Dataset Information

Modeling the instantaneous pressure-volume relation of the left ventricle: a comparison of six models.

ABSTRACT: Simulations are useful to study the heart's ability to generate flow and the interaction between contractility and loading conditions. The left ventricular pressure-volume (PV) relation has been shown to be nonlinear, but it is unknown whether a linear model is accurate enough for simulations. Six models were fitted to the PV-data measured in five sheep and the estimated parameters were used to simulate PV-loops. Simulated and measured PV-loops were compared with the Akaike information criterion (AIC) and the Hamming distance, a measure for geometric shape similarity. The compared models were: a time-varying elastance model with fixed volume intercept (LinFix); a time-varying elastance model with varying volume intercept (LinFree); a Langewouter's pressure-dependent elasticity model (Langew); a sigmoidal model (Sigm); a time-varying elastance model with a systolic flow-dependent resistance (Shroff) and a model with a linear systolic and an exponential diastolic relation (Burkh). Overall, the best model is LinFree (lowest AIC), closely followed by Langew. The remaining models rank: Sigm, Shroff, LinFix and Burkh. If only the shape of the PV-loops is important, all models perform nearly identically (Hamming distance between 20 and 23%). For realistic simulation of the instantaneous PV-relation a linear model suffices.

SUBMITTER: Lankhaar JW

PROVIDER: S-EPMC3233835 | biostudies-literature | 2009 Sep

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Modeling the instantaneous pressure-volume relation of the left ventricle: a comparison of six models.

Lankhaar Jan-Willem JW Rövekamp Fleur A FA Steendijk Paul P Faes Theo J C TJ Westerhof Berend E BE Kind Taco T Vonk-Noordegraaf Anton A Westerhof Nico N

Annals of biomedical engineering 20090625 9

Simulations are useful to study the heart's ability to generate flow and the interaction between contractility and loading conditions. The left ventricular pressure-volume (PV) relation has been shown to be nonlinear, but it is unknown whether a linear model is accurate enough for simulations. Six models were fitted to the PV-data measured in five sheep and the estimated parameters were used to simulate PV-loops. Simulated and measured PV-loops were compared with the Akaike information criterion ...[more]

PMID: 19554450

Similar Datasets

Project description:Background: Optimal adjustment of cardiac preload is essential for improving left ventricle stroke volume (LVSV) and tissue perfusion. Changes in LVSV caused by central venous pressure (CVP) are the most important concerns in the treatment of critically ill patients. Objectives: This study aimed to clarify the changes in LVSV after negative fluid balance in patients with elevated CVP, and to elucidate the relationship between the parameters of right ventricle (RV) filling state and LVSV changes. Methods: This prospective cohort study included patients with high central venous pressure (CVP) (≥8 mmHg) within 24 h of ICU admission in the Critical Medicine Department of Peking Union Medical College Hospital. Patients were classified into two groups based on the LVSV changes after negative fluid balance. The cutoff value was 10%. The hemodynamic and echo parameters of the two groups were recorded at baseline and after negative fluid balance. Results: A total of 71 patients included in this study. Forty in VI Group (LVOT VTI increased ≥10%) and 31 in VNI Group (LVOT VTI increased <10%). Of all patients, 56.3% showed increased LVSV after negative fluid balance. In terms of hemodynamic parameters at T0, patients in VI Group had a higher CVP (p < 0.001) and P(v-a)CO2 (p < 0.001) and lower ScVO2 (p < 0.001) relative to VNI Group, regarding the echo parameters at T0, the RVD/LVD ratio (p < 0.001), DIVC end-expiratory (p < 0.001), and ΔLVOT VTI (p < 0.001) were higher, while T0 LVOT VTI (p < 0.001) was lower, in VI Group patients. The multifactor logistic regression analysis suggested that a high CVP and RVD/LVD ratio ≥0.6 were significant associated with LVSV increase after negative fluid balance in critically patients. The AUC of CVP was 0.894. A CVP >10.5 mmHg provided a sensitivity of 87.5% and a specificity of 77.4%. The AUC of CVP combined with the RVD/LVD ratio ≥0.6 was 0.926, which provided a sensitivity of 92.6% and a specificity of 80.4%. Conclusion: High CVP and RVD/LVD ratio ≥0.6 were significant associated with RV stressed in critically patients. Negative fluid balance will not always lead to a decrease, even an increase, in LVSV in these patients.

Project description:Aims: Cardiomyocyte-specific nitric oxide synthase 3 (NOS3) overexpression reduces left ventricular (LV) remodelling after myocardial infarction in mice, but its effect on sustained LV pressure-overload remains incompletely understood. We investigated LV structural and functional adaptation to elevated afterload in mice with cardiomyocyte-restricted NOS3 overexpression (NOS3TG) and wild type littermates (WT). Methods and Results: Hemodynamic indices, cardiac hypertrophy and interstitial fibrosis were measured 10 weeks after transverse aortic constriction (TAC). After 10 weeks TAC, NOS3TG had better preserved systolic function (maximum rates of pressure development normalized to maximal pressure 77Â±6 versus 65Â±2 ms-1, P=0.05), reduced heart weight-body weight ratio (HW/BW, 5.0Â±0.3 versus 5.8Â±0.1, P<0.05), and cardiomyocyte width than WT (14.9Â±0.4 vs 16.7Â±0.2 ?m, P<0.05). After 10 weeks TAC, a 44k cDNA chip-based microarray analysis was validated using real time PCR and revealed significantly altered expression pattern of genes involved in cellular growth, matrix remodelling, and inflammation between genotypes. Conclusions: Cardiomyocyte-restricted NOS3 overexpression attenuates TAC-induced hypertrophy via autocrine inhibition of cardiomyocyte cell growth, but does not mitigate myocardial fibrosis. The subsequent diastolic dysfunction suggests that inhibition of matrix producing cells during hypertrophic stress is necessary to prevent functional and structural deterioration of the pressure-overloaded heart. Left ventricular mRNA expression profiles were compared between alpha-myosin heavy chain driven nitric oxide synthase 3 (alpha-MHC-NOS3) transgenic and wild type (WT) littermate mice at baseline and 10 weeks after transversal aortic constrcition-induced pressure-overload. Biological repeats: n=4, two males and two females, for each group and condition. Transgenic mice were backcrossed for seven generations (F7) to a C57Bl/6 N background and age and weight matched animals were used for microarray experiments.

Project description:BACKGROUND:Aortic valve regurgitation (AR) results in left ventricle (LV) volume overload (VO) leading to its dilation and hypertrophy (H). We study a rat model of severe AR induced by puncturing one or two leaflets using a catheter. Most of our studies were conducted in male animals. Recently, we started investigating if sex dimorphism existed in the AR rat model. We observed that AR females developed as much LVH as males but morphological remodeling differences were present. A head-to-head comparison of LV morphological and functional changes had never been performed in AR males (M) and females (F) using the latest modalities in cardiac imaging by echocardiography. METHODS:We performed a longitudinal study to evaluate the development of LV hypertrophy caused by chronic AR in male and female rats over 6?months. Sham-operated (sham) animals were used as controls. RESULTS:LV diastolic volumes (EDV) increased more over 6?months in sham males than in females (38% vs. 23% for EDV, both p?<?0.01). AR resulted in significant LV dilation for both sexes (54% vs. 51% increase in EDV) vs. baseline values. Since normal cardiac growth was less in females, dilation from AR was relatively more important for them (88% (M) vs. 157% (F) increase in EDV over sham). AR caused LV wall thickening in both males and females. It happened sooner for AR females and was more important than in males (25% (M) vs. 56% (F) increase in septum thickness at 2?months and 10% (M) vs. 30% (F) at 6?months). We then evaluated if AR was associated with changes in LV strain using speckle-tracking 2D echocardiography. Global longitudinal strain remained similar between AR and sham animals. Circumferential strain was negatively modulated by AR but only in females and early after VO induction (13% (M) vs. 26% (F)). CONCLUSION:AR resulted in more LV dilation and quicker wall thickening in female AR rats compared to males. Global circumferential strain was negatively modulated in AR females but not in males. AR also seemed to lead to a more spherical LV shape in females whereas; it kept mostly an ellipsoid shape in males. This can influence validity of mass estimation of the dilated LV in females by echocardiography.

Project description:Introduction: Low cardiac output syndrome is one of the postoperative complications that are associated with significant morbidity and mortality after surgical closure of atrial septal defect (ASD) with small-sized left ventricle (LV). This study investigated whether preoperative left ventricular end-diastolic volume index (LVEDVi) could accurately predict low cardiac output syndrome (LCOS) after surgical closure of ASD with small-sized LV. Method: This retrospective cohort study involved adult ASD patients with small-sized LV from January 2018 to December 2019 in National Cardiovascular Center Harapan Kita. Preoperative MRI data to assess the left and right ventricle volume were collected. A bivariate analysis using independent Student's t-test was done. Diagnostic test using receiver operating characteristic (ROC) curve was also done to obtain the area under the curve (AUC) value. The best cutoff point was determined by Youden's index. Result: Fifty-seven subjects were involved in this study [age (mean ± SD) 32.56 ± 13.15 years; weight (mean ± SD) 48.82 ± 12.15 kg]. Subjects who had post-operative LCOS (n = 30) have significantly lower LVEDVi (45.0 ± 7.42 ml/m2 vs. 64.15 ± 13.37 ml/m2; p < 0.001), LVEDV (64.6 ± 16.0 ml vs. 85.9 ± 20.7 ml; p < 0.001), LVSV (38.97 ± 11.5 ml vs. 53.13 ± 7.5 ml; p < 0.001), and LVSVi (27.28 ± 8.55 ml/m2 vs. 37.42 ± 5.35 ml/m2; p < 0.001) compared to subjects who did not have post-operative LCOS (n = 27). ROC analysis showed that the best AUC was found on LVEDVi (AUC 95.3%; 95% confidence interval: 90.6-100%). The best cutoff value for LVEDVi to predict the occurrence of LCOS after surgical closure of ASD was 53.3 ml/m2 with a sensitivity of 86.7% and a specificity of 85.2%. Conclusion: This study showed that preoperative LVEDVi could predict LCOS after surgical closure of ASD with small-sized LV with a well-defined cutoff. The best cutoff value of LVEDVi to predict the occurrence of LCOS after surgical ASD closure was 53.5 ml/m2.

Dataset Information

Modeling the instantaneous pressure-volume relation of the left ventricle: a comparison of six models.

Publications

Modeling the instantaneous pressure-volume relation of the left ventricle: a comparison of six models.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets