Left Ventricular Geometric Remodeling and Residual Stress in the Rat Heart

1998 ◽  
Vol 120 (6) ◽  
pp. 715-719 ◽  
Author(s):  
J. H. Omens ◽  
S. M. Vaplon ◽  
B. Fazeli ◽  
A. D. McCulloch
Keyword(s):  
Residual Stress ◽  
Wall Thickness ◽  
Residual Strain ◽  
Left Ventricular ◽  
Radius Ratio ◽  
Area Fraction ◽  
Heart Weight ◽  
Left Ventricular Geometry ◽  
Opening Angle ◽  
Internal Radius

Theoretical considerations and observations of residual stress suggest that geometric remodeling in the heart may also alter residual stress and strain. We investigated whether changes in left ventricular geometry during physiologic growth were associated with corresponding changes in myocardial residual strain. In anesthetized rats from eight age groups ranging from 2–25+ weeks, the heart was arrested and isolated, and equatorial slices were obtained. The geometry of the intact, unloaded state was recorded, as well as the “opening angle” of the stress-free configuration after radial resection of the tissue slice. The tissue was fixed and embedded for histological examination of collagen area fraction. Heart weight increased 10-fold with age and unloaded internal radius increased almost 4-fold. However, wall thickness increased only 66 percent, so that the ratio of wall thickness to internal radius decreased significantly from 2.22 ± 0.29 (mean ± SD) at 2 weeks to 0.81 ± 0.47 at 25 weeks. Opening angle of the stress-free slice decreased significantly from 87 ± 16 deg at 2 weeks to 51 ± 16 deg, and correlated linearly with wall thickness/radius ratio. Collagen area fraction increased with age. Hence physiologic ventricular remodeling in rats decreases myocardial residual strain in proportion to the relative reduction in wall thickness–radius ratio.

The Effect of Age on Residual Strain in the Rat Aorta

1996 ◽  
Vol 118 (4) ◽  
pp. 440-444 ◽  
Author(s):  
A. Badreck-Amoudi ◽  
C. K. Patel ◽  
T. P. C. Kane ◽  
S. E. Greenwald
Keyword(s):  
Residual Stress ◽  
Wall Thickness ◽  
Residual Strain ◽  
Normal Growth ◽  
Rat Aorta ◽  
Opening Angle ◽  
Steady Increase ◽  
The Relationship ◽  
Effect Of Age ◽  
Intravascular Pressure

Residual stress is observed in many parts of the cardiovascular system and is thought to reduce transmural stress gradients due to intravascular pressure. Its development is closely associated with normal growth and pathological remodeling, although there appear to be few previous reports of the relationship between aging and residual stress. We have estimated residual strain (an indicator of the magnitude of residual stress) at ten sites along the aorta of rats aged 2.5 to 56 weeks by measuring the degree to which rings of vessel spring open when cut (opening angle). At all ages the opening angle decreased along the aorta, reaching a minimum near the renal arteries and increasing toward the aorto-iliac bifurcation, a result that confirms previous studies. During growth, although the unloaded circumference of the aorta increased steadily, the wall thickness and medial surface area fell to a minimum at the age of 6 weeks before continuing a steady increase. Similarly, the opening angle decreased between the ages of 2.5 and 6 weeks, thereafter increasing with age. In the abdominal aorta, a strong correlation between opening angle and wall thickness relative to midwall radius (h/R) was seen; whereas in the thoracic segment, in which no increase in h/R with age occurred, no such relationship was found. These observations are in keeping with a recently proposed hypothesis that residual stress will change in response to growth-related changes in vessel geometry driven by a tendency to minimize the nonuniform stress distribution inevitably found in pressurized thick-walled cylinders.

Abstract 16165: Inorganic Arsenic Induces Sex-Dependent Pathological Cardiac Hypertrophy

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Raihan Kabir ◽  
Prithvi Sinha ◽  
Sumita Mishra ◽  
Obialunanma V Ebenebe ◽  
Nicole Taube ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Hypertrophy ◽  
Inorganic Arsenic ◽  
Left Ventricular ◽  
Luciferase Assay ◽  
Heart Weight ◽  
Left Ventricular Geometry ◽  
Wall Thickening ◽  
Pathological Cardiac Hypertrophy ◽  
Relevant Dose

Exposure to inorganic arsenic (iAS) through drinking water is well-associated with adverse cardiovascular outcomes, yet the mechanisms through which it induces these effects are not fully understood. Recent epidemiological findings highlight an association between iAS exposure and altered left ventricular geometry in both the presence and absence of hypertension. We therefore tested the hypothesis that iAS exposure has a bimodal impact on cardiac-intrinsic and hemodynamic mechanisms that together induce pathological remodeling of the myocardium. Adult male and female mice were exposed to an environmentally relevant dose of 615 μg/L NaAsO 2 for eight weeks. Males (n=9-10 mice/group) exhibited increased systolic blood pressure (115.1±3.0 vs. 106.0±2.3 mmHg, p=0.0350) via tail cuff photoplethysmography, left ventricular wall thickening (0.98±0.01 vs. 0.88±0.01 mm, p<0.0001) via transthoracic echocardiography, increased heart weight to tibia length (8.56±0.21 vs. 7.15±0.24 mg/mm; n=24 mice/group), and increased plasma atrial natriuretic peptide (47.85±12.0 vs. 15.14±3.73 pg/mL, p=0.0379) via enzyme immunoassay. Myocardial mRNA transcript levels (n=10 hearts/group) of Acta1 (1.36±0.18 vs. 0.73±0.11, p=0.0037), Myh7 (1.53±0.15 vs. 1.04±0.10, p=0.0138), and Nppa (2.40±0.29 vs. 1.02±0.07, p=0.0001) were increased, and Myh6 (0.92±0.17 vs. 1.14±0.23, p=0.0001) was decreased, evidencing pathological hypertrophy in the male heart. Female hearts, however, were largely protected at this eight-week timepoint as similar changes were not detected. Further investigation found that Rcan1 was upregulated (1.47±0.19 vs. 0.97±0.04, p=0.0161; n=10 hearts/group) in male hearts, suggesting that calcineurin-NFAT was activated. Interestingly, iAS was sufficient to activate NFAT (0.82±0.11 vs. 0.46±0.05, p=0.0214; n=8 wells/group) independent of blood pressure via luciferase assay. In conclusion, these results demonstrate for the first time that iAS may cause pathological cardiac hypertrophy not only by increasing hemodynamic load, but also by activating calcineurin-NFAT and inducing fetal gene expression in the male heart, thus providing novel mechanistic insight into the threat of iAS exposure to the cardiovascular system.

scholarly journals A Reduction in ADAM17 Expression Is Involved in the Protective Effect of the PPAR-α Activator Fenofibrate on Pressure Overload-Induced Cardiac Hypertrophy

PPAR Research ◽  
2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Si-Yu Zeng ◽  
Hui-Qin Lu ◽  
Qiu-Jiang Yan ◽  
Jian Zou
Keyword(s):  
Body Weight ◽  
Angiotensin Ii ◽  
Cardiac Hypertrophy ◽  
Wall Thickness ◽  
Protective Action ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Heart Weight ◽  
Hypertensive Rats ◽  
Protein Levels

The peroxisome proliferator-activated receptor-α (PPAR-α) agonist fenofibrate ameliorates cardiac hypertrophy; however, its mechanism of action has not been completely determined. Our previous study indicated that a disintegrin and metalloproteinase-17 (ADAM17) is required for angiotensin II-induced cardiac hypertrophy. This study aimed to determine whether ADAM17 is involved in the protective action of fenofibrate against cardiac hypertrophy. Abdominal artery constriction- (AAC-) induced hypertensive rats were used to observe the effects of fenofibrate on cardiac hypertrophy and ADAM17 expression. Primary cardiomyocytes were pretreated with fenofibrate (10 μM) for 1 hour before being stimulated with angiotensin II (100 nM) for another 24 hours. Fenofibrate reduced the ratios of left ventricular weight to body weight (LVW/BW) and heart weight to body weight (HW/BW), left ventricular anterior wall thickness (LVAW), left ventricular posterior wall thickness (LVPW), and ADAM17 mRNA and protein levels in left ventricle in AAC-induced hypertensive rats. Similarly, in vitro experiments showed that fenofibrate significantly attenuated angiotensin II-induced cardiac hypertrophy and diminished ADAM17 mRNA and protein levels in primary cardiomyocytes stimulated with angiotensin II. In summary, a reduction in ADAM17 expression is associated with the protective action of PPAR-α agonists against pressure overload-induced cardiac hypertrophy.

scholarly journals The visceral pericardium: macromolecular structure and contribution to passive mechanical properties of the left ventricle

2007 ◽  
Vol 293 (6) ◽  
pp. H3379-H3387 ◽  
Author(s):  
Paul D. Jöbsis ◽  
Hiroshi Ashikaga ◽  
Han Wen ◽  
Emily C. Rothstein ◽  
Keith A. Horvath ◽  
...  
Keyword(s):  
Mechanical Properties ◽  
Residual Stress ◽  
Ex Vivo ◽  
Second Harmonic ◽  
Three Dimensional ◽  
Left Ventricular ◽  
Opening Angle ◽  
Passive Stiffness ◽  
Photon Excitation ◽  
Before And After

Much attention has been focused on the passive mechanical properties of the myocardium, which determines left ventricular (LV) diastolic mechanics, but the significance of the visceral pericardium (VP) has not been extensively studied. A unique en face three-dimensional volumetric view of the porcine VP was obtained using two-photon excitation fluorescence to detect elastin and backscattered second harmonic generation to detect collagen, in addition to standard light microscopy with histological staining. Below a layer of mesothelial cells, collagen and elastin fibers, extending several millimeters, form several distinct layers. The configuration of the collagen and elastin layers as well as the location of the VP at the epicardium providing a geometric advantage led to the hypothesis that VP mechanical properties play a role in the residual stress and passive stiffness of the heart. The removal of the VP by blunt dissection from porcine LV slices changed the opening angle from 53.3 ± 10.3 to 27.3 ± 5.7° (means ± SD, P < 0.05, n = 4). In four porcine hearts where the VP was surgically disrupted, a significant decrease in opening angle was found (35.5 ± 4.0°) as well as a rightward shift in the ex vivo pressure-volume relationship before and after disruption and a decrease in LV passive stiffness at lower LV volumes ( P < 0.05). These data demonstrate the significant and previously unreported role that the VP plays in the residual stress and passive stiffness of the heart. Alterations in this layer may occur in various disease states that effect diastolic function.

Left ventricular geometry and risk of incident hypertension

Heart ◽  
2019 ◽  
Vol 105 (18) ◽  
pp. 1402-1407 ◽  
Author(s):  
Sung Keun Park ◽  
Ju Young Jung ◽  
Jeong Gyu Kang ◽  
Pil-Wook Chung ◽  
Chang-Mo Oh
Keyword(s):  
Wall Thickness ◽  
Proportional Hazards ◽  
Proportional Hazards Model ◽  
Left Ventricular ◽  
Cox Proportional Hazards ◽  
Cox Proportional Hazards Model ◽  
Left Ventricular Geometry ◽  
Incident Hypertension ◽  
Increased Risk ◽  
Echocardiographic Parameters

ObjectiveLeft ventricular (LV) geometry change is an independent predictor for cardiovascular disease. However, data are equivocal on the association of echocardiographic parameters of LV geometry with incident hypertension. Thus, we were to investigate the risk of hypertension according to the baseline echocardiographic parameters of LV geometry.MethodsStudy participants were 12 562 Koreans without hypertension who received echocardiography as an item of health check-up. They were divided into normotensive or prehypertensive group according to baseline blood pressure. In each group, study subjects were classified by quintiles of baseline echocardiographic parameters including left ventricular mass index (LVMI), relative wall thickness (RWT), interventricular septal thickness (IVST), posterior wall thickness (PWT) and IVST plus PWT and followed up for 5 years. Cox proportional hazards model was used in calculating adjusted HRs and their 95% CI for hypertension according to each quintile group. Area under the curve (AUC) analysis (AUC [95% CI]) was performed to compare the predictability of LVMI, RWT, IVST, PWT, IVST plus PWT for hypertension.ResultsPrehypertensive group had the worse clinical and echocardiographic parameters in baseline analysis than normotensive group. The risk of hypertension significantly increased proportionally to baseline LVMI, RWT, IVST, PWI and IVST plus PWT above specific quintile levels, which was identified in both normotensive and prehypertensive group. In AUC analysis, IVST, PWT and IVST plus PWT showed a significantly increased AUC, compared with LVMI.ConclusionLV geometry change was significantly associated with the increased risk for hypertension in non-hypertensive individuals.

Reference Values for Valve Circumferences and Ventricular Wall Thicknesses of Fetal and Neonatal Hearts

2004 ◽  
Vol 7 (5) ◽  
pp. 499-505 ◽  
Author(s):  
Calvin E. Oyer ◽  
C. James Sung ◽  
Rebecca Friedman ◽  
Katrine Hansen ◽  
Monique De Paepe ◽  
...  
Keyword(s):  
Reference Values ◽  
Wall Thickness ◽  
Mean Value ◽  
Left Ventricular ◽  
Heart Weight ◽  
Ventricular Wall ◽  
Linear Measurements ◽  
Foot Length ◽  
Valvular Stenosis ◽  
The Mean

To evaluate valvular stenosis, cardiac dilation, and/or cardiac hypertrophy, measurements of valve circumference and ventricular wall thickness are of importance. To establish reference values in fetuses and neonates, we reviewed pathology reports at Women and Infants Hospital from 1978 through 2002 and found measurements in 776 cases that were suitable for analysis. Gestational ages (GA) ranged from 15 to 42 wk. The tabulated data include the mean, standard deviation, and 10th and 90th percentile values for foot length, body weight, body length, heart weight, valve measurements, and ventricular wall thicknesses for each week of GA. In cases in which clinical dating is not reliable, we estimated the GA by the mean value nearest that of the observed foot length. All linear measurements increased in a linear fashion throughout the second and third trimesters of development. The circumferences of cardiac valves at all ages, in descending order of magnitude, are: tricuspid, mitral, pulmonary, and aortic. Mean left ventricular (LV) wall thickness is greater than mean right ventricular (RV) wall thickness throughout gestation. The tables offer a means of determining valvular stenosis, or cardiac dilation and/or hypertrophy, based on various gestational ages.

Abstract 18623: Evaluation of Left Ventricular Geometry Changes in Patients with Tight Aortic Stenosis Using Multi-detector Computed Tomography

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Jeong Yoon Jang ◽  
Dong Hyun Yang ◽  
Sang Soo Cheon ◽  
Hee-Soon Park ◽  
Min Su Kim ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Aortic Stenosis ◽  
Wall Thickness ◽  
Left Ventricular ◽  
Left Ventricular Geometry ◽  
Aortic Valve Area ◽  
Normal Range ◽  
Lv Remodeling ◽  
Normal Controls ◽  
Multi Detector Computed Tomography

Background: Although aortic stenosis (AS) is a prototype of left ventricular hypertrophy (LVH) due to pressure overloading, patterns of LV geometric changes in patients with tight AS and their potential impact remain to be established. Methods: LV mass index (LVMI), LV end-diastolic volume (LVEDV) and regional LV wall thickness in 16 segments were measured in 147 patients with tight AS (indexed aortic valve area [AVA] < 0.6 cm 2 /m 2 ) using multi-detector computed tomography and compared with those of 32 normal controls. LVH was defined as LVMI >95 th percentile of normal controls and LV remodeling as increased LVM/LVEDV with normal range of LVMI. Asymmetric remodeling or hypertrophy were used for patients with septal wall thickness >1.5 fold compared to the opposite segment. Patients with increased LVMI but normal range of LVM/LVEDV were classified to have eccentric LVH and those with eccentric LVH and decreased LV systolic function were defined to have de-compensation. Results: AS patients with mean indexed AVA of 0.36 ± 0.08 cm 2 /m 2 showed 7 different patterns of LV geometry including normal LV geometry (n=44), remodeling (n=7), asymmetric remodeling (n=7), concentric hypertrophy (n=16), asymmetric hypertrophy (n=23), eccentric hypertrophy (n=38), and de-compensation (n=12). Peak transaortic velocity (r=0.31, p<0.001) and E/E’ (r=0.29, p<0.001) showed positive correlation with LVMI: compared to other groups, patients with LVH (concentric or asymmetric or eccentric) showed higher peak velocity and E/E’ with smaller AVA (all, p<0.001). Despite similar AVA and mean pressure gradient, patients with E/E’ ≥ 15 (n=110) showed different LV remodeling patterns (p=0.028) with higher LVMI (97.8 ± 21.1 vs 86.4 ± 20.2 g/m 2 , p=0.005). Conclusions: Various remodeling patterns of LV geometry were observed in tight AS and individual variation in LVH severity under similar LV pressure overloading could explain different severity of diastolic dysfunction.

Comparison of effects of exercise and diuretic on left ventricular geometry, mass, and insulin resistance in older hypertensive adults

2004 ◽  
Vol 287 (2) ◽  
pp. R360-R368 ◽  
Author(s):  
Morton R. Rinder ◽  
Robert J. Spina ◽  
Linda R. Peterson ◽  
Christopher J. Koenig ◽  
Christa R. Florence ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Exercise Training ◽  
Wall Thickness ◽  
Exercise Group ◽  
Left Ventricular ◽  
Left Ventricular Geometry ◽  
Endurance Exercise Training ◽  
Improve Insulin Resistance ◽  
Lv Mass ◽  
Plasma Insulin Levels

To compare the effects of exercise training and hydrochlorothiazide on left ventricular (LV) geometry and mass, blood pressure (BP), and hyperinsulinemia in older hypertensive adults, we studied 28 patients randomized either to a group (age 66.4 ± 1.3 yr; n = 16) that exercised or to a group (age 65.3 ± 1.2 yr; n = 12) that received hydrochlorothiazide for 6 mo. Endurance exercise training induced a 15% increase in peak aerobic power. The reduction in systolic BP was twofold greater with thiazide than with exercise (26.6 ± 12.2 vs. 11.5 ± 10.9 mmHg). Exercise and thiazide reduced LV wall thickness, LV mass index (14% in each group), and the LV wall thickness-to-radius ratio ( h/ r) similarly (exercise: before 0.48 ± 0.2, after 0.42 ± 0.01; thiazide: before 0.47 ± 0.04, after 0.40 ± 0.04; P = 0.017). The reductions in systolic BP and h/ r were correlated in the exercise group ( r = 0.70, P = 0.005) but not in the thiazide group. Exercise training reduced glucose-stimulated hyperinsulinemia (before: 13.65 ± 2.6 vs. 9.84 ± 1.5 mU·ml−1·min; P = 0.04) and insulin resistance. Thiazide did not affect plasma insulin levels. The results suggest that although exercise is less effective in reducing systolic BP than thiazide, it can induce regression of LV hypertrophy similar in magnitude to thiazide. Unlike hydrochlorothiazide, exercise training can improve insulin resistance and aerobic capacity in older hypertensive people.

Regional arterial stress-strain distributions referenced to the zero-stress state in the rat

2002 ◽  
Vol 282 (2) ◽  
pp. H622-H629 ◽  
Author(s):  
Jingbo Zhao ◽  
Judd Day ◽  
Zhuang Feng Yuan ◽  
Hans Gregersen
Keyword(s):  
Stress State ◽  
Pulmonary Artery ◽  
Thoracic Aorta ◽  
Wall Thickness ◽  
Femoral Artery ◽  
Residual Strain ◽  
Mechanical Test ◽  
Opening Angle ◽  
Outer Diameter ◽  
Stress Strain

Morphometric and stress-strain properties were studied in isolated segments of the thoracic aorta, abdominal aorta, left common carotid artery, left femoral artery, and the left pulmonary artery in 16 male Wistar rats. The mechanical test was performed as a distension experiment where the proximal end of the arterial segment was connected via a tube to the container used for applying pressures to the segment and the distal end was left free. Outer wall dimensions were obtained from digitized images of the arterial segments at different pressures as well as at no-load and zero-stress states. The results showed that the morphometric data, such as inner and outer circumference, wall and lumen area, wall thickness, wall thickness-to-inner radius ratio, and normalized outer diameter, as a function of the applied pressures, differed between the five arteries ( P < 0.01). The opening angle was largest in the pulmonary artery and smallest in thoracic aorta ( P < 0.01). The absolute value of both the inner and outer residual strain and the residual strain gradient were largest in the femoral artery and smallest in the thoracic aorta ( P < 0.01). In the circumferential and longitudinal direction, the arterial wall was stiffest in the femoral artery and in the thoracic aorta, respectively, and most compliant in the pulmonary artery. These results show that the morphometric and biomechanical properties referenced to the zero-stress state differed between the five arterial segments.

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