scholarly journals A Computationally Efficient Formal Optimization of Regional Myocardial Contractility in a Sheep With Left Ventricular Aneurysm

2009 ◽  
Vol 131 (11) ◽  
Author(s):  
Kay Sun ◽  
Nielen Stander ◽  
Choon-Sik Jhun ◽  
Zhihong Zhang ◽  
Takamaro Suzuki ◽  
...  
Keyword(s):  
Myocardial Contractility ◽  
Active Material ◽  
Left Ventricular ◽  
Left Ventricular Aneurysm ◽  
Fe Model ◽  
Mr Images ◽  
Material Parameters ◽  
Lv Volumes ◽  
Formal Optimization

A noninvasive method for estimating regional myocardial contractility in vivo would be of great value in the design and evaluation of new surgical and medical strategies to treat and/or prevent infarction-induced heart failure. As a first step toward developing such a method, an explicit finite element (FE) model-based formal optimization of regional myocardial contractility in a sheep with left ventricular (LV) aneurysm was performed using tagged magnetic resonance (MR) images and cardiac catheterization pressures. From the tagged MR images, three-dimensional (3D) myocardial strains, LV volumes, and geometry for the animal-specific 3D FE model of the LV were calculated, while the LV pressures provided physiological loading conditions. Active material parameters (Tmax_B and Tmax_R) in the noninfarcted myocardium adjacent to the aneurysm (borderzone) and in the myocardium remote from the aneurysm were estimated by minimizing the errors between FE model-predicted and measured systolic strains and LV volumes using the successive response surface method for optimization. The significant depression in optimized Tmax_B relative to Tmax_R was confirmed by direct ex vivo force measurements from skinned fiber preparations. The optimized values of Tmax_B and Tmax_R were not overly sensitive to the passive material parameters specified. The computation time of less than 5 h associated with our proposed method for estimating regional myocardial contractility in vivo makes it a potentially very useful clinical tool.

scholarly journals Regional Left Ventricular Myocardial Contractility and Stress in a Finite Element Model of Posterobasal Myocardial Infarction

2011 ◽  
Vol 133 (4) ◽  
Author(s):  
Jonathan F. Wenk ◽  
Kay Sun ◽  
Zhihong Zhang ◽  
Mehrdad Soleimani ◽  
Liang Ge ◽  
...  
Keyword(s):  
Finite Element ◽  
Myocardial Contractility ◽  
Left Ventricular ◽  
Border Zone ◽  
Left Ventricular Aneurysm ◽  
Fe Model ◽  
Ventricular Aneurysm ◽  
Computationally Efficient ◽  
Lv Volumes ◽  
Formal Optimization

Recently, a noninvasive method for determining regional myocardial contractility, using an animal-specific finite element (FE) model-based optimization, was developed to study a sheep with anteroapical infarction (Sun et al., 2009, “A Computationally Efficient Formal Optimization of Regional Myocardial Contractility in a Sheep With Left Ventricular Aneurysm,” ASME J. Biomech. Eng., 131(11), p. 111001). Using the methodology developed in the previous study (Sun et al., 2009, “A Computationally Efficient Formal Optimization of Regional Myocardial Contractility in a Sheep With Left Ventricular Aneurysm,” ASME J. Biomech. Eng., 131(11), p. 111001), which incorporates tagged magnetic resonance images, three-dimensional myocardial strains, left ventricular (LV) volumes, and LV cardiac catheterization pressures, the regional myocardial contractility and stress distribution of a sheep with posterobasal infarction were investigated. Active material parameters in the noninfarcted border zone (BZ) myocardium adjacent to the infarct (Tmax_B), in the myocardium remote from the infarct (Tmax_R), and in the infarct (Tmax_I) were estimated by minimizing the errors between FE model-predicted and experimentally measured systolic strains and LV volumes using the previously developed optimization scheme. The optimized Tmax_B was found to be significantly depressed relative to Tmax_R, while Tmax_I was found to be zero. The myofiber stress in the BZ was found to be elevated, relative to the remote region. This could cause further damage to the contracting myocytes, leading to heart failure.

scholarly journals Computational Investigation of Transmural Differences in Left Ventricular Contractility

2016 ◽  
Vol 138 (11) ◽  
Author(s):  
Hua Wang ◽  
Xiaoyan Zhang ◽  
Shauna M. Dorsey ◽  
Jeremy R. McGarvey ◽  
Kenneth S. Campbell ◽  
...  
Keyword(s):  
Myocardial Contractility ◽  
Ex Vivo ◽  
Experimental Studies ◽  
Contractile Force ◽  
Left Ventricular ◽  
Lv Function ◽  
Fe Model ◽  
Myocardial Layers ◽  
Best Fit

Myocardial contractility of the left ventricle (LV) plays an essential role in maintaining normal pump function. A recent ex vivo experimental study showed that cardiomyocyte force generation varies across the three myocardial layers of the LV wall. However, the in vivo distribution of myocardial contractile force is still unclear. The current study was designed to investigate the in vivo transmural distribution of myocardial contractility using a noninvasive computational approach. For this purpose, four cases with different transmural distributions of maximum isometric tension (Tmax) and/or reference sarcomere length (lR) were tested with animal-specific finite element (FE) models, in combination with magnetic resonance imaging (MRI), pressure catheterization, and numerical optimization. Results of the current study showed that the best fit with in vivo MRI-derived deformation was obtained when Tmax assumed different values in the subendocardium, midmyocardium, and subepicardium with transmurally varying lR. These results are consistent with recent ex vivo experimental studies, which showed that the midmyocardium produces more contractile force than the other transmural layers. The systolic strain calculated from the best-fit FE model was in good agreement with MRI data. Therefore, the proposed noninvasive approach has the capability to predict the transmural distribution of myocardial contractility. Moreover, FE models with a nonuniform distribution of myocardial contractility could provide a better representation of LV function and be used to investigate the effects of transmural changes due to heart disease.

scholarly journals A Novel Method for Quantifying In-Vivo Regional Left Ventricular Myocardial Contractility in the Border Zone of a Myocardial Infarction

2011 ◽  
Vol 133 (9) ◽  
Author(s):  
Lik Chuan Lee ◽  
Jonathan F. Wenk ◽  
Doron Klepach ◽  
Zhihong Zhang ◽  
David Saloner ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Myocardial Contractility ◽  
Active Material ◽  
Left Ventricular ◽  
Magnetic Resonance Images ◽  
Border Zone ◽  
Remote Region ◽  
Strain Fields ◽  
Mean Square Errors

Homogeneous contractility is usually assigned to the remote region, border zone (BZ), and the infarct in existing infarcted left ventricle (LV) mathematical models. Within the LV, the contractile function is therefore discontinuous. Here, we hypothesize that the BZ may in fact define a smooth linear transition in contractility between the remote region and the infarct. To test this hypothesis, we developed a mathematical model of a sheep LV having an anteroapical infarct with linearly–varying BZ contractility. Using an existing optimization method (Sun et al., 2009, “A Computationally Efficient Formal Optimization of Regional Myocardial Contractility in a Sheep With Left Ventricular Aneurysm,” J. Biomech. Eng., 131(11), pp. 111001), we use that model to extract active material parameter Tmax and BZ width dn that “best” predict in–vivo systolic strain fields measured from tagged magnetic resonance images (MRI). We confirm our hypothesis by showing that our model, compared to one that has homogeneous contractility assigned in each region, reduces the mean square errors between the predicted and the measured strain fields. Because the peak fiber stress differs significantly (∼15%) between these two models, our result suggests that future mathematical LV models, particularly those used to analyze myocardial infarction treatment, should account for a smooth linear transition in contractility within the BZ.

Effects of Rest and Exercise on Cardiac Blood Volume Determinations

1997 ◽  
Vol 36 (08) ◽  
pp. 259-264
Author(s):  
N. Topuzović
Keyword(s):  
Radionuclide Ventriculography ◽  
Left Ventricular ◽  
Peak Exercise ◽  
Volume Determination ◽  
Group I ◽  
Lv Volumes ◽  
Group Ii ◽  
Lv Volume

Summary Aim: The purpose of this study was to investigate the changes in blood activity during rest, exercise and recovery, and to assess its influence on left ventricular (LV) volume determination using the count-based method requiring blood sampling. Methods: Forty-four patients underwent rest-stress radionuclide ventriculography; Tc-99m-human serum albumin was used in 13 patients (Group I), red blood cells was labeled using Tc-99m in 17 patients (Group II) in vivo, and in 14 patients (Group III) by modified in vivo/in vitro method. LV volumes were determined by a count-based method using corrected count rate in blood samples obtained during rest, peak exercise and after recovery. Results: In group I at stress, the blood activity decreased by 12.6 ± 5.4%, p <0.05, as compared to the rest level, and increased by 25.1 ± 6.4%, p <0.001, and 12.8 ± 4.5%, p <0.05, above the resting level in group II and III, respectively. This had profound effects on LV volume determinations if only one rest blood aliquot was used: during exercise, the LV volumes significantly decreased by 22.1 ± 9.6%, p <0.05, in group I, whereas in groups II and III it was significantly overestimated by 32.1 ± 10.3%, p <0.001, and 10.7 ± 6.4%, p <0.05, respectively. The changes in blood activity between stress and recovery were not significantly different for any of the groups. Conclusion: The use of only a single blood sample as volume aliquot at rest in rest-stress studies leads to erroneous estimation of cardiac volumes due to significant changes in blood radioactivity during exercise and recovery.

Resizable Ventricular Patch Plasty in the Porcine Left Ventricle a Pilot Study

2010 ◽  
Vol 5 (1) ◽  
pp. 16-21 ◽  
Author(s):  
Willemijn H. F. Huijgen ◽  
Paul F. Gründeman ◽  
Tycho van der Spoel ◽  
Maarten-Jan Cramer ◽  
Paul Steendijk ◽  
...  
Keyword(s):  
Pilot Study ◽  
Animal Experiments ◽  
Ventricular Volume ◽  
Left Ventricular ◽  
Left Ventricular Aneurysm ◽  
Patch Shape ◽  
End Diastolic Volume ◽  
Patch Plasty

Objective Endoventricular circular patch plasty is a method used to reconstruct the ventricular cavity in patients with (post) ischemic left ventricular aneurysm or global dilatation. However, late redilatation with mitral regurgitation has been reported, in which postoperative apex shape seems to play an important role. We studied the feasibility of ventricular volume downsizing with a variably shaped patch in porcine hearts. Methods In five in vitro and two acute animal experiments, a dyskinetic aneurysm was simulated with a pericardial insert. Reducing patch surface by changing patch shape diminished end-diastolic volume. In vitro, static end-diastolic volume was determined for each patch shape using volumetry and echocardiography. In the acute animal experiments, preliminary observations of patch behavior in live material were made, and pressure/time relationship, dPdTmax, was registered. Results In vitro, bringing the convex patch into a flat plane reduced LV volume from 66 ± 7 mL (aneurysm) to 49 ± 5 mL. Four of 5 patch shapes further reduced volume to a mean of 38 ± 7 mL (P = 0.03). The in vitro echocardiographic measurements correlated with volumetry findings (r = 0.81). In the acute animal experiments, dPdTmax varied with patch shape, independent of volume changes. Conclusions In this pilot study, in vitro shape configuration of the resizable ventricular patch resulted in a calibrated end-diastolic volume reduction. The data of the two in vivo pilot experiments clearly indicate that change in patch configuration in the situation of more or less unchanged end-diastolic volume had impact on cardiac performance. Future studies must substantiate the results of this observation.

Modulation of force-frequency relation by phospholamban in genetically engineered mice

1999 ◽  
Vol 276 (6) ◽  
pp. H2245-H2250 ◽  
Author(s):  
Vivek J. Kadambi ◽  
Nancy Ball ◽  
Evangelia G. Kranias ◽  
Richard A. Walsh ◽  
Brian D. Hoit
Keyword(s):  
Heart Rate ◽  
Myocardial Contractility ◽  
Left Ventricular ◽  
Atrial Pacing ◽  
Force Frequency ◽  
Cardiac Sarcoplasmic Reticulum ◽  
Peak Rate ◽  
Genetically Engineered Mice ◽  
Frequency Relation

Phospholamban levels regulate cardiac sarcoplasmic reticulum Ca2+ pump activity and myocardial contractility. To determine whether and to what extent phospholamban modulates the force-frequency relation and ventricular relaxation in vivo, we studied transgenic mice overexpressing phospholamban (PLBOE), gene-targeted mice without phospholamban (PLBKO), and isogenic wild-type controls. Contractility was assessed by the peak rate of left ventricular (LV) isovolumic contraction (+dP/d t max), and diastolic function was assessed by both the peak rate (−dP/d t max) and the time constant (τ) of isovolumic LV relaxation, using a high-fidelity LV catheter. Incremental atrial pacing was used to generate heart rate vs. −dP/d t max(force-frequency) relations. Biphasic force-frequency relations were produced in all animals, and the critical heart rate (HRcrit) was taken as the heart rate at which dP/d t max was maximal. The average LV +dP/d t maxincreased in both PLBKO and PLBOE compared with their isogenic controls (both P < 0.05). The HRcrit for LV +dP/d t max was significantly higher in PLBKO (427 ± 20 beats/min) compared with controls (360 ± 18 beats/min), whereas the HRcrit in PLBOE (340 ± 30 beats/min) was significantly lower compared with that in isogenic controls (440 ± 25 beats/min). The intrinsic heart rates were significantly lower, and the HRcrit and the ±dP/d t max at HRcrit were significantly greater in FVB/N than in SvJ control mice. We conclude that 1) the level of phospholamban is a critical negative determinant of the force-frequency relation and myocardial contractility in vivo, and 2) contractile parameters may differ significantly between strains of normal mice.

The inotropic effect of digoxin on an isolated rat heart in hypercapnia and (or) hypoxia

1990 ◽  
Vol 68 (3) ◽  
pp. 455-461
Author(s):  
M. Allam ◽  
C. Saunier ◽  
A. Sautegeau ◽  
D. Hartemann
Keyword(s):  
Rat Heart ◽  
Myocardial Contractility ◽  
Diastolic Pressure ◽  
Isolated Heart ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Gas Mixture ◽  
Constant Frequency

The explanation for the increased frequency of troubles with digoxin therapy in patients with chronic pulmonary diseases is debated. The reported effects of hypoxia in vivo on myocardial levels of digoxin are contradictory, and there have been few studies on the effects of hypercapnia. In the past, it has been shown in rat myocardial tissue at rest in vitro that hypoxia decreased and hypercapnia acidosis increased the digoxin uptake. We performed a new study in vitro in an isolated beating rat heart perfused at constant flow (37 °C) and stimulated at a constant frequency (6 Hz). The performances were recorded with an intraventricular balloon equipped with a tip-manometer catheter. The action of digoxin was studied by recording systolic pressure (PS) and diastolic pressure (PD), the left ventricular developed pressure (LVDP = PS − PD), the (dP/dt)max, and the ratio (dP/dt)max/PS. First, the heart was perfused for 30 min with a modified Tyrode's solution perfusate aerated with carbogen (pH = 7.40; [Formula: see text]; [Formula: see text]) (1 mmHg = 133.32 Pa). Various parameters of contractions were recorded (initial control values). Then the heart was perfused for 15 min with Tyrode's solution aerated either with a hypoxic gas mixture (pH = 7.41; [Formula: see text]; [Formula: see text]), a hypercapnic gas mixture (pH = 7.08; [Formula: see text]; [Formula: see text]), or a hypoxic–hypercapnic gas mixture (pH = 7.09; [Formula: see text]; [Formula: see text]). Control hearts were continuously perfused with Tyrode's solution aerated with carbogen. During heart perfusion with hypercapnic, hypoxic, or hypoxic–hypercapnic Tyrode's solution, a decrease in LVDP and (dP/dt)max was observed. Finally, the heart was perfused with the same Tyrode's solution plus 1.75 × 10−5 M digoxin. The increase in myocardial contractility produced by digoxin was enhanced by hypercapnia and abolished by hypoxia. The addition of hypercapnia to hypoxia in Tyrode's solution seems to enhance the depressor action of the hypoxia.Key words: isolated heart, digoxin, hypoxia, hypercapnia, myocardial contractility.

scholarly journals Improved Left Ventricular Aneurysm Repair with Cell- and Cytokine-Seeded Collagen Patches

2018 ◽  
Vol 2018 ◽  
pp. 1-16 ◽  
Author(s):  
Hui Qu ◽  
Bao-dong Xie ◽  
Jian Wu ◽  
Bo Lv ◽  
Jun-bo Chuai ◽  
...  
Keyword(s):  
Human Mesenchymal Stem Cells ◽  
Collagen Scaffold ◽  
Left Ventricular ◽  
Left Ventricular Aneurysm ◽  
Ventricular Aneurysm ◽  
Surgical Ventricular Restoration ◽  
Promising Alternative ◽  
Postmyocardial Infarction

Background. Engineered heart tissues (EHTs) present a promising alternative to current materials for surgical ventricular restoration (SVR); however, the clinical application remains limited by inadequate vascularization postimplantation. Moreover, a suitable and economic animal model for primary screening is another important issue. Methods. Recently, we used 1-ethyl-3-(3-dimethylaminopropyl)carbodiimide hydrochloride chemistry (EDC) to initiate a strengthened, cytokine-conjugated collagenous platform with a controlled degradation speed. In vitro, the biomaterial exhibited an enhanced mechanical strength maintaining a porous ultrastructure, and the constant release of cytokines promoted the proliferation of seeded human mesenchymal stem cells (hMSCs). In vivo, with the hMSC-seeded, cytokine-immobilized patch (MSCs + GF patch), we performed modified SVR for rats with left ventricular aneurysm postmyocardial infarction (MI). Overall, the rats that underwent modified SVR lost less blood and had lower mortality. After 4 weeks, the rats repaired with this cell-seeded, cytokine-immobilized patch presented preserved cardiac function, beneficial morphology, enhanced cell infiltration, and functional vessel formation compared with the cytokine-free (MSC patch), cell-free (GF patch), or blank controls (EDC patch). Furthermore, the degradable period of the collagen patch in vivo extended up to 3 months after EDC treatment. Conclusions. EDC may substantially modify collagen scaffold and provide a promising and practical biomaterial for SVR.

MRI-based finite-element analysis of left ventricular aneurysm

2005 ◽  
Vol 289 (2) ◽  
pp. H692-H700 ◽  
Author(s):  
Joseph C. Walker ◽  
Mark B. Ratcliffe ◽  
Peng Zhang ◽  
Arthur W. Wallace ◽  
Bahar Fata ◽  
...  
Keyword(s):  
Finite Element ◽  
Myocardial Strain ◽  
Left Ventricular ◽  
Fe Analysis ◽  
Border Zone ◽  
Fe Model ◽  
Tagged Mri ◽  
Fiber Stress ◽  
Material Parameters ◽  
Biaxial Stretching

Tagged MRI and finite-element (FE) analysis are valuable tools in analyzing cardiac mechanics. To determine systolic material parameters in three-dimensional stress-strain relationships, we used tagged MRI to validate FE models of left ventricular (LV) aneurysm. Five sheep underwent anteroapical myocardial infarction (25% of LV mass) and 22 wk later underwent tagged MRI. Asymmetric FE models of the LV were formed to in vivo geometry from MRI and included aneurysm material properties measured with biaxial stretching, LV pressure measurements, and myofiber helix angles measured with diffusion tensor MRI. Systolic material parameters were determined that enabled FE models to reproduce midwall, systolic myocardial strains from tagged MRI (630 ± 187 strain comparisons/animal). When contractile stress equal to 40% of the myofiber stress was added transverse to the muscle fiber, myocardial strain agreement improved by 27% between FE model predictions and experimental measurements (RMS error decreased from 0.074 ± 0.016 to 0.054 ± 0.011, P < 0.05). In infarct border zone (BZ), end-systolic midwall stress was elevated in both fiber (24.2 ± 2.7 to 29.9 ± 2.4 kPa, P < 0.01) and cross-fiber (5.5 ± 0.7 to 11.7 ± 1.3 kPa, P = 0.02) directions relative to noninfarct regions. Contrary to previous hypotheses but consistent with biaxial stretching experiments, active cross-fiber stress development is an integral part of LV systole; FE analysis with only uniaxial contracting stress is insufficient. Stress calculations from these validated models show 24% increase in fiber stress and 115% increase in cross-fiber stress at the BZ relative to remote regions, which may contribute to LV remodeling.

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