Ventricular Remodeling in Pressure vs. Volume Overload

2005 ◽  
pp. 9-26
Author(s):  
Blase A. Carabello
Keyword(s):  
Ventricular Remodeling ◽  
Volume Overload

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 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.

Effect of Digoxin on Ventricular Remodeling and Responsiveness of β-Adrenoceptors in Chronic Volume Overload

1998 ◽  
Vol 3 (4) ◽  
pp. 281-290 ◽  
Author(s):  
J. Thompson Sullebarger ◽  
Paula M. D'Ambra ◽  
Linda C. Clark ◽  
Lisa Thanikarry ◽  
Hector L. Fontanet
Keyword(s):  
Ventricular Remodeling ◽  
Volume Overload ◽  
Chronic Volume Overload

scholarly journals Moderate Exercise Training Improves Survival and Ventricular Remodeling in an Animal Model of Left Ventricular Volume Overload

2009 ◽  
Vol 2 (5) ◽  
pp. 437-445 ◽  
Author(s):  
Dominic Lachance ◽  
Éric Plante ◽  
Andrée-Anne Bouchard-Thomassin ◽  
Serge Champetier ◽  
Élise Roussel ◽  
...  
Keyword(s):  
Animal Model ◽  
Exercise Training ◽  
Left Ventricular Volume ◽  
Ventricular Remodeling ◽  
Volume Overload ◽  
Ventricular Volume ◽  
Left Ventricular ◽  
Moderate Exercise ◽  
Moderate Exercise Training

scholarly journals Pleiotropic effects of neutrophils on myocyte apoptosis and left ventricular remodeling during early volume overload

2009 ◽  
Vol 47 (5) ◽  
pp. 634-645 ◽  
Author(s):  
Mikhail A. Kolpakov ◽  
Rachid Seqqat ◽  
Khadija Rafiq ◽  
Hang Xi ◽  
Kennneth B. Margulies ◽  
...  
Keyword(s):  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Volume Overload ◽  
Left Ventricular ◽  
Pleiotropic Effects ◽  
Myocyte Apoptosis

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.

Response of cardiac mast cells to atrial natriuretic peptide

2007 ◽  
Vol 293 (2) ◽  
pp. H1216-H1222 ◽  
Author(s):  
David B. Murray ◽  
Jason D. Gardner ◽  
Scott P. Levick ◽  
Gregory L. Brower ◽  
Loren G. Morgan ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Ventricular Remodeling ◽  
Volume Overload ◽  
Mast Cell Degranulation ◽  
Aortocaval Fistula ◽  
Chronic Volume Overload ◽  
Atrial Natriuretic

Previously, our laboratory demonstrated that cardiac mast cell degranulation induces adverse ventricular remodeling in response to chronic volume overload. The purpose of this study was to investigate whether atrial natriuretic peptide (ANP), which is known to be elevated in chronic volume overload, causes cardiac mast cell degranulation. Relative to control, ANP induced significant histamine release from peritoneal mast cells, whereas isolated cardiac mast cells were not responsive. Infusion of ANP (225 pg/ml) into blood-perfused isolated rat hearts produced minimal activation of cardiac mast cells, similar to that seen in the control group. ANP also did not increase matrix metalloproteinase-2 activity, reduce collagen volume fraction, or alter diastolic or systolic cardiac function compared with saline-treated controls. In a subsequent study to evaluate the effects of natriuretic peptide receptor antagonism on volume overload-induced ventricular remodeling, anantin was administered to rats with an aortocaval fistula. Comparable increases of myocardial MMP-2 activity in treated and untreated rats with an aortocaval fistula were associated with equivalent decreases in ventricular collagen ( P < 0.05 vs. sham-operated controls). Cardiac functional parameters and left ventricular hypertrophy were unaffected by anantin. We conclude that ANP is not a cardiac mast cell secretagogue and is not responsible for the cardiac mast cell-mediated adverse ventricular remodeling in response to volume overload.

scholarly journals Time-dependent remodeling of transmural architecture underlying abnormal ventricular geometry in chronic volume overload heart failure

2004 ◽  
Vol 287 (5) ◽  
pp. H1994-H2002 ◽  
Author(s):  
Hiroshi Ashikaga ◽  
Jeffrey H. Omens ◽  
James W. Covell
Keyword(s):  
Wall Thickness ◽  
Ventricular Remodeling ◽  
Volume Overload ◽  
Wall Stress ◽  
Anterior Wall ◽  
Left Ventricular ◽  
Ventricular Geometry ◽  
Final Study ◽  
Chronic Volume Overload ◽  
Apical Site

To test the hypothesis that the abnormal ventricular geometry in failing hearts may be accounted for by regionally selective remodeling of myocardial laminae or sheets, we investigated remodeling of the transmural architecture in chronic volume overload induced by an aortocaval shunt. We determined three-dimensional finite deformation at apical and basal sites in left ventricular anterior wall of six dogs with the use of biplane cineradiography of implanted markers. Myocardial strains at end diastole were measured at a failing state referred to control to describe remodeling of myofibers and sheet structures over time. After 9 ± 2 wk (means ± SE) of volume overload, the myocardial volume within the marker sets increased by >20%. At 2 wk, the basal site had myofiber elongation (0.099 ± 0.030; P < 0.05), whereas the apical site did not [ P = not significant (NS)]. Sheet shear at the basal site increased progressively toward the final study (0.040 ± 0.003 at 2 wk and 0.054 ± 0.021 at final; both P < 0.05), which contributed to a significant increase in wall thickness at the final study (0.181 ± 0.047; P < 0.05), whereas the apical site did not ( P = NS). We conclude that the remodeling of the transmural architecture is regionally heterogeneous in chronic volume overload. The early differences in fiber elongation seem most likely due to a regional gradient in diastolic wall stress, whereas the late differences in wall thickness are most likely related to regional differences in the laminar architecture of the wall. These results suggest that the temporal progression of ventricular remodeling may be anatomically designed at the level of regional laminar architecture.

Sign in / Sign up

Export Citation Format

Share Document