scholarly journals ET-receptor antagonism, myocardial gene expression, and ventricular remodeling during CHF in rats

1998 ◽  
Vol 275 (3) ◽  
pp. H868-H877 ◽  
Author(s):  
Erik Øie ◽  
Reidar Bjønerheim ◽  
Haakon K. Grøgaard ◽  
Heidi Kongshaug ◽  
Otto A. Smiseth ◽  
...  
Keyword(s):  
Gene Expression ◽  
Ventricular Remodeling ◽  
Myocardial Hypertrophy ◽  
Oral Treatment ◽  
Left Ventricular ◽  
Receptor Antagonism ◽  
Hypertrophic Response ◽  
Lv Remodeling ◽  
Program Characteristic ◽  
Myocardial Gene Expression

Both myocardial and plasma endothelin-1 (ET-1) are elevated in congestive heart failure (CHF). However, the role played by endogenous ET-1 in the progression of CHF remains unknown. The aim of the present study was to investigate and correlate myocardial gene expression programs and left ventricular (LV) remodeling during chronic ET-receptor antagonism in CHF rats. After ligation of the left coronary artery, rats were randomized to oral treatment with a nonselective ET-receptor antagonist (bosentan, 100 mg ⋅ kg−1 ⋅ day−1, n = 11) or vehicle (saline, n = 13) for 15 days, starting 24 h after induction of myocardial infarction. Bosentan substantially attenuated LV dilatation during postinfarction failure as evaluated by echocardiography. Furthermore, bosentan decreased LV systolic and end-diastolic pressures and increased fractional shortening. Myocardial expression of preproET-1 mRNA and a fetal gene program characteristic of myocardial hypertrophy were increased in the CHF rats and were not affected by bosentan. Consistently, right ventricular-to-body weight ratios, diameters of cardiomyocytes, and echocardiographic analysis demonstrated a sustained hypertrophic response and a normalized relative wall thickness after intervention with bosentan. Thus the modest reduction of preload and afterload provided by bosentan substantially attenuates LV dilatation, causing improved pressure-volume relationships. However, the compensatory hypertrophic response was not altered by ET-receptor antagonism. Therefore, ET-1 does not appear to play a crucial role in the mechanisms of myocardial hypertrophy during the early phase of postinfarction failure.

Abstract 169: Angiotensin-II Induced Left Ventricular Remodeling Differs Between C57bl/6 Substrains

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Sophie Cardin ◽  
Marie-Pier Scott-Boyer ◽  
Sylvie Picard ◽  
Tim L Reudelhuber ◽  
Christian F Deschepper
Keyword(s):  
Gene Expression ◽  
Angiotensin Ii ◽  
Cardiac Fibrosis ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Left Ventricular ◽  
Cardiovascular Research ◽  
Lv Remodeling ◽  
Fold Induction ◽  
Subsequent Activation

Background: Although C57Bl/6 mice are widely used in cardiovascular research, little is known about possible substrain differences. We compared the left ventricular (LV) remodeling induced by angiotensin II (angII) in C57Bl/6J and C57Bl/6N mice, these 2 substrains corresponding to two main branches having diverged since 1951. Methods and Results: Male C57Bl/6J and C57Bl/6N mice were treated with angII (350ng/kg/min) or vehicle via mini-osmotic pumps for either 48h (for microarray profiling of gene expression and macrophage cytofluorometry counting) or 15 days (for both gene expression and histology). AngII (15d) induced fibrosis in LV from C57BL/6N (as shown by histology and col1a expression), but not in C57BL/6J. After 48h of treatment, about 100 genes responded in a strain-specific fashion, most responses being specific for C57Bl/6N mice. Among genes showing greater than 2-fold induction by angII (48h) in C57Bl/6N mice, there was enrichment for markers of macrophages activation and M2 polarization (including osteopontin, arginase1 and galectin3). These strain-specific differences were confirmed (both in LV tissues and macrophages isolated from LVs) by Q-RT-PCR, and occurred despite that fact that AngII increased the abundance of Cd11b+ macrophages to the same extent in both strains. Moreover, AngII (48h) increased expression of several markers of fibroblast activation (including Timp1, Lox and tenascin) in C57Bl/6N (both in LV tissue and fibroblasts isolated from LVs), but not in C57Bl/6J. Although one of the best known genetic differences in both substrains is the inactivation of the Nnt gene in C57Bl6/J mice, experiments performed in F2 mice do not indicate that the fibrotic response co-segregates with the Nnt mutation. Conclusions: Although angII-treatment induces macrophage recruitment in the LVs of both C57Bl/6J and C57Bl/6N mice, activation of cardiac macrophages and their M2 pro-reparative polarization (with subsequent activation of fibroblasts and synthesis of collagen) occurs only in the genetic C57Bl/6N background. The absence of macrophage activation and cardiac fibrosis in C57BL/6J may possibly explain some differences in experimental results obtained by various investigators using different C57BL/6 substrains.

Cardiac magnetic resonance T1 mapping allows for predicting adverse left ventricular remodeling post-reperfused st-elevation myocardial infarction

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
L Zhang ◽  
Y.K Guo ◽  
Z.G Yang ◽  
M.X Yang ◽  
K.Y Diao ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
T1 Mapping ◽  
Ventricular Remodeling ◽  
Tissue Injury ◽  
Left Ventricular ◽  
Funding Source ◽  
Native T1 ◽  
End Diastolic Volume ◽  
Significant Difference ◽  
Lv Remodeling

Abstract Background Cardiac magnet resonance (CMR) T1 mapping allows the quantitative characterization of the severity of tissue injury and predict functional recovery in acute myocardial infarction (AMI). Purpose The study aimed to investigate whether native T1 and ECV of infarct myocardium are influenced by microvascular obstruction (MVO) and have predictive value for adverse left ventricular (LV) remodeling post-infarction. Method A cohort of 54 patients with successfully reperfused STEMI underwent CMR imaging at a 3T scanner in AMI and 3 months post-infarction. Native T1 data was acquired using a modified Look-Locker inversion recovery (MOLLI) sequence, and ECV maps were calculated using blood sampled hematocrit. Manual regions-of-interest were drawn within the infarct myocardium to measure native T1 and ECV (native T1infarct and ECVinfarct, respectively). MVO identified as a low-intensity area within the infarct zone on LGE was eliminated. Results MVO was present in 36 patients (66.67%) in AMI. ECVinfarct in patients with MVO was different from those without (58.66±8.71% vs. 49.64±8.82%, P=0.001), while no significant difference in T1infarct was observed between patients with and without MVO (1474.7±63.5ms vs. 1495.4±98.0ms, P=0.352). ECV correlated well with the change in end-diastolic volume (all patients: r=0.564, P<0.001) and predicted LV remodeling in patients with and without MVO (rMVO absent = 0.626, P=0.005; rMVO present = 0.686, P<0.001; all patients: r=0.622, P<0.001); Native T1 was only associated with a 3-month change in LV end-diastolic volume (rMVO absent= 0.483, P=0.042) and predicted LV remodeling in patients without MVO (rMVO absent = 0.659, P=0.003). Furthermore, ECV had an association with LV remodeling (β=0.312, P=0.007) in multivariable logistic analysis. Conclusion Absolute native T1 in infarct myocardium might be affected by MVO but ECV isn't. ECV could predict LV remodeling in MI patients with and without MVO, while native T1 predict it in MI with MVO absent. Funding Acknowledgement Type of funding source: Public hospital(s). Main funding source(s): 1·3·5 project for disciplines of excellence, West China Hospital, Sichuan University

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 Dietary fatty acids alter left ventricular myocardial gene expression in Wistar rats

2014 ◽  
Vol 34 (8) ◽  
pp. 694-706 ◽  
Author(s):  
Kimberly M. Jeckel ◽  
Gerrit J. Bouma ◽  
Ann M. Hess ◽  
Erin B. Petrilli ◽  
Melinda A. Frye
Keyword(s):  
Gene Expression ◽  
Fatty Acids ◽  
Wistar Rats ◽  
Left Ventricular ◽  
Dietary Fatty Acids ◽  
Myocardial Gene Expression

Biphasic temporal pattern in exercise capacity after myocardial infarction in the rat: relationship to left ventricular remodeling

2005 ◽  
Vol 288 (1) ◽  
pp. H244-H249 ◽  
Author(s):  
Nathan A. Trueblood ◽  
Patrick R. Inscore ◽  
Daniel Brenner ◽  
Daniel Lugassy ◽  
Carl S. Apstein ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Exercise Capacity ◽  
Time Course ◽  
Ventricular Remodeling ◽  
Contractile Function ◽  
Left Ventricular ◽  
Coronary Artery Ligation ◽  
Early Recovery ◽  
Functional Changes ◽  
Lv Remodeling

After myocardial infarction (MI), there is progressive left ventricular (LV) remodeling and impaired exercise capacity. We tested the hypothesis that LV remodeling results in structural and functional changes that determine exercise impairment post-MI. Rats underwent coronary artery ligation ( n = 12) or sham ( n = 11) surgery followed by serial exercise tests and echocardiography for 16 wk post-MI. LV pressure-volume relationships were determined using a blood-perfused Langendorff preparation. Exercise capacity was 60% of shams immediately post-MI ( P < 0.05) followed by a recovery to near normal during weeks 5– 8. Thereafter, there was a progressive decline in exercise capacity to ±40% of shams ( P < 0.01). At both 8 and 16 wk post-MI, fractional shortening (FS) was reduced and end-diastolic diameter (EDD) was increased ( P < 0.01). However, neither FS nor EDD correlated with exercise at 8 or 16 wk ( r2 < 0.12, P > 0.30). LV septal wall thickness was increased at both 8 ( P = 0.17 vs. shams) and 16 wk ( P = 0.035 vs. shams) post-MI and correlated with exercise at both times ( r2 ≥ 0.50 and P ≤ 0.02 at 8 and 16 wk). Neither end-diastolic volume nor maximum LV developed pressure at 16 wk correlated with exercise capacity. Exercise capacity follows a biphasic time course post-MI. An immediate decrease is followed by an early recovery phase that is associated with compensatory LV hypertrophy. Subsequently, there is a progressive decrease in exercise capacity that is independent of further changes in LV volume or contractile function.

CHRONIC KIDNEY DISEASE AND THE STATE OF THE CARDIOVASCULAR SYSTEM IN LOCOMOTIVE CREW WORKERS

2021 ◽  
Author(s):  
V.A. Zhmurov ◽  
◽  
D.V. Zhmurov ◽  
V.G. Yarkova
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Cardiovascular System ◽  
Cardiovascular Events ◽  
Ventricular Remodeling ◽  
Myocardial Hypertrophy ◽  
Left Ventricular Remodeling ◽  
Left Ventricular ◽  
Professional Activities ◽  
Ckd Stage

Abstract: 967 employees of locomotive crews (drivers and their assistants of the Sverdlovsk railway of JSC «Russian Railways») were examined. It was revealed that CKD occurs in 12, 09% of employees of locomotive crews. As the CKD stage increases, the progression of changes in the cardiovascular system was found in locomotive crew workers. A high percentage of the prognostically unfavorable variant of left ventricular remodeling - eccentric myocardial hypertrophy (25% - 39.1%, depending on the stage of CKD) was found. These changes may be a factor of adverse cardiovascular events in employees of locomotive crews, which must be taken into account when admitting to professional activities.

scholarly journals Assessment of the Utility of the SeptalE/(E′×S′)Ratio and Tissue Doppler Index in Predicting Left Ventricular Remodeling after Acute Myocardial Infarction

2016 ◽  
Vol 2016 ◽  
pp. 1-6
Author(s):  
Selma Kenar Tiryakioglu ◽  
Hakan Ozkan ◽  
Hasan Ari ◽  
Kıvanc Yalin ◽  
Senol Coskun ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Doppler Echocardiography ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Tissue Doppler ◽  
Left Ventricular ◽  
Tissue Doppler Echocardiography ◽  
Anterior Myocardial Infarction ◽  
Lv Remodeling ◽  
Group 1

Background. The aim of this study is to show whether the septalE/(E′×S′)ratio assessed by tissue Doppler echocardiography can predict left ventricular remodeling after first ST segment elevation myocardial infarction treated successfully with primary percutaneous intervention.Methods. Consecutive patients (n=111) presenting with acute anterior myocardial infarction for the first time in their life were enrolled. All patients underwent successful primary percutaneous coronary intervention. Standard and tissue Doppler echocardiography were performed in the first 24-36 hours of admission. Echocardiographic examination was repeated after 6 months to reassess left ventricular volumes. SeptalE/(E′×S′)ratio was assessed by pulsed Doppler echocardiography.Results. Group 1 consisted of 33 patients with left ventricular (LV) remodeling, and Group 2 had 78 patients without LV remodeling.E/(E′×S′)was significantly higher in Group 1 (4.1±1.9versus1.65±1.32,p=0.001). The optimal cutoff value forE/(E′×S′)ratio was 2.34 with 87.0% sensitivity and 82.1% specificity.Conclusion. SeptalE/(E′×S′)values measured after the acute anterior myocardial infarction can strongly predict LV remodeling in the 6-month follow-up. In the risk assessment, the septalE/(E′×S′)can be evaluated together with the conventional echocardiographic techniques.

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