scholarly journals Personalization of electro-mechanical models of the pressure-overloaded left ventricle: fitting of Windkessel-type afterload models

2020 ◽  
Vol 378 (2173) ◽  
pp. 20190342 ◽  
Author(s):  
Laura Marx ◽  
Matthias A. F. Gsell ◽  
Armin Rund ◽  
Federica Caforio ◽  
Anton J. Prassl ◽  
...  
Keyword(s):  
Clinical Data ◽  
Strong Dependence ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Data Uncertainty ◽  
Model Parameters ◽  
Input Uncertainty ◽  
Mechanical Models ◽  
Local Optimizer ◽  
The Impact

Computer models of left ventricular (LV) electro-mechanics (EM) show promise as a tool for assessing the impact of increased afterload upon LV performance. However, the identification of unique afterload model parameters and the personalization of EM LV models remains challenging due to significant clinical input uncertainties. Here, we personalized a virtual cohort of N  = 17 EM LV models under pressure overload conditions. A global–local optimizer was developed to uniquely identify parameters of a three-element Windkessel (Wk3) afterload model. The sensitivity of Wk3 parameters to input uncertainty and of the EM LV model to Wk3 parameter uncertainty was analysed. The optimizer uniquely identified Wk3 parameters, and outputs of the personalized EM LV models showed close agreement with clinical data in all cases. Sensitivity analysis revealed a strong dependence of Wk3 parameters on input uncertainty. However, this had limited impact on outputs of EM LV models. A unique identification of Wk3 parameters from clinical data appears feasible, but it is sensitive to input uncertainty, thus depending on accurate invasive measurements. By contrast, the EM LV model outputs were less sensitive, with errors of less than 8.14% for input data errors of 10%, which is within the bounds of clinical data uncertainty. This article is part of the theme issue ‘Uncertainty quantification in cardiac and cardiovascular modelling and simulation’.

scholarly journals Comment on Can assimilation of crowdsourced data in hydrological modelling improve flood prediction? by Mazzoleni et al. (2017)

2017 ◽  
Author(s):  
Daniele P. Viero
Keyword(s):  
Real Time ◽  
Data Uncertainty ◽  
Model Parameters ◽  
Design Strategies ◽  
Actual System ◽  
Recent Contribution ◽  
Flood Prediction ◽  
Irregular Frequency ◽  
Crowdsourced Data ◽  
The Impact

Abstract. In their recent contribution, Mazzoleni et al. (2017) investigated the integration of crowdsourced data (CSD) in hydrological models to improve the accuracy of real-time flood forecast. They showed that assimilation of CSD improves the overall model performance in all the considered case studies. The impact of irregular frequency of available crowdsourced data, and that of data uncertainty, were also deeply assessed. However, it has to be remarked that, in their work, the Authors used synthetic (i.e., not actually measured) crowdsourced data, because actual crowdsourced data were not available at the moment of the study. This point, briefly mentioned by the authors, deserves further discussion. In most real-world applications, rainfall-runoff models are calibrated using data from traditional sensors. Typically, CSD are collected at different locations, where semi-distributed models are not calibrated. In a context of equifinality and of poor identifiability of model parameters, the model internal states can hardly mimic the actual system states away from calibration points, thus reducing the chances of success in assimilating real (i.e., not synthetic) CSD. Additional criteria are given that are useful for the a-priori evaluation of crowdsourced data for real-time flood forecasting and, hopefully, to plan apt design strategies for both model calibration and collection of crowdsourced data.

Pressure overload-induced LV hypertrophy and dysfunction in mice are exacerbated by congenital NOS3 deficiency

2004 ◽  
Vol 286 (3) ◽  
pp. H1070-H1075 ◽  
Author(s):  
Fumito Ichinose ◽  
Kenneth D. Bloch ◽  
Justina C. Wu ◽  
Ryuji Hataishi ◽  
H. Thomas Aretz ◽  
...  
Keyword(s):  
Wall Thickness ◽  
Maximum Rate ◽  
Pressure Overload ◽  
Posterior Wall ◽  
Left Ventricular ◽  
Mouse Strains ◽  
Term Administration ◽  
And Function ◽  
The Impact ◽  
Fractional Shortening

To investigate the role of endothelial nitric oxide synthase (NOS3) in left ventricular (LV) remodeling induced by chronic pressure overload, the impact of transverse aortic constriction (TAC) on LV structure and function was compared in wild-type (WT) and NOS3-deficient (NOS3–/–) mice. Before TAC, LV wall thickness, mass, and fractional shortening were similar in the two mouse strains. Twenty-eight days after TAC, both WT and NOS3–/– mice had increased LV wall thickness and mass as well as decreased fractional shortening. Although the pressure gradient across the TAC was similar in both strains of mice 28 days after TAC, LV mass and posterior wall thickness were greater in NOS3–/– than in WT mice, whereas fractional shortening and the maximum rate of developed LV pressure were less. Diastolic function, as measured by the time constant of isovolumic relaxation and the maximum rate of LV pressure decay, was impaired to a greater extent in NOS3–/– than in WT mice. The degree of myocyte hypertrophy and LV fibrosis was greater in NOS3–/– than in WT mice at 28 days after TAC. Mortality was greater in NOS3–/– than in WT mice 28 days after TAC. Long-term administration of hydralazine normalized the blood pressure and prevented the LV dilation in NOS3–/– mice but did not prevent the LV hypertrophy, dysfunction, and fibrosis associated with NOS3 deficiency after TAC. These results suggest that the absence of NOS3 augments LV dysfunction and remodeling in a murine model of chronic pressure overload.

scholarly journals A short duration of high-fat diet induces insulin resistance and predisposes to adverse left ventricular remodeling after pressure overload

2008 ◽  
Vol 295 (6) ◽  
pp. H2495-H2502 ◽  
Author(s):  
Michael J. Raher ◽  
Helene B. Thibault ◽  
Emmanuel S. Buys ◽  
Darshini Kuruppu ◽  
Nobuyuki Shimizu ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Myocardial Perfusion ◽  
Short Duration ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Systemic Hypertension ◽  
High Fat ◽  
Lv Remodeling ◽  
And Function ◽  
The Impact

Insulin resistance is an increasingly prevalent condition in humans that frequently clusters with disorders characterized by left ventricular (LV) pressure overload, such as systemic hypertension. To investigate the impact of insulin resistance on LV remodeling and functional response to pressure overload, C57BL6 male mice were fed a high-fat (HFD) or a standard diet (SD) for 9 days and then underwent transverse aortic constriction (TAC). LV size and function were assessed in SD- and HFD-fed mice using serial echocardiography before and 7, 21, and 28 days after TAC. Serial echocardiography was also performed on nonoperated SD- and HFD-fed mice over a period of 6 wk. LV perfusion was assessed before and 7 and 28 days after TAC. Nine days of HFD induced systemic and myocardial insulin resistance (assessed by myocardial 18F-fluorodeoxyglucose uptake), and myocardial perfusion response to acetylcholine was impaired. High-fat feeding for 28 days did not change LV size and function in nonbanded mice; however, TAC induced greater hypertrophy, more marked LV systolic and diastolic dysfunction, and decreased survival in HFD-fed compared with SD-fed mice. Compared with SD-fed mice, myocardial perfusion reserve was decreased 7 days after TAC, and capillary density was decreased 28 days after TAC in HFD-fed mice. A short duration of HFD induces insulin resistance in mice. These metabolic changes are accompanied by increased LV remodeling and dysfunction after TAC, highlighting the impact of insulin resistance in the development of pressure-overload-induced heart failure.

scholarly journals Parametric Identification of the Models with Specified Quality Characteristics

2019 ◽  
Vol 29 (4) ◽  
pp. 480-495
Author(s):  
Olga G. Kantor ◽  
Semen I. Spivak ◽  
Nikolay D. Morozkin
Keyword(s):  
Experimental Data ◽  
Factor Model ◽  
Parametric Identification ◽  
Reaction Rate Constant ◽  
Quality Characteristics ◽  
Data Uncertainty ◽  
Parameter Estimates ◽  
Model Parameters ◽  
Chemical Reaction Rate Constant ◽  
The Impact

Introduction. The model of a given structure should be identified based on the results of solving the problem of parametric identification. This model should provide the best possible the database development reproduction of the experimental data. The concept of “best” is not strictly structured. Therefore, the procedure for identifying such a model is subject to natural logic and includes the stages of data a determination of a set of acceptable models and subsequent selection of the best of them. If the set of acceptable models is large, the procedure for determining the best one can be time-consuming. In this regard, the development of methods for parametric identification, which at the stage of creating a set of acceptable models allows taking into account the qualitative aspects of the identified dependence, which are of interest to the researcher, is of particular importance. Materials and Methods. The set of acceptable methods in the problems of parametric identification largely depends on the type of the experimental data. Uncertainty for example, probabilistic and statistical methods are useful if the observed factors are random and subject to any law of probability distribution. If the conditions for the use of such methods are not met, it may be useful to present an approach based on identifying the boundaries of location of the model parameters that ensure the achievement of specified levels of quality characteristics. Results. The procedure of parametric identification of models is formalized. It is based on the use of maximum permissible parameter estimates and allows one to determining the set of parameter values that guarantee the achievement of the required qualitative level of experimental data description, including from the standpoint of analyzing the impact of changes in accord with requirements to the accuracy of their reproduction. The approbation of the developed method on the example of the construction of a one-factor model of chemical kinetics is presented. Discussion and Conclusion. It is shown that the obtained value of the chemical reaction rate constant, in accordance with the introduced criteria, provides acceptable accuracy, adequacy, and stability of the identified kinetic model. At the same time, the results of calculations revealed the information that can form the basis for planning experiments carried out in order to improve the accuracy of the experimental data.

scholarly journals Protective Effects of Thyroid Hormone Deprivation on Progression of Maladaptive Cardiac Hypertrophy and Heart Failure

2021 ◽  
Vol 8 ◽  
Author(s):  
Helena Kerp ◽  
Georg Sebastian Hönes ◽  
Elen Tolstik ◽  
Judith Hönes-Wendland ◽  
Janina Gassen ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Hypertrophy ◽  
Cardiac Function ◽  
Heart Function ◽  
Pressure Overload ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Cardiovascular Morbidity And Mortality ◽  
The Impact

Purpose: Thyroid hormones (TH) play a central role for cardiac function. TH influence heart rate and cardiac contractility, and altered thyroid function is associated with increased cardiovascular morbidity and mortality. The precise role of TH in onset and progression of heart failure still requires clarification.Methods: Chronic left ventricular pressure overload was induced in mouse hearts by transverse aortic constriction (TAC). One week after TAC, alteration of TH status was induced and the impact on cardiac disease progression was studied longitudinally over 4 weeks in mice with hypo- or hyperthyroidism and was compared to euthyroid TAC controls. Serial assessment was performed for heart function (2D M-mode echocardiography), heart morphology (weight, fibrosis, and cardiomyocyte cross-sectional area), and molecular changes in heart tissues (TH target gene expression, apoptosis, and mTOR activation) at 2 and 4 weeks.Results: In diseased heart, subsequent TH restriction stopped progression of maladaptive cardiac hypertrophy and improved cardiac function. In contrast and compared to euthyroid TAC controls, increased TH availability after TAC propelled maladaptive cardiac growth and development of heart failure. This was accompanied by a rise in cardiomyocyte apoptosis and mTOR pathway activation.Conclusion: This study shows, for the first time, a protective effect of TH deprivation against progression of pathological cardiac hypertrophy and development of congestive heart failure in mice with left ventricular pressure overload. Whether this also applies to the human situation needs to be determined in clinical studies and would infer a critical re-thinking of management of TH status in patients with hypertensive heart disease.

Left ventricular wall stress normalization in chronic pressure-overloaded heart: a mathematical model study

2000 ◽  
Vol 279 (3) ◽  
pp. H1120-H1127 ◽  
Author(s):  
Patrick Segers ◽  
Nikos Stergiopulos ◽  
Jan J. Schreuder ◽  
Berend E. Westerhof ◽  
Nico Westerhof
Keyword(s):  
Blood Pressure ◽  
Wall Thickness ◽  
Alternative Hypothesis ◽  
Pressure Overload ◽  
Wall Stress ◽  
Quantitative Agreement ◽  
Left Ventricular ◽  
Lumped Parameter Model ◽  
Model Parameters

It is generally accepted that the left ventricle (LV) hypertrophies (LVH) to normalize systolic wall stress (ςs) in chronic pressure overload. However, LV filling pressure (Pv) may be elevated as well, supporting the alternative hypothesis of end-diastolic wall stress (ςd) normalization in LVH. We used an LV time-varying elastance model coupled to an arterial four-element lumped-parameter model to study ventricular-arterial interaction in hypertension-induced LVH. We assessed model parameters for normotensive controls and applied arterial changes as observed in hypertensive patients with LVH (resistance +40%, compliance −25%) and assumed 1) no cardiac adaptation, 2) normalization of ςs by LVH, and 3) normalization of ςs by LVH and increase in Pv, such that ςd is normalized as well. In patients, systolic and diastolic blood pressures increase by ∼40%, cardiac output (CO) is constant, and wall thickness increases by 30–55%. In scenarios 1 and 2, blood pressure increased by only 10% while CO dropped by 20%. In scenario 2, LV wall thickness increased by only 10%. The predictions of scenario 3 were in qualitative and quantitative agreement with in vivo human data. LVH thus contributes to the elevated blood pressure in hypertension, and cardiac adaptations include an increase in Pv, normalization of ςs, and preservation of CO in the presence of an impaired diastolic function.

scholarly journals Comparing impacts of parameter and spatial data uncertainty for a grid-based distributed watershed model

2016 ◽  
Vol 18 (6) ◽  
pp. 961-974 ◽  
Author(s):  
Younggu Her ◽  
Conrad Heatwole
Keyword(s):  
Land Cover ◽  
Parameter Uncertainty ◽  
Input Data ◽  
Hydrologic Model ◽  
Data Uncertainty ◽  
Model Parameters ◽  
Model Output ◽  
Model Errors ◽  
Land Cover Data ◽  
The Impact

Parameter uncertainty in hydrologic modeling is commonly evaluated, but assessing the impact of spatial input data uncertainty in spatially descriptive ‘distributed’ models is not common. This study compares the significance of uncertainty in spatial input data and model parameters on the output uncertainty of a distributed hydrology and sediment transport model, HYdrology Simulation using Time-ARea method (HYSTAR). The Shuffled Complex Evolution Metropolis (SCEM-UA) algorithm was used to quantify parameter uncertainty of the model. Errors in elevation and land cover layers were simulated using the Sequential Gaussian/Indicator Simulation (SGS/SIS) techniques and then incorporated into the model to evaluate their impact on the outputs relative to those of the parameter uncertainty. This study demonstrated that parameter uncertainty had a greater impact on model output than did errors in the spatial input data. In addition, errors in elevation data had a greater impact on model output than did errors in land cover data. Thus, for the HYSTAR distributed hydrologic model, accuracy and reliability can be improved more effectively by refining parameters rather than further improving the accuracy of spatial input data and by emphasizing the topographic data over the land cover data.

scholarly journals Lack of Contribution of p66shc to Pressure Overload-Induced Right Heart Hypertrophy

2020 ◽  
Vol 21 (24) ◽  
pp. 9339
Author(s):  
Christine Hirschhäuser ◽  
Akylbek Sydykov ◽  
Annemarie Wolf ◽  
Azadeh Esfandiary ◽  
Julia Bornbaum ◽  
...  
Keyword(s):  
Pressure Overload ◽  
Left Ventricular ◽  
Sham Operation ◽  
Ros Production ◽  
Mitochondrial Ros ◽  
Ros Formation ◽  
Pulmonary Arterial ◽  
Genetic Deletion ◽  
And Function ◽  
The Impact

The leading cause of death in pulmonary arterial hypertension (PAH) is right ventricular (RV) failure (RVF). Reactive oxygen species (ROS) have been suggested to play a role in the development of RV hypertrophy (RVH) and the transition to RVF. The hydrogen peroxide-generating protein p66shc has been associated with left ventricular (LV) hypertrophy but its role in RVH is unclear. The purpose of this study was to determine whether genetic deletion of p66shc affects the development and/or progression of RVH and RVF in the pulmonary artery banding (PAB) model of RV pressure overload. The impact of p66shc on mitochondrial ROS formation, RV cardiomyocyte function, as well as on RV morphology and function were studied three weeks after PAB or sham operation. PAB in wild type mice did not affect mitochondrial ROS production or RV cardiomyocyte function, but induced RVH and impaired cardiac function. Genetic deletion of p66shc did also not alter basal mitochondrial ROS production or RV cardiomyocyte function, but impaired RV cardiomyocyte shortening was observed following PAB. The development of RVH and RVF following PAB was not affected by p66shc deletion. Thus, our data suggest that p66shc-derived ROS are not involved in the development and progression of RVH or RVF in PAH.

scholarly journals Moderate exercise training provides left ventricular tolerance to acute pressure overload

2011 ◽  
Vol 300 (3) ◽  
pp. H1044-H1052 ◽  
Author(s):  
Daniel Moreira-Gonçalves ◽  
Tiago Henriques-Coelho ◽  
Hélder Fonseca ◽  
Rita Maria Ferreira ◽  
Francisco Amado ◽  
...  
Keyword(s):  
Exercise Training ◽  
Systolic Pressure ◽  
Pressure Overload ◽  
Left Ventricular Pressure ◽  
Myocardial Damage ◽  
Left Ventricular ◽  
Cardiac Response ◽  
Moderate Exercise ◽  
The Impact ◽  
Moderate Exercise Training

The present study evaluated the impact of moderate exercise training on the cardiac tolerance to acute pressure overload. Male Wistar rats were randomly submitted to exercise training or sedentary lifestyle for 14 wk. At the end of this period, the animals were anaesthetized, mechanically ventilated, and submitted to hemodynamic evaluation with biventricular tip pressure manometers. Acute pressure overload was induced by banding the descending aorta to induce a 60% increase of peak systolic left ventricular pressure during 120 min. This resulted in the following experimental groups: 1) sedentary without banding (SED + Sham), 2) sedentary with banding (SED + Band), and 3) exercise trained with banding (EX + Band). In response to aortic banding, SED + Band animals could not sustain the 60% increase of peak systolic pressure for 120 min, even with additional narrowing of the banding. This was accompanied by a reduction of dP/d tmax and dP/d tmin and a prolongation of the time constant tau, indicating impaired systolic and diastolic function. This impairment was not observed in EX + Band ( P < 0.05 vs. SED + Band). Additionally, compared with SED + Band, EX + Band presented less myocardial damage, exhibited attenuated protein expression of active caspase-3 and NF-κB ( P < 0.016), and showed less protein carbonylation and nitration ( P < 0.05). These findings support our hypothesis that exercise training has a protective role in the modulation of the early cardiac response to pressure overload.

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