Abstract 38: Important Role of Adiponectin in Volume Overload Induced Heart Failure

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Lili Wang ◽  
Desiree Wanders ◽  
Gayani Nanayakkara ◽  
Rajesh Amin ◽  
Robert L Judd ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Myocyte ◽  
Ventricular Remodeling ◽  
Vena Cava ◽  
Volume Overload ◽  
Infrarenal Aorta ◽  
Protective Effects ◽  
Fistula Surgery ◽  
Myocyte Contractility

Adiponectin (ADP) has been reported to exert cardiac protective effects during ventricular remodeling following pressure overload and myocardial ischemia. However, the potential role of ADP in the volume overload induced heart failure has not been reported. In this study we examined the effect of ADP in cardiac myocyte contractile dysfunction following sustained volume overload. Rat model of volume overload induced heart failure was created by infrarenal aorta-vena cava (A-V) fistula. Some rats were administered with adenoviral ADP (Ad-ADP) at 2-, 6-, and 9-weeks following fistula surgery. Serum total ADP levels were measured at 3 days before, 5 weeks and 10 weeks after fistula surgery. Myocyte contractility and intracellular Ca2+ transients were evaluated at 10 weeks following fistula. Results indicated a progressive reduction of serum ADP levels. In ventricular myocytes isolated from 10-week fistula rats, protein expression of ADP, AdipoR1/R2 and T-cadherin were decreased, and AMPK phosphorylation was reduced. Consistent with these, myocytes exhibited significant depression in cell shortening and intracellular Ca2+ transient. In vivo overexpression of adenovirus-mediated ADP in fistula rats significantly increased ADP serum levels, and prevented the depression of myocyte contractile performance. Moreover, in vitro treatment with ADP significantly improved myocyte contractility and intracellular Ca2+ transient from 10-week fistula rats, but had no effect on myocyte performance in control and Ad-ADP animals. These results demonstrate a positive correlation of ADP reduction and ventricular remodeling induced by volume overload. Adiponectin plays a protective role in volume overload-induced heart failure.

scholarly journals Pulmonary Congestion Assessment in Heart Failure: Traditional and New Tools

Diagnostics ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 1306
Author(s):  
Filippo Pirrotta ◽  
Benedetto Mazza ◽  
Luigi Gennari ◽  
Alberto Palazzuoli
Keyword(s):  
Heart Failure ◽  
Adverse Outcome ◽  
Volume Overload ◽  
Pulmonary Congestion ◽  
X Ray ◽  
Persistent Symptoms ◽  
Biochemical Evaluation ◽  
Cardiac Filling ◽  
Symptoms And Signs

Congestion related to cardiac pressure and/or volume overload plays a central role in the pathophysiology, presentation, and prognosis of heart failure (HF). Most HF exacerbations are related to a progressive rise in cardiac filling pressures that precipitate pulmonary congestion and symptomatic decompensation. Furthermore, persistent symptoms and signs of congestion at discharge or among outpatients are strong predictors of an adverse outcome. Pulmonary congestion is also one of the most important diagnostic and therapeutic targets in chronic heart failure. The aim of this review is to analyze the importance of clinical, instrumental, and biochemical evaluation of congestion in HF by describing old and new tools. Lung ultrasonography (LUS) is an emerging method to assess pulmonary congestion. Accordingly, we describe the additive prognostic role of chest ultrasound with respect to traditional clinical and X-ray assessment in acute and chronic HF setting.

Role of oxidative stress in left ventricular remodeling and heart failure after myocardial infarction

1999 ◽  
Vol 5 (3) ◽  
pp. 79
Author(s):  
Shintaro Kinugawa ◽  
Hiroyuki Tsutsui ◽  
Tomomi Ide ◽  
Hideo Ustumi ◽  
Nobuhiro Suematsu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Heart Failure ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Left Ventricular

scholarly journals Biomarkers for the diagnosis and management of heart failure

2021 ◽  
Author(s):  
Vincenzo Castiglione ◽  
Alberto Aimo ◽  
Giuseppe Vergaro ◽  
Luigi Saccaro ◽  
Claudio Passino ◽  
...  
Keyword(s):  
Heart Failure ◽  
Risk Stratification ◽  
Adverse Outcome ◽  
Volume Overload ◽  
High Sensitivity ◽  
Circulating Biomarkers ◽  
Diagnosis And Management ◽  
Conflicting Evidence ◽  
Galectin 3

AbstractHeart failure (HF) is a significant cause of morbidity and mortality worldwide. Circulating biomarkers reflecting pathophysiological pathways involved in HF development and progression may assist clinicians in early diagnosis and management of HF patients. Natriuretic peptides (NPs) are cardioprotective hormones released by cardiomyocytes in response to pressure or volume overload. The roles of B-type NP (BNP) and N-terminal pro-B-type NP (NT-proBNP) for diagnosis and risk stratification in HF have been extensively demonstrated, and these biomarkers are emerging tools for population screening and as guides to the start of treatment in subclinical HF. On the contrary, conflicting evidence exists on the role of NPs as a guide to HF therapy. Among the other biomarkers, high-sensitivity troponins and soluble suppression of tumorigenesis-2 are the most promising biomarkers for risk stratification, with independent value to NPs. Other biomarkers evaluated as predictors of adverse outcome are galectin-3, growth differentiation factor 15, mid-regional pro-adrenomedullin, and makers of renal dysfunction. Multi-marker scores and genomic, transcriptomic, proteomic, and metabolomic analyses could further refine HF management.

Contribution of ventricular remodeling to pathogenesis of heart failure in rats

2001 ◽  
Vol 280 (2) ◽  
pp. H674-H683 ◽  
Author(s):  
Gregory L. Brower ◽  
Joseph S. Janicki
Keyword(s):  
Heart Failure ◽  
Ventricular Remodeling ◽  
Volume Fraction ◽  
Volume Overload ◽  
Left Ventricular ◽  
Morbidity And Mortality ◽  
Compliance Matrix ◽  
Hypertrophic Response ◽  
Lv Volume ◽  
And Function

We previously reported an approximately 50% incidence of rats with symptoms of congestive heart failure (CHF) at 8 wk postinfrarenal aorto-caval fistula. However, it was not clear whether compensatory ventricular remodeling could continue beyond 8 wk or whether the remaining animals would have developed CHF or died. Therefore, the intent of this study was to complete the characterization of this model of sustained volume overload by determining the morbidity and mortality and the temporal response of left ventricular (LV) remodeling and function beyond 8 wk. The findings demonstrate an upper limit to LV hypertrophy and substantial increases in LV volume and compliance, matrix metalloproteinase activity, and collagen volume fraction associated with the development of CHF. There was an 80% incidence of morbidity and mortality following 21 wk of chronic volume overload. These findings indicate that the development of CHF is triggered by marked ventricular dilatation and increased compliance occurring once the myocardial hypertrophic response is exhausted.

scholarly journals Role of Lung Ultrasound and Inferior Vena Cava Diameter in Assessment of Patients with Heart Failure

2021 ◽  
Vol 85 (2) ◽  
pp. 4102-4107
Author(s):  
Hussein Abd El-Fattah Mohammed ◽  
Mohamed Salah El-Feshawy ◽  
Fareed Shawky Basiony ◽  
Mustafa Abu shady
Keyword(s):  
Heart Failure ◽  
Inferior Vena Cava ◽  
Inferior Vena ◽  
Lung Ultrasound ◽  
Vena Cava ◽  
Patients With Heart Failure ◽  
Inferior Vena Cava Diameter

Abstract 865: Gata-4 Is An Angiogenic Survival Factor Of The Infarcted Heart

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Olli Tenhunen ◽  
Hanna Leskinen ◽  
Raisa Serpi ◽  
Jaana Rysä ◽  
Harri Pennanen ◽  
...  
Keyword(s):  
Heart Failure ◽  
Stem Cells ◽  
Gene Transfer ◽  
Dna Binding ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Left Ventricular ◽  
Therapeutic Interventions ◽  
Cardiac Stem Cells

Recent data suggest that the cardiac-restricted transcription factor GATA-4 is an anti-apoptotic factor required for adaptive responses as well as a key regulator of hypertrophy and hypertrophy-associated genes in the heart. As a leading cause of chronic heart failure, reversal of post-infarction left ventricular remodeling represents an important target for therapeutic interventions. Here we studied the role of GATA-4 as a mediator of post-infarction remodeling. Rats were subjected to experimental myocardial infarction (MI) by ligating the left anterior descending coronary artery (LAD). Ligation of the LAD decreased the DNA binding activity of GATA-4 by 69 % at day 1 after MI (P<0.001, n=7– 8) as assessed by gel mobility shift assays. At 2 weeks the GATA-4 DNA binding was significantly upregulated (2.4-fold, P<0.05, n=7), and returned to baseline at 4 weeks. To determine the functional role of GATA-4, rats underwent LAD ligation followed by peri-infarct intramyocardial delivery of adenoviral vector expressing GATA-4. Hearts treated with the GATA-4 gene transfer exhibited significantly increased ejection fraction (58±5% vs. 38±3% in LacZ-treated control animals with MI, P<0.001, n=8 –9) and fractional shortening (28±3% vs. 16±1%, P<0.001, n=8 –9) 2 weeks after MI. Accordingly, the infarct size was significantly reduced (26±4% vs. 45±4%, P<0.01, n=8 –9). To determine the cardioprotective mechanisms of GATA-4, the number of cardiac stem cells, apoptotic cardiomyocytes and capillaries were assessed. The number of capillaries (59±4/field vs. 48±3/field, P<0.051, n=7– 8) and c-kit positive stem cells (13±5 cells vs. 4±2 cells, P<0.05, n=7– 8) were increased in GATA-4 treated hearts, and a tendency to decreased apoptosis was observed in TUNEL-stained histological sections. These results indicate that the reversal of reduced GATA-4 activity prevents adverse post-infarction remodeling through increased angiogenesis, recruitment of cardiac stem cells and anti-apoptosis. GATA-4-based gene transfer may represent a novel, efficient therapeutic approach for heart failure.

Role of nitric oxide and cGMP in human septic serum-induced depression of cardiac myocyte contractility

1999 ◽  
Vol 276 (1) ◽  
pp. R265-R276 ◽  
Author(s):  
Anand Kumar ◽  
Rupinder Brar ◽  
Peter Wang ◽  
Linda Dee ◽  
Greg Skorupa ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Septic Shock ◽  
Cardiac Myocytes ◽  
Guanylate Cyclase ◽  
Cardiac Myocyte ◽  
Intracellular Cgmp ◽  
Human Septic Shock ◽  
Tnf Α ◽  
Myocyte Contractility

Previous studies have demonstrated the existence of a circulating myocardial depressant substance during human septic shock. We have recently identified this substance as a synergistic combination of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). This study utilized an in vitro cardiac myocyte assay to evaluate the potential mechanistic role of nitric oxide (NO) and cGMP in depression of myocyte contractility induced by TNF-α, IL-1β, TNF-α + IL-1β (at low concentrations), and human septic shock serum (HSS). TNF-α, IL-1β, TNF-α + IL-1β, and each of 5 sera from patients with acute septic shock caused depression of both maximum extent and peak velocity of cardiac myocyte shortening and an increase in intracellular cGMP concentration during 30 min of exposure (minimum P < 0.01). NO synthetase (NOS) and guanylate cyclase inhibitors such as N-methyl-l-arginine (l-NMA) and methylene blue prevented these effects; an excess ofl-arginine withl-NMA restored them (minimum P < 0.01). In contrast,d-arginine failed to reestablish cytokine-induced myocyte depression and cGMP accumulation prevented byl-NMA. Exposure of myocytes to TNF-α, IL-1β, or TNF-α + IL-1β produced a concentration-dependent increase in intracellular cGMP that paralleled the depression of cardiac myocyte contractility (minimum P < 0.001). In addition, TNF-α, IL-1β, TNF-α + IL-1β, or HSS application to cardiac myocytes resulted in increased NO gas generation, which was inhibited byl-NMA (minimum P < 0.01). Furthermore, unstimulated cardiac myocytes were shown to harbor constitutive but not inducible NOS activity. These data suggest that the sequential generation of NO by a constitutive NOS and cGMP by guanylate cyclase represents an important mechanism of cardiac myocyte depression by TNF-α, IL-1β, TNF-α + IL-1β, and the myocardial depressant substance(s) of septic shock.

Interactive role of diastolic dysfunction and ventricular remodeling in asymptomatic subjects at increased risk of heart failure

2019 ◽  
Vol 35 (7) ◽  
pp. 1231-1240 ◽  
Author(s):  
Iacopo Fabiani ◽  
◽  
Nicola Riccardo Pugliese ◽  
Salvatore La Carrubba ◽  
Lorenzo Conte ◽  
...  
Keyword(s):  
Heart Failure ◽  
Diastolic Dysfunction ◽  
Ventricular Remodeling ◽  
Increased Risk ◽  
Asymptomatic Subjects

scholarly journals Modification of a Volume-Overload Heart Failure Model to Track Myocardial Remodeling and Device-Related Reverse Remodeling

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Egemen Tuzun ◽  
Roger Bick ◽  
Cihan Kadipasaoglu ◽  
Jeffrey L. Conger ◽  
Brian J. Poindexter ◽  
...  
Keyword(s):  
Heart Failure ◽  
Wall Thickness ◽  
Ventricular Remodeling ◽  
Diastolic Pressure ◽  
Volume Overload ◽  
Left Ventricular ◽  
Reverse Remodeling ◽  
Sheep Model ◽  
Dystrophin Expression ◽  
Cellular Markers

Purpose. To provide an ovine model of ventricular remodeling and reverse remodeling by creating congestive heart failure (CHF) and then treating it by implanting a left ventricular assist device (LVAD). Methods. We induced volume-overload heart failure in 2 sheep; 20 weeks later, we implanted an LVAD and assessed recovery 11 weeks thereafter. We examined changes in histologic and hemodynamic data and levels of cellular markers of CHF. Results. After CHF induction, we found increases in LV end-diastolic pressure, LV systolic and diastolic dimensions, wall thickness, left atrial diameter, and atrial natriuretic protein (ANP) and endothelin-1 (ET-1) levels; β-adrenergic receptor (BAR) and dystrophin expression decreased markedly. Biopsies confirmed LV remodeling. After LVAD support, LV systolic and diastolic dimensions, wall thickness, and mass, and ANP and ET-1 levels decreased. Histopathologic and hemodynamic markers improved, and BAR and dystrophin expression normalized. Conclusions. We describe a successful sheep model for ventricular and reverse remodeling.

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