes

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
I Bytyci ◽  
N R Pugliese ◽  
A Bajraktari ◽  
M Mazzola ◽  
G Bajraktari ◽  
...  
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Left Atrial ◽  
Ventricular Remodeling ◽  
Systolic Function ◽  
Left Ventricular ◽  
Diabetic Patients ◽  
Reduced Ejection Fraction ◽  
Patients With Heart Failure ◽  
The Impact

Abstract Background and Aim Diabetes mellitus (DM) affects left ventricular remodeling in patients with heart failure (HF), but its effect on left atrial (LA) remodeling and their combined effect on survival and other clinical events (CE) remain to be elucidated. We evaluated in this study the relationship between DM and left atrial (LA) remodeling in a group of HF patients with reduced ejection fraction (HFrEF), Methods This studied 136 consecutive HFrEF patients (65 ± 11 years), 36 diabetics, using conventional and tissue Doppler echocardiography. LA dimension and function were measured and cavity stiffness was calculated with the formula: LA stiffness = E/e’ratio/LA strain. Results The age, gender, LV end-systolic dimension, LV end-diastolic dimension, LV EF and BNP level did not differ between diabetic and non-diabetic patients. Diabetic patients with HFrEF had higher NYHA functional class (p = 0.02), reduced right ventricle (RV) systolic function (p = 0.01) and increased LA stiffness (p = 0.02) . At follow up of 55 ± 37 months, survival free from CE was 69% in non-diabetics compared with 44.4% in diabetics (X2 12.7; p&lt; 0.0001). The CE free survival was lower in patients with increased LA stiffnes, irrespective of the presence of DM: 1) Patients with HFrEF without DM and normal LA stiffness (85%); 2) Patients with HFrEF without DM and with increased LA stiffness (50%); 3) Patients with HFrEF with DM and with normal LA stiffness (71%) and patients with HFrEF with DM and with increased LA stiffness (27%) (X2 29.6; p&lt; 0.0001, Figure 1). Conclusion Compromised LA stiffness as surrogate of LA remodeling is associated with poor outcome in patients with heart failure and reduced EF. The presence of diabetes in patients with HFrEF and increased LA stiffness has incremental prognostic value. Abstract P791 Figure.

scholarly journals Characterization of left ventricular myocardial sodium-glucose cotransporter 1 expression in patients with end-stage heart failure

2020 ◽  
Vol 19 (1) ◽  
Author(s):  
Alex Ali Sayour ◽  
Attila Oláh ◽  
Mihály Ruppert ◽  
Bálint András Barta ◽  
Eszter Mária Horváth ◽  
...  
Keyword(s):  
Heart Failure ◽  
Protein Expression ◽  
Immunohistochemical Staining ◽  
Systolic Function ◽  
Left Ventricular ◽  
Idiopathic Dilated Cardiomyopathy ◽  
Cardiac Resynchronization ◽  
Sodium Glucose Cotransporter ◽  
Protein Expressions ◽  
End Stage

Abstract Background Whereas selective sodium-glucose cotransporter 2 (SGLT2) inhibitors consistently showed cardiovascular protective effects in large outcome trials independent of the presence of type 2 diabetes mellitus (T2DM), the cardiovascular effects of dual SGLT1/2 inhibitors remain to be elucidated. Despite its clinical relevance, data are scarce regarding left ventricular (LV) SGLT1 expression in distinct heart failure (HF) pathologies. We aimed to characterize LV SGLT1 expression in human patients with end-stage HF, in context of the other two major glucose transporters: GLUT1 and GLUT4. Methods Control LV samples (Control, n = 9) were harvested from patients with preserved LV systolic function who went through mitral valve replacement. LV samples from HF patients undergoing heart transplantation (n = 71) were obtained according to the following etiological subgroups: hypertrophic cardiomyopathy (HCM, n = 7); idiopathic dilated cardiomyopathy (DCM, n = 12); ischemic heart disease without T2DM (IHD, n = 14), IHD with T2DM (IHD + T2DM, n = 11); and HF patients with cardiac resynchronization therapy (DCM:CRT, n = 9, IHD:CRT, n = 9 and IHD-T2DM:CRT, n = 9). We measured LV SGLT1, GLUT1 and GLUT4 gene expressions with qRT-PCR. The protein expression of SGLT1, and activating phosphorylation of AMP-activated protein kinase (AMPKα) and extracellular signal-regulated kinase 1/2 (ERK1/2) were quantified by western blotting. Immunohistochemical staining of SGLT1 was performed. Results Compared with controls, LV SGLT1 mRNA and protein expressions were significantly and comparably upregulated in HF patients with DCM, IHD and IHD + T2DM (all P < 0.05), but not in HCM. LV SGLT1 mRNA and protein expressions positively correlated with LVEDD and negatively correlated with EF (all P < 0.01). Whereas AMPKα phosphorylation was positively associated with SGLT1 protein expression, ERK1/2 phosphorylation showed a negative correlation (both P < 0.01). Immunohistochemical staining revealed that SGLT1 expression was predominantly confined to cardiomyocytes, and not fibrotic tissue. Overall, CRT was associated with reduction of LV SGLT1 expression, especially in patients with DCM. Conclusions Myocardial LV SGLT1 is upregulated in patients with HF (except in those with HCM), correlates significantly with parameters of cardiac remodeling (LVEDD) and systolic function (EF), and is downregulated in DCM patients with CRT. The possible role of SGLT1 in LV remodeling needs to be elucidated.

Changes in Expressions of HSP27, HSP70 and Soluble Glycoprotein in Heart Failure Rats Complicated with Pulmonary Edema and Correlations with Cardiopulmonary Functions Running title: Expressions of HSP27, HSP70 and Soluble Glycoprotein in Heart Failure

2021 ◽  
Vol 7 (5) ◽  
pp. 4286-4295
Author(s):  
Yan Tan ◽  
Bo Gao ◽  
Dongming Gu ◽  
Shuyun Wang ◽  
Zhinua Wang
Keyword(s):  
Heart Failure ◽  
Protein Expression ◽  
Pulmonary Edema ◽  
Airway Resistance ◽  
Lung Compliance ◽  
Left Ventricular ◽  
Normal Group ◽  
Model Group ◽  
Expression Levels ◽  
Gene And Protein Expression

Objective: The study aimed to investigate the changes in expressions of heat shock protein 27 (HSP27), HSP70 and soluble glycoprotein (SGP) in heart failure (HF) rats complicated with pulmonary edema, and explore their potential correlations with cardiopulmonary functions. Methods: The rat model of HF was established, and the rats were divided into HF model group (model group, n=15) and normal group (n=15). After successful modeling, MRI and ECG were applied to detect the cardiac function indexes of the rats. The myocardial function indexes were determined, the injury of myocardial tissues was observed via hematoxylin and eosin (HE) staining, and the content of myeloperoxidase (MPO), matrix metalloproteinase-9 (MMP-9) and tumor necrosis factor-alpha (TNF-a) in the blood was measured. The partial pressure of oxygen (Pa02) and oxygenation index (01) were observed, and the airway resistance and lung compliance were examined. Moreover, quantitative polymerase chain reaction (qPCR) and Western blotting assay were performed to detect the gene and protein expression levels of HSP27, HSP70 and SGP130. Results: The levels of serum creatine kinase (CK), creatine (Cr) and blood urea nitrogen (BUN) were increased markedly in model group (p<0.05). Model group had notably decreased fractional shortening (FS) and ejection fraction (EF) compared with normal group (p<0.05), while the opposite results of left ventricular end-diastolic diameter (LVEDD) and left ventricular end-systolic diameter (LVESD) were detected. In model group, the content of serum MPO, MMP-9 and TNF-a was raised remarkably (p<0.05), 01 and Pa02were reduced notably (p<0.05), the airway resistance was increased (p<0.05), and the lung compliance was decreased (p<0.05). Obviously elevated gene and protein expression levels of HSP27, HSP70 and SGP130 were detected in model group (p<0.05). Conclusion: The expressions of HSP27, HSP70 and SGP130 are increased in HF rats complicated with pulmonary edema, seriously affecting the cardiopulmonary functions of the rats.

Estrogen improves TIMP-MMP balance and collagen distribution in volume-overloaded hearts of ovariectomized females

2010 ◽  
Vol 299 (2) ◽  
pp. R683-R693 ◽  
Author(s):  
Tetyana G. Voloshenyuk ◽  
Jason D. Gardner
Keyword(s):  
Heart Failure ◽  
Estrogen Receptor ◽  
Protein Expression ◽  
Volume Overload ◽  
Estrogen Receptor Α ◽  
Left Ventricular ◽  
Ovariectomized Rats ◽  
Type I ◽  
Female Rat ◽  
The Impact

Our previous studies demonstrate that 17β-estradiol limits chronic volume overload-induced hypertrophy and improves heart function in ovariectomized rats. One possible cardioprotective mechanism involves the interaction between estrogen, estrogen receptors, and proteins of the extracellular matrix (ECM). The impact of estrogen deficiency and replacement on left ventricular (LV) hypertrophy and ECM protein expression was studied using five female rat groups: intact sham-operated, ovariectomized sham-operated, intact with volume overload, ovariectomized with volume overload, and ovariectomized with volume overload treated with estrogen. After 8 wk, LV protein extracts were evaluated by Western blot analysis for matrix metalloproteinase-2 (MMP-2) and MMP-9, MT1-MMP, tissue inhibitors of MMPs (TIMP)-1, TIMP-2, TIMP-3 and TIMP-4, collagens type I and III, and estrogen receptor α and β expression. MMP proteolytic activity was assessed by zymography. All volume-overloaded groups exhibited LV hypertrophy, which was associated with a loss of interstitial collagen and perivascular fibrosis. After 8 wk of volume overload, 70% of ovariectomized rats developed heart failure, in contrast to only one intact rat. A downregulation of MMP-2, estrogen receptor-α (ERα), and ERβ, and upregulation of MMP-9 and MT1-MMP were found in the volume-overloaded hearts of ovariectomized rats. Estrogen treatment improved TIMP-2/MMP-2 and TIMP-1/MMP-9 protein balance, restored ERα expression, and prevented MMP-9 activation, perivascular collagen accumulation and development of heart failure. However, estrogen did not fully restore ERβ expression and did not prevent the increase of MMP-9 expression or loss of interstitial collagen. These results support that estrogen limits undesirable ECM remodeling and LV dilation, in part, through modulation of ECM protein expression in volume-overloaded hearts of ovariectomized rats.

Abstract 17053: Cardiac AKAP12 Signalosome Overexpression Exacerbation of Heart Failure and Cardiac Calcium Handling

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Hanan Qasim ◽  
Bradley K McConnell
Keyword(s):  
Heart Failure ◽  
Protein Expression ◽  
Left Ventricular ◽  
Cardiac Contraction ◽  
Calcium Handling ◽  
Left Ventricular Ejection ◽  
Mrna Levels ◽  
Control Groups ◽  
Ventricular Ejection Fraction ◽  
Males And Females

Introduction: Heart failure (HF) is responsible for 1 out of 8 deaths per year in the U.S.A. and is the major cause of death globally. Calcium cycling is crucial for proper signaling processes and efficient cardiac contraction. In failing hearts, remodeled calcium handling contributes to cardiac dysfunction. Previously we reported enhanced cardiac function in mice lacking a functional A-Kinase Anchoring Protein 12 (AKAP12). In this study, we aim to investigate the role of AKAP12 overexpression (oxAKAP12) on heart failure progression through assessing Sarco/Endoplasmic Reticulum Ca2+-ATPase (SERCA2) and its regulatory protein Phospholamban (PLN). Hypothesis: Cardiac AKAP12 overexpression potentiates HF development through its action on SERCA2. Methods: HF was developed in WT and oxAKAP12-Tg mice of 8-10 weeks old males and females, through chronic Isoproterenol (ISO) administration (60 mg/kg/day for 14-days). Left ventricular homogenates were used for gene expression analysis. Furthermore, AKAP12 was transiently overexpressed in AC16 cells (human cardiomyocytes cell line), to assess protein expression levels upon treatment with 100 nM of ISO for 12-hrs. Results: Cardiac oxAKAP12 in both males and females reduced left ventricular ejection fraction (EF) by 14.5±2.5% and fractional shortening (FS) by 22.7±2.0% after 14-days of chronic ISO treatment when compared to control groups. Both RNA sequencing and RTqPCR analysis showed a significant reduction of SERCA2 and PLN mRNA levels, respectively, in left ventricular homogenates of male (53.5±2.0%, 39.0±2.5%) and female (50.0±2.5%, 45.0±2.0%) groups overexpressing AKAP12 treated with ISO (14-days) compared to control groups (p<0.005). In AC16 cells overexpressing AKAP12 and treated with ISO, SERCA2 protein expression was reduced by 37% (p=0.0413) while PLN protein expression was not significantly reduced compared to control groups. Conclusions: Cardiac oxAKAP12 negatively influences systolic function in both male and female mice, potentially through affecting calcium handling, which will be assessed in future experiments by evaluating calcium transients and sarcomere shortening in isolated primary cardiomyocytes from oxAKAP12 and control mice.

ACCESSMENT OF RIGHT VENTRICULAR SYSTOLIC FUNCTION USING TAPSE

2011 ◽  
pp. 62-70
Author(s):  
Lien Nhut Nguyen ◽  
Anh Vu Nguyen
Keyword(s):  
Heart Failure ◽  
Left Ventricular Ejection Fraction ◽  
Ejection Fraction ◽  
Right Ventricular ◽  
Systolic Function ◽  
Systolic Heart Failure ◽  
Left Ventricular ◽  
Ventricular Ejection ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction

Background: The prognostic importance of right ventricular (RV) dysfunction has been suggested in patients with systolic heart failure (due to primary or secondary dilated cardiomyopathy - DCM). Tricuspid annular plane systolic excursion (TAPSE) is a simple, feasible, reality, non-invasive measurement by transthoracic echocardiography for evaluating RV systolic function. Objectives: To evaluate TAPSE in patients with primary or secondary DCM who have left ventricular ejection fraction ≤ 40% and to find the relation between TAPSE and LVEF, LVDd, RVDd, RVDd/LVDd, RA size, severity of TR and PAPs. Materials and Methods: 61 patients (36 males, 59%) mean age 58.6 ± 14.4 years old with clinical signs and symtomps of chronic heart failure which caused by primary or secondary DCM and LVEF ≤ 40% and 30 healthy subject (15 males, 50%) mean age 57.1 ± 16.8 were included in this study. All patients and controls were underwent echocardiographic examination by M-mode, two dimentional, convensional Dopler and TAPSE. Results: TAPSE is significant low in patients compare with the controls (13.93±2.78 mm vs 23.57± 1.60mm, p<0.001). TAPSE is linearly positive correlate with echocardiographic left ventricular ejection fraction (r= 0,43; p<0,001) and linearly negative correlate with RVDd (r= -0.39; p<0.01), RVDd/LVDd (r=-0.33; p<0.01), RA size (r=-0.35; p<0.01), TR (r=-0.26; p<0.05); however, no correlation was found with LVDd and PAPs. Conclusions: 1. Decreased RV systolic function as estimated by TAPSE in patients with systolic heart failure primary and secondary DCM) compare with controls. 2. TAPSE is linearly positive correlate with LVEF (r= 0.43; p<0.001) and linearly negative correlate with RVDd (r= -0.39; p<0.01), RVDd/LVDd (r=-0.33; p<0.01), RA size (r=-0.35; p<0.01), TR (r=-0.26; p<0.05); however, no correlation is found with LVDd and PAPs. 3. TAPSE should be used routinely as a simple, feasible, reality method of estimating RV function in the patients systolic heart failure DCM (primary and secondary).

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