scholarly journals Ventricular remodeling induced by retinoic acid supplementation in adult rats

2003 ◽  
Vol 284 (6) ◽  
pp. H2242-H2246 ◽  
Author(s):  
Sergio Alberto Rupp de Paiva ◽  
Leonardo Antonio Mamede Zornoff ◽  
Marina Politi Okoshi ◽  
Katashi Okoshi ◽  
Luiz Shiguero Matsubara ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Papillary Muscle ◽  
Ventricular Remodeling ◽  
Volume Fraction ◽  
Maximum Velocity ◽  
Left Ventricular ◽  
Control Group ◽  
Adult Rats ◽  
Cross Sectional ◽  
Morphological Studies

Retinoic acid (RA) plays a role in regulating cardiac geometry and function throughout life. The aim of this study was to analyze the cardiac effects of RA in adult rats. Wistar rats were randomly allocated to a control group ( n = 18) receiving standard rat chow and a group treated with RA ( n = 14) receiving standard rat chow supplemented with RA for 90 days. All animals were evaluated by echocardiography, isolated papillary muscle function, and morphological studies. Whereas the RA-treated group developed an increase in both left ventricular (LV) mass and LV end-diastolic diameter, the ratio of LV wall thickness to LV end-diastolic diameter remained unchanged when compared with the control group. In the isolated papillary muscle preparation, RA treatment decreased the time to peak developed tension and increased the maximum velocity of isometric relengthening, indicating that systolic and diastolic function was improved. Although RA treatment produced an increase in myocyte cross-sectional area, the myocardial collagen volume fraction was similar to controls. Thus our study demonstrates that small physiological doses of RA induce ventricular remodeling resembling compensated volume-overload hypertrophy in rats.

Severe myocardial dysfunction induced by ventricular remodeling in aging rat hearts

1990 ◽  
Vol 259 (4) ◽  
pp. H1086-H1096 ◽  
Author(s):  
J. M. Capasso ◽  
T. Palackal ◽  
G. Olivetti ◽  
P. Anversa
Keyword(s):  
Ventricular Remodeling ◽  
Volume Fraction ◽  
Diastolic Pressure ◽  
Structural Characteristics ◽  
Myocardial Dysfunction ◽  
Pressure Rise ◽  
Wall Stress ◽  
Left Ventricular ◽  
Cross Sectional

To determine if aging engenders alterations in the functional properties of the myocardium and ventricular remodeling, the hemodynamic performance and structural characteristics of the left ventricle of male Fischer 344 rats at 4, 12, 20, and 29 mo of age were studied by quantitative physiology and morphology. In vivo assessment of cardiac pump function showed no change up to 20 mo, whereas left ventricular end-diastolic pressure was increased at 29 mo. Moreover, peak rates of pressure rise and decay, stroke volume, ejection fraction, and cardiac output were depressed at the later age interval, demonstrating the presence of ventricular failure at this time. The measurements of chamber size and wall thickness showed that ventricular end-diastolic and end-systolic volumes progressively increased with age with the greatest change occurring at 20-29 mo. Aging was also accompanied by a marked augmentation in the volume fraction of fibrotic areas in the ventricular myocardium that was due to an increase in their number and cross-sectional area with time. These architectural rearrangements, in combination with the abnormalities in ventricular function, resulted in an elevation in the volume of wall stress throughout the cardiac cycle. Wall stress increased by 64, 44, and 50% from 4 to 12, 12 to 20, and 20 to 29 mo of age. In conclusion, aging leads to a continuous rise in wall stress that is not normalized by ventricular remodeling. These two independent processes appear to be responsible for the onset of heart failure in the senescent rat.

The Pattern of Ventricular Remodeling Influences the Level of Oxidative Stress in Heart Failure Patients

2017 ◽  
Vol 68 (7) ◽  
pp. 1506-1511
Author(s):  
Cerasela Mihaela Goidescu ◽  
Anca Daniela Farcas ◽  
Florin Petru Anton ◽  
Luminita Animarie Vida Simiti
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Ventricular Remodeling ◽  
Clinical Laboratory ◽  
Left Ventricular ◽  
Control Group ◽  
Reactive Protein ◽  
Lv Mass ◽  
Few Data

Oxidative stress (OS) is increased in chronic diseases, including cardiovascular (CV), but there are few data on its effects on the heart and vessels. The isoprostanes (IsoP) are bioactive compounds, with 8-iso-PGF25a being the most representative in vivo marker of OS. They correlate with the severity of heart failure (HF), but because data regarding OS levels in different types of HF are scarce, our study was aimed to evaluate it by assessing the urinary levels of 8-iso-PGF2aand its correlations with various biomarkers and parameters. Our prospective study included 53 consecutive patients with HF secondary to ischemic heart disease or dilative cardiomyopathy, divided according to the type of HF (acute, chronic decompensated or chronic compensated HF). The control group included 13 hypertensive patients, effectively treated. They underwent clinical, laboratory - serum NT-proBNP, creatinine, uric acid, lipids, C reactive protein (CRP) and urinary 8-iso-PGF2a and echocardiographic assessment. HF patients, regardless the type of HF, had higher 8-iso-PGF2a than controls (267.32pg/�mol vs. 19.82pg/�mol, p[0.001). The IsoP level was directly correlated with ejection fraction (EF) (r=-0.31, p=0.01) and NT-proBNP level (r=0.29, p=0.019). The relative wall thickness (RWT) was negatively correlated with IsoP (r=-0.55, p[0.001). Also 8-iso-PGF25a was higher by 213.59pg/�mol in the eccentric left ventricular (LV) hypertrophy subgroup comparing with the concentric subgroup (p=0.014), and the subgroups with severe mitral regurgitation (MR) and moderate/severe pulmonary hypertension (PAH) had the highest 8-iso-PGF2a levels. Male sex, severe MR, moderate/severe PAH, high LV mass and low RWT values were predictive for high OS level in HF patients.Eccentric cardiac remodeling, MR severity and PAH severity are independent predictors of OS in HF patients.

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.

Cardiac vasculature and flow during pressure-overload hypertrophy

1986 ◽  
Vol 251 (5) ◽  
pp. H1031-H1037 ◽  
Author(s):  
E. A. Breisch ◽  
F. C. White ◽  
L. E. Nimmo ◽  
C. M. Bloor
Keyword(s):  
Blood Flow ◽  
Myocardial Blood Flow ◽  
Weight Ratio ◽  
Pressure Overload ◽  
Capillary Density ◽  
Left Ventricular ◽  
Control Group ◽  
Cross Sectional ◽  
Ventricle Hypertrophy ◽  
Aortic Cuff

The effects of pressure-overload hypertrophy (H) on myocardial blood flow and microvasculature were studied in the porcine left ventricle. Hypertrophy was produced in nine adult pigs by an aortic cuff constriction of the ascending aorta. Eight pigs served as controls. After 30 days the aortic cuff was released, and the hypertrophy group was studied 1 day postrelease. The degree of hypertrophy, determined by left ventricular-to-body weight ratio, was 45%. With hypertrophy, left ventricular blood flows were normal at rest. During exercise with adenosine infusion, myocardial blood flow to the endomyocardium was reduced compared with the control (C) group (H = 4.02 +/- 0.35, P less than 0.05; C = 5.33 +/- 0.41 ml X min-1 X g-1). Minimal coronary vascular resistance in the endomyocardium was increased during exercise with adenosine in the hypertrophy group compared with the control group. Anatomic studies revealed that hypertrophy causes a reduction in the endomyocardial capillary density (H = 1,654 +/- 168, P less than 0.025; C = 2,168 +/- 106, no./mm2) with a similar trend noted for the transmural arteriolar density. Arteriolar media wall cross-sectional area was unaffected by the pressure overload. These results indicate that changes in the vascular bed do not parallel myocyte growth during pressure-overload hypertrophy. The resultant anatomic imbalance compromises endomyocardial flow, making this region vulnerable to ischemia.

scholarly journals Plasma Level of High-Sensitive C-Reactive Protein in Patients with Acute Myocardial Infarction and Arterial Hypertension

2017 ◽  
Vol 23 (1) ◽  
Author(s):  
Wael Rumaneh
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Plasma Level ◽  
Arterial Hypertension ◽  
Ventricular Remodeling ◽  
Left Ventricular ◽  
Control Group ◽  
Blood Levels ◽  
C Reactive Protein ◽  
Reactive Protein

Arterial hypertension is an independent predictor of acute myocardial infarction. Nowadays, plasma level of high-sensitive C-reactive protein is a marker of cardiovascular risk. The objective of the research was to evaluate plasma level of high-sensitive C-reactive protein in patients with acute myocardial infarction and arterial hypertension depending on myocardial remodeling type. Materials and methods. 130 patients with myocardial infarction (63 individuals with concomitant arterial hypertension and 67 individuals without it) were observed. Transthoracic echocardiogram was used. To evaluate plasma level of high-sensitive C-reactive protein the ELISA method was applied. Results. Plasma level of high-sensitive C-reactive protein in patients with acute myocardial infarction increased by 5.11 times compared to the control group: (10.67 [5.43; 12.89]) mg/l and (2.09 [1.40; 4.60]) mg/l, respectively (p<0.001). In myocardial infarction and arterial hypertension, this parameter increased by 6.57 times (to (13.73 [7.05; 15.17]) mg/l) (p<0.001), and by 1.27 times (p<0.05) as compared to patients without arterial hypertension. No differences in plasma level of high-sensitive C-reactive protein were detected in patients with different types of left ventricular remodeling.Conclusions. Acute myocardial infarction caused by high plasma level of high-sensitive C-reactive protein is severer in co-existent arterial hypertension. There are no differences in blood levels of high-sensitive C-reactive protein depending on the type of left ventricular remodeling.

Abstract P471: Mechanisms Controlling Regression Of Cardiac Fibrosis By Removal Of Pressure Overload

2021 ◽  
Vol 129 (Suppl_1) ◽  
Author(s):  
Lily Neff ◽  
An Van Laer ◽  
Catalin F Baicu ◽  
Michael R Zile ◽  
Amy Bradshaw
Keyword(s):  
Cardiac Fibrosis ◽  
Volume Fraction ◽  
Lysyl Oxidase ◽  
Cardiac Fibroblasts ◽  
Pressure Overload ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Cellular Mechanisms ◽  
Cross Sectional ◽  
Fibroblast Activation

Background: Antecedent conditions, like aortic stenosis, can induce left ventricular pressure overload (LVPO), that can lead to Heart Failure with Preserved Ejection Fraction (HFpEF). Myocardial fibrosis and stiffness are key characteristics of HFpEF. Cardiac fibroblasts are the primary cell type regulating ECM production and deposition. In previous studies, biopsies isolated at the time of SAVR surgery, to correct stenosis, and then at 1-year and 5-years post-SAVR showed reductions in hypertrophy and fibrosis demonstrating these processes can regress. However, cellular mechanisms, including fibroblast activity, are poorly defined. Objective: Define mechanisms that contribute to remodeling of ECM before and after LVPO. Methods: LVPO was induced using transverse aortic constriction (TAC). LVPO was relieved by removal of the band (unTAC) at 4 wks. Cardiomyocyte cross-sectional area (CSA), collagen volume fraction (CVF), and protein production was measured by histology and immunoblot for five time points: nonTAC, 2wk TAC, 4wk TAC, 4wk TAC+2wk unTAC, and 4wk TAC+4wk unTAC. Results: In response to LVPO, myocyte CSA increased by 23% at 2wk TAC and by 47% at 4wk. CVF increased by 64% and 204% at 2wk and 4wk TAC, respectively, versus nonTAC. In 2wk TAC hearts, SMA, a marker of fibroblast activation was increased as was production of two collagen cross-linking enzymes, lysyl oxidase (LOX) and LOXL2, in the absence of significant increases in markers of ECM degradation. After unloading, myocyte CSA decreased by 20% in 2wk unTAC versus 4wk TAC and CVF decreased by 38% in 4wk unTAC versus 4wk TAC. Coincident with decreases in CVF, levels of pro-MMP2 increased at 2wk unTAC as did levels of degraded collagen measured by collagen hybridizing peptide reactivity. Whereas markers of ECM deposition, LOX and LOXL2, were not increased in unTAC myocardium, a resurgence of SMA production occurred in 2wk unTAC. Conclusions: In LVPO hearts, hypertrophy was characterized by increases in myocyte CSA, greater CVF, and fibroblast activation with increased production of pro-fibrotic ECM. After unloading, hypertrophy and fibrosis significantly decreased accompanied by increases in ECM degrading activity and reductions in proteins that contribute to collagen assembly.

Abstract 16771: Longitudinal Segmental Shape Analysis of the Remodeling Left Ventricle in Chronic Mitral Regurgitation

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Daniella Corporan ◽  
Muralidhar Padala
Keyword(s):  
Mitral Regurgitation ◽  
Systolic Function ◽  
Left Ventricular ◽  
Control Group ◽  
Adult Rats ◽  
Mitral Valve Leaflet ◽  
Area Index ◽  
Sphericity Index ◽  
Left Ventricular Shape ◽  
Apical Area

Introduction: Severe mitral regurgitation (MR) initiates left ventricular (LV) dilatation, but preserves systolic function. Due to preserved EF, patients are not referred for correction of their MR, and the ventricle continues to enlarge. Identifying patients at risk of heart failure, just from assessing LV size is challenging. In this study, we sought to investigate if ventricular shape and sphericity can represent the pathological remodeling process in this disease. Methods: Sixty adult rats (N=60) were induced with severe MR by puncturing the mitral valve leaflet with a 23G needle on the beating heart, using echo guidance (Fig.A1). Transthoracic echocardiography was performed at 2, 10, 20, and 40 weeks (n=15 rats/group) for analysis of the left ventricular shape. Fifteen healthy rats (N=15) were used as a sham group for comparison. Results: Severe MR was confirmed in all the rats in the MR group with a MR jet area of 40.99±9.40% ( Fig.A2 ), MR volume of 119.50±32.43μl ( Fig.A3 ), and pulmonary flow reversal ( Fig.A4 ). None of these were observed in the control group. LV dilation was observed in MR rats compared to sham ( Fig.B ). Diastolic sphericity index, LV area, and diastolic apical area index was significantly increased at 2, 10, 20, and 40 weeks after MR compared to sham (p<0.05) ( Fig.C1-C3 ). Systolic sphericity index was not significantly increased compared to sham at any time-point ( Fig.D1 ). LV area was unchanged at 2 weeks, and was significantly increased at 10, 20, and 40 weeks ( Fig.D2 ). Systolic apical area index was significantly increased at 2, 20, and 40 weeks compared to sham (p<0.05) ( Fig.D3 ). Conclusions: Analysis of left ventricular shape and its longitudinal changes can help detect remodeling patterns that are not visible using traditional functional indices.

Influence of exercise on excitation-contraction coupling in rat myocardium

1981 ◽  
Vol 240 (4) ◽  
pp. H472-H480 ◽  
Author(s):  
G. F. Tibbits ◽  
R. J. Barnard ◽  
K. M. Baldwin ◽  
N. Cugalj ◽  
N. K. Roberts
Keyword(s):  
Binding Sites ◽  
Action Potentials ◽  
Left Ventricular ◽  
Female Rats ◽  
Contractile Element ◽  
Resting Membrane Potential ◽  
Control Group ◽  
Cross Sectional ◽  
Significant Prolongation ◽  
Isometric Twitch

The present studies were conducted to investigate further the mechanisms by which the myocardium adapts to exercise training. Sixty female rats were randomly divided into sedentary control (group C) and trained (group T) groups. Group T was progressively trained for 12 wk. After the rats were killed, left ventricular papillary muscles were mounted in a tissue bath for mechanical studies. Muscles from group T generated greater peak isometric twitch tension per unit cross-sectional area than muscles from group C with [Ca2+]o ranging from 0.25 to 3.5 mM. Analyses of these data indicated that the Km for Ca2+ was not different but that the predicted number of sarcolemmal Ca2+ binding sites was 63% higher in group T. The ATPase activity of the purified cardiac myofibrils was not different between the two groups in the pCa range of 8.53-4.42. Action potentials were recorded with microelectrodes impaled into left ventricular muscle fibers of the subendocardium. Although there was no difference in the resting membrane potential, overshoot, or 90% duration, there was a significant prolongation of the action potential at 0 mV (20.2 +/- 1.0 vs 30.0 +/- 1.3 ms) in group T. These data further support the hypothesis that treadmill exercise enhances cardiac performance by increasing Ca2+ availability to the contractile element. This adaptation is mediated, at least in part, by a sarcolemmal adaptation induced by the exercise paradigm.

scholarly journals Alterations in myocardial collagen content affect rat papillary muscle function

2000 ◽  
Vol 279 (4) ◽  
pp. H1534-H1539 ◽  
Author(s):  
Luiz S. Matsubara ◽  
Beatriz B. Matsubara ◽  
Marina P. Okoshi ◽  
Antonio C. Cicogna ◽  
Joseph S. Janicki
Keyword(s):  
Papillary Muscle ◽  
Muscle Function ◽  
Volume Fraction ◽  
Systolic Function ◽  
Collagen Content ◽  
Passive Stiffness ◽  
Collagen Concentration ◽  
Cross Sectional ◽  
Rat Papillary Muscle ◽  
Myocardial Collagen

We investigated the influence of myocardial collagen volume fraction (CVF, %) and hydroxyproline concentration (μg/mg) on rat papillary muscle function. Collagen excess was obtained in 10 rats with unilateral renal ischemia for 5 wk followed by 3-wk treatment with ramipril (20 mg · kg−1· day−1) (RHTR rats; CVF = 3.83 ± 0.80, hydroxyproline = 3.79 ± 0.50). Collagen degradation was induced by double infusion of oxidized glutathione (GSSG rats; CVF = 2.45 ± 0.52, hydroxyproline = 2.85 ± 0.18). Nine untreated rats were used as controls (CFV = 3.04 ± 0.58, hydroxyproline = 3.21 ± 0.30). Active stiffness (AS; g · cm−2· % Lmax−1) and myocyte cross-sectional area (MA; μm2) were increased in the GSSG rats compared with controls [AS 5.86 vs. 3.96 ( P < 0.05); MA 363 ± 59 vs. 305 ± 28 ( P < 0.05)]. In GSSG and RHTR groups the passive tension-length curves were shifted downwards, indicating decreased passive stiffness, and upwards, indicating increased passive stiffness, respectively. Decreased collagen content induced by GSSG is related to myocyte hypertrophy, decreased passive stiffness, and increased AS, and increased collagen concentration causes myocardial diastolic dysfunction with no effect on systolic function.

scholarly journals Relationship between obesity and left ventricular hypertrophy in children

2016 ◽  
Vol 50 (6) ◽  
pp. 331
Author(s):  
Johnny Rompis ◽  
Erling David Kaunang
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Cross Sectional Study ◽  
Left Ventricular ◽  
Control Group ◽  
Obese Children ◽  
Cross Sectional ◽  
Diastolic Compliance ◽  
And Function ◽  
And Control

Background Obesity is a chronic metabolic disorder associated with cardiovascular disease (CVD) increasing morbidity-mortality rates. It is apparent that a variety of adaptations/alterations in cardiac structure and function occurs as excessive adipose tissue accumulates. This leads to a decrease in diastolic compliance, eventually resulting in an increase in left ventricular filling pressure and left ventricular enlargement.Objective To evaluate left ventricular hypertrophy (LVH) among  obese using electrocardiographic (ECG) criteria.Methods A cross-sectional study was conducted on 74 children aged 10-15 years from February 2009 to October 2009. The subjects were divided into obese and control groups. Physical examination and standard 12 lead electrocardiography (ECG) were done in both groups.Results Of 37 obese children, LVH were featured in 3 subjects, while in control group, only 1 child had LVH (P= 0.304). We found that mean RV6 in obese and control group were 9.8446 (SD 3.5854) and 11.9662 (SD 3.2857), respectively (P=0.005). As an additional findings, we found that birth weight was related to obesity in children.Conclusion There is no relation between obesity and left ventricular using ECG criteria in obese children aged 10-15 years.

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