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Objective: Atrial fibrillation is a strong independent risk factor for cardioembolic stroke, with a significant impact on morbidity, mortality and healthcare costs. The aim of our study is to investigate left atrial mechanical function in healthy subjects and patients with atrial fibrillation paroxysms less than 48 hours with low risk of thromboembolic complications at 1 and 28 days after restoration of sinus rhythm. Methods: Thirty-six healthy controls and patients with paroxysms of non-valvular atrial fibrillation less than 48 hours (n=25) with low-risk CHA2DS2VASc score were included in the study. The mechanical function of the left atrium (LA) was investigated by the 2D speckle tracking program. Transthoracic echocardiography was performed on the 1st and 28th days after restoration of sinus rhythm by pharmacological cardioversion. Results: Despite the absence of differences in left ventricular systolic function and LA size between the groups, there was a significant decrease in LA deformation and strain rate on day 1 immediately after sinus rhythm recovery in the patients. In the pump phase, the decrease was about 3%, reservoir phase -- 10%, and conduit phase -- 7% compared to the control group. The strain rate also decreased in the patient group: -1.5 s-1 versus control: -2.14 s-1 (p<0.0001). On the 28th day after restoration of sinus rhythm, there were significant changes in reservoir and conduit functions in patients group in comparison with control group. Global longitudinal LA strain (reservoir phase) decreased to 7%, conduit phase decreased to 11% compared with the control group. In patients group we can see the dynamics during 28 days: pump phase and strain rate were significantly improved, however reservoir and conduit did not significantly change and were lower than in healthy. Conclusion: Mechanical function of the LA in patients with non-valvular atrial fibrillation and low risk of thromboembolic complications, studied with speckle tracking on the first day was significantly impaired compared with the control group (reservoir phase and strain rate). By day 28, mechanical function improved compared to day 1, but reservoir phase remained significantly lower than normal. [ABSTRACT FROM AUTHOR]

Geopolymer binder has the advantages of early strength, fast solidification, high volume stability, and low permeability. It is beneficial to improve the mechanical performance of silty sands, saving cement consumption and being environmentally friendly. However, the strength improvement of silty sand stabilized with steel slag-based geopolymer was significantly controlled by their material composition and technical parameters. This study conducted a series of unconfined compression tests to investigate the material composition of steel slag-based geopolymer binders and their reasonable mixing ratio for silty sand stabilization. The optimum mixing ratio of precursor (steel slag) to alkaline activator (the combination of Na2SiO3 and CaO) and the optimum dosage of steel slag-based geopolymer for silty sand stabilization were explored. The strengthening mechanism of geopolymer-stabilized silty sands was discussed based on microstructural images and elemental concentrations of primary components observed by SEM and EDS. The results show that when the mass ratio of steel slag: Na2SiO3: CaO was 80:35:21, and the steel slag-based geopolymer material was 15%, the silty sand could achieve the best mechanical performance improvement. The microstructural characteristics of geopolymer-stabilized silty sands at different curing ages illustrated that the compactness and integrity of silty sand structures were enhanced over the curing age. The improving cementitious contact among particles and enlarging particle size was responsible for the strength improvement of silty sand. This research can provide a reference for applying steel slag-based geopolymer in silty sand stabilization in engineering practices. [ABSTRACT FROM AUTHOR]

In order to study the influencing factors of fire evacuation bottlenecks and evacuation time in subway transfer stations, a subway transfer station model was built using Pathfinder to simulate the emergency evacuation of passengers in a fire. Using the control variable method, the evacuation under different conditions is simulated by changing the parameters. The effects of the use of escalators, the speed of escalators, preference for stairs and escalators, the use of escalators, the familiarity of exits, the speed of personnel movement and the width of stairs on evacuation time are discussed and analyzed. The results show that the fire evacuation bottlenecks of subway transfer stations is each stair entrance. Evacuation time can be shortened by increasing the speed of escalators, increasing the proportion of escalator walkers, reducing the proportion of passengers who choose familiar exits to escape, increasing the speed of passengers and increasing the width of stairs. [ABSTRACT FROM AUTHOR]

Hypoxic exposure increases right ventricular (RV) afterload by triggering pulmonary hypertension, with consequent effects on the structure and function of the RV. Improved myocardial contractility is a critical circulatory adaptation to exercise training. However, the types of exercise that enhance right cardiac mechanics during hypoxic stress have not yet been identified. This study investigated how high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) influence right cardiac mechanics during hypoxic exercise A total of 54 young and healthy sedentary males were randomly selected to engage in either HIIT (3-min intervals at 40% and 80% of oxygen uptake reserve, n = 18) or MICT (sustained 60% of oxygen uptake reserve, n = 18) for 30 min/day and 5 days/week for 6 weeks or were included in a control group (CTL, n = 18) that did not engage in any exercise. The primary outcome was the change in right cardiac mechanics during semiupright bicycle exercise under hypoxic conditions (i.e., 50 watts under 12% FiO2 for 3 min) as measured by two-dimensional speckle tracking echocardiography.: After 6 weeks of training, HIIT was superior to MICT in improving maximal oxygen consumption (VO2max). Furthermore, the HIIT group showed reduced pulmonary vascular resistance (PVR, pre-HIIT:1.16 ± 0.05 WU; post-HIIT:1.05 ± 0.05 WU, p < 0.05) as well as an elevated right ventricular ejection fraction (RVEF, pre-HIIT: 59.5 ± 6.0%; post-HIIT: 69.1 ± 2.8%, p < 0.05) during hypoxic exercise, coupled with a significant enhancement of the right atrial (RA) reservoir and conduit functions. HIIT is superior to MICT in dilating RV chamber and reducing radial strain but ameliorating radial strain rate in either systole (post-HIIT: 2.78 ± 0.14 s-1; post-MICT: 2.27 ± 0.12 s-1, p < 0.05) or diastole (post-HIIT: − 2.63 ± 0.12 s-1; post-MICT: − 2.36 ± 0.18 s-1, p < 0.05). In the correlation analysis, the changes in RVEF were directly associated with improved RA reservoir (r = 0.60, p < 0.05) and conduit functions (r = 0.64, p < 0.01) but inversely associated with the change in RV radial strain (r = − 0.70, p < 0.01) and PVR (r = − 0.70, p < 0.01) caused by HIIT. HIIT is superior to MICT in improving right cardiac mechanics by simultaneously increasing RA reservoir and conduit functions and decreasing PVR during hypoxic exercise. [ABSTRACT FROM AUTHOR]

The previously more frequently implanted pulsatile blood pumps (PBPs) showed higher recovery rates than the currently preferred rotary blood pumps (RBPs), with unclear causality. The aim of this study was to comparatively assess the capability of PBPs and RPBs to unload the left ventricle and maintain cardiac energetics as a possible implication for recovery. An RBP and a heartbeat synchronized PBP were alternately connected to isolated porcine hearts. Rotational speed of RBPs was set to different support levels. For PBP support, the start of ejection was phased to different points during the cardiac cycle, prescribed as percentage delays from 0% to 90%. Cardiac efficiency, quantified by the ratio of external work over myocardial oxygen consumption, was determined. For RBP support, higher degrees of RBP support correlated with lower left atrial pressures (LAP) and lower cardiac efficiency (r = 0.91 ± 0.12). In contrast, depending on the phase delay of a PBP, LAP and cardiac efficiency exhibited a sinusoidal relationship with the LAP minimum at 90% and efficiency maximum at 60%. Phasing of a PBP offers the possibility to maintain a high cardiac efficiency and simultaneously unload the ventricle. These results warrant future studies investigating whether optimized cardiac energetics promotes functional recovery with LVAD therapy. [ABSTRACT FROM AUTHOR]

Summary: In the present research, a nitrogen‐based flame‐retardant, melamine cyanurate (MCA) was surface‐treated with low‐molecular‐weight nylon through a solvent process to further improve its flowability and dispersion. The surface energy and flow energy of the modified MCA were investigated. The properties of polyamide 66 (PA66) prepared with surface‐treated and with conventional MCA were evaluated and compared. Because of lower surface energy and flow energy for modified MCA, its agglomeration degree and flow resistance are obviously decreased compared with conventional MCA, thus achieving finer and more homogenous dispersion in the PA66 matrix. Moreover, the low‐molecular‐weight nylon resin encapsulating MCA surface will melt at lower temperature during compounding with PA66; hence, it serves as a lubricant and carrier to further improve the flowability and dispersion of the flame retardants. Based on these advantages, the modified MCA flame‐retardant PA66 achieves much better flame retardancy, flowability, and mechanical properties compared with conventional MCA/PA66 under the same loading level of flame retardant (10 wt%). [ABSTRACT FROM AUTHOR]

Abstract Cardiac mechanics plays a crucial role in atrial and ventricular function, in the regulation of growth and remodelling, in the progression of disease, and the response to treatment. The spatial scale of the critical mechanisms ranges from nm (molecules) to cm (hearts) with the fastest events occurring in milliseconds (molecular events) and the slowest requiring months (growth and remodelling). Due to its complexity and importance, cardiac mechanics has been studied extensively both experimentally and through mathematical models and simulation. Models of cardiac mechanics evolved from seminal studies in skeletal muscle, and developed into cardiac specific, species specific, human specific and finally patient specific calculations. These models provide a formal framework to link multiple experimental assays recorded over nearly 100 years into a single unified representation of cardiac function. This review first provides a summary of the proteins, physiology and anatomy involved in the generation of cardiac pump function. We then describe the evolution of models of cardiac mechanics starting with the early theoretical frameworks describing the link between sarcomeres and muscle contraction, transitioning through myosin-level models to calcium-driven systems, and ending with whole heart patient-specific models. [ABSTRACT FROM AUTHOR]

Quantifying dynamic strain fields from time-resolved volumetric medical imaging and microscopy stacks is a pressing need for radiology and mechanobiology. A critical limitation of all existing techniques is regularization: because these volumetric images are inherently noisy, the current strain mapping techniques must impose either displacement regularization and smoothing that sacrifices spatial resolution, or material property assumptions that presuppose a material model, as in hyperelastic warping. Here, we present, validate, and apply the first three-dimensional (3D) method for estimating mechanical strain directly from raw 3D image stacks without either regularization or assumptions about material behavior. We apply the method to high-frequency ultrasound images of mouse hearts to diagnose myocardial infarction. We also apply the method to present the first ever in vivo quantification of elevated strain fields in the heart wall associated with the insertion of the chordae tendinae. The method shows promise for broad application to dynamic medical imaging modalities, including high-frequency ultrasound, tagged magnetic resonance imaging, and confocal fluorescence microscopy. [ABSTRACT FROM AUTHOR]

Hydrogen bonds are known to play an important role in prescribing the mechanical performance of certain hydrogels such as polyether‐based polyurethanes. The quantitative contribution of hydrogen bonds to the toughness of polymer networks, however, has not been elucidated to date. Here, a new physical model is developed to predict the threshold fracture energies of hydrogels physically crosslinked via hydrogen bonds. The model is based on consecutive and sequential dissociation of hydrogen‐bonded crosslinks during crack propagation. It is proposed that the scission of hydrogen bonds during crack propagation allows polymer strands in the deformation zone to partially relax and release stored elastic energy. The summation of these partial chain relaxations leads to amplified threshold fracture energies which are 10–45 times larger than those predicted by the classical Lake–Thomas theory. Experiments were performed on a hydrophilic polyurethane hydrogel where urea additions were used to control the density of hydrogen bonds. The measured fracture energies were in good agreement with the calculated values. © 2018 Wiley Periodicals, Inc. J. Polym. Sci., Part B: Polym. Phys. 2018, 56, 1287–1293 Hydrogen‐bonded hydrogels are easily fabricated highly swollen polymer networks that are mechanically robust. The origin of their high toughness is explored by using urea to control the density of hydrogen bonds. The gel toughness is shown to be much greater than predicted by the classical Lake‐Thomas theory. A new model supported by experiments is introduced based on the sequential debonding of successive hydrogen bonds along polymer chains that span the crack plane. [ABSTRACT FROM AUTHOR]

The bicuspid aortic valve (BAV) generates wall shear stress (WSS) abnormalities in the ascending aorta (AA) that may be responsible for the high prevalence of aortopathy in BAV patients. While previous studies have analyzed the magnitude and oscillatory characteristics of the total or streamwise WSS in BAV AAs, the assessment of the circumferential component is lacking despite its expected significance in this highly helical flow environment. This gap may have hampered the identification of a robust hemodynamic predictor of BAV aortopathy. The objective of this study was to perform a global and component-specific assessment of WSS magnitude, oscillatory and directional characteristics in BAV AAs. The WSS environments were computed in the proximal and middle convexity of tricuspid aortic valve (TAV) and BAV AAs using our previous valve-aorta fluid-structure interaction (FSI) models. Component-specific WSS characteristics were investigated in terms of temporal shear magnitude (TSM) and oscillatory shear index (OSI). WSS directionality was quantified in terms of mean WSS vector magnitude and angle, and angular dispersion index (Da). Local WSS magnitude and multidirectionality were captured in a new shear magnitude and directionality index (SMDI) calculated as the product of the mean WSS magnitude and Da. BAVs subjected the AA to circumferential TSM overloads (2.4-fold increase vs. TAV). TAV and BAV AAs exhibited a unidirectional circumferential WSS (OSI < 0.04) and an increasingly unidirectional longitudinal WSS between the proximal (OSI > 0.21) and middle (OSI < 0.07) sections. BAVs generated mean WSS vectors skewed toward the anterior wall and WSS angular distributions exhibiting decreased uniformity in the proximal AA (0.27-point increase in Dα vs. TAV). SMDI was elevated in all BAV AAs but peaked in the proximal LR-BAV AA (3.6-fold increase vs. TAV) and in themiddle RN-BAV AA (1.6-fold increase vs. TAV). This analysis demonstrates the significance of the circumferential WSS component and the existence of substantial WSS directional abnormalities in BAV AAs. SMDI abnormality distributions in BAV AAs follow the morphotype-dependent occurrence of dilation in BAV AAs, suggesting the predictive potential of this metric for BAV aortopathy. [ABSTRACT FROM AUTHOR]

Patient specific models of ventricular mechanics require the optimization of their many parameters under the uncertainties associated with imaging of cardiac function. We present a strategy to reduce the complexity of parametric searches for 3-D FE models of left ventricular contraction. The study employs automatic image segmentation and analysis of an image database to gain geometric features for several classes of patients. Statistical distributions of geometric parameters are then used to design parametric studies investigating the effects of: (1) passive material properties during ventricular filling, and (2) infarct geometry on ventricular contraction in patients after a heart attack. Gaussian Process regression is used in both cases to build statistical models trained on the results of biophysical FEM simulations. The first statistical model estimates unloaded configurations based on either the intraventricular pressure or the end-diastolic fiber strain. The technique provides an alternative to the standard fixed-point iteration algorithm, which is more computationally expensive when used to unload more than 10 ventricles. The second statistical model captures the effects of varying infarct geometries on cardiac output. For training, we designed high resolution models of non-transmural infarcts including refinements of the border zone around the lesion. This study is a first effort in developing a platform combining HPC models and machine learning to investigate cardiac function in heart failure patients with the goal of assisting clinical diagnostics. [ABSTRACT FROM AUTHOR]

Computational modeling has been used routinely in the pre-clinical development of medical devices such as coronary artery stents. The ability to simulate and predict physiological and structural parameters such as flow disturbance, wall shear-stress, and mechanical strain patterns is beneficial to stent manufacturers. These methods are now emerging as useful clinical tools, used by physicians in the assessment and management of patients. Computational models, which can predict the physiological response to intervention, offer clinicians the ability to evaluate a number of different treatment strategies in silico prior to treating the patient in the cardiac catheter laboratory. For the first time clinicians can perform a patient-specific assessment prior to making treatment decisions. This could be advantageous in patients with complex disease patterns where the optimal treatment strategy is not clear. This article reviews the key advances and the potential barriers to clinical adoption and translation of these virtual treatment planning models. [ABSTRACT FROM AUTHOR]

We previously found that vascular guided wave imaging (VGWI) could non-invasively quantify transmural wall stiffness in both the longitudinal (r-z plane, 0°) and circumferential (r-θ plane, 90°) directions of soft hollow cylinders. Arterial stiffness estimation in multiple directions warrants further comprehensive characterization of arterial health, especially in the presence of asymmetric plaques, but is currently lacking. This study therefore investigated the multidirectional estimation of the arterial Young's modulus in a finite-element model, in vitro artery-mimicking phantoms and an excised porcine aorta. A longitudinal pre-stretch of 20% and/or lumen pressure (15 or 70 mm Hg) was additionally introduced to pre-condition the phantoms for emulating the intrinsic mechanical anisotropy of the real artery. The guided wave propagation was approximated by a zero-order antisymmetric Lamb wave model. Shape factor, which was defined as the ratio of inner radius to thickness, was calculated over the entire segment of each planar cross section of the hollow cylindrical structure at a full rotation (0°-360° at 10° increments) about the radial axis. The view-dependent geometry of the cross segment was found to affect the guided wave propagation, causing Young's modulus overestimation in four angular intervals along the propagation pathway, all of which corresponded to wall regions with low shape factors (<1.5). As validated by mechanical tensile testing, the results indicate not only that excluding the propagation pathway with low shape factors could correct the overestimation of Young's modulus, but also that VGWI could portray the anisotropy of hollow cylindrical structures and the porcine aorta based on the derived fractional anisotropy values from multidirectional modulus estimates. This study may serve as an important step toward 3-D assessment of the mechanical properties of the artery. [ABSTRACT FROM AUTHOR]

Pressure overload and heart failure electrophysiological remodeling (HF-ER) in pigs are associated with decreased conduction velocity (CV) and dispersion of repolarization, which lead to higher risk of ventricular arrhythmia. This work aimed to establish the correlation between QRS complex duration and underlying changes in CV during increased intraventricular pressure (IVP) and/or HF-ER ex-vivo , and to determine whether QRS duration could be sensitive to an acute increase in left ventricular (LV) afterload in-vivo . HF-ER was induced in 7 pigs by high-rate ventricular pacing. Seven weight-matched animals were used as controls. Isolated Langendorff-perfused hearts underwent programmed ventricular stimulation to study QRS complex duration and CV under low/high IVP, using volume-conducted ECG and epicardial optical mapping, respectively. Four additional pigs underwent open-chest surgery to increase LV afterload by partially clamping the ascending aorta, while measuring QRS complex duration during sinus rhythm (SR). In 13 hearts included for analysis, both HF-ER and increased IVP showed significantly slower epicardial CV (−40% and −15%, p < 0.001 and p = 0.004, respectively), which correlated with similar widening of the QRS complex (+41% and +17%, p = 0.005 and p < 0.001, respectively). HF-ER hearts shower larger prolongation of the QRS complex than controls upon increasing the IVP (+21% vs. +12%, respectively. HF-ER*IVP interaction: p = 0.004). QRS complex widened after increasing LV afterload in-vivo ( n = 3 ), with correlation between QRS duration and aortic diastolic pressures (R = 0.58, p < 0.001). In conclusion, high IVP and/or HF-ER significantly decrease CV, which correlates with QRS widening on the ECG during ventricular pacing. Increased myocardial wall stress also widens the QRS complex during SR in-vivo . [ABSTRACT FROM AUTHOR]

Mechanically-induced alterations in cardiac electrophysiology are referred to as mechano-electric feedback (MEF), and play an important role in electrical regulation of cardiac performance. The influence of mechanical stress and strain on electrophysiology has been investigated at all levels, however the role of MEF in arrhythmia remains poorly understood. During the normal contraction of the heart, mechano-sensitive processes are an implicit component of cardiac activity. Under abnormal mechanical events, stretch-activated mechanisms may contribute to local or global changes in electrophysiology (EP). While such mechanisms have been hypothesised to be involved in mechanically-initiated arrhythmias, the details of these mechanisms and their importance remain elusive. We assess the theoretical role of stretch mechanisms using coupled models of cellular electrophysiology and sarcomere contraction dynamics. Using models of single ventricular myocytes, we first investigated the potential MEF contributions of stretch-activated currents (SAC), and stretch-induced myofilament calcium release, to test how strain and fibrosis may alter cellular electrophysiology. For all models investigated, SACs were alone not sufficient to create a pro-arrhythmic perturbation of the action potential with stretch. However, when combined with stretch-induced myofilament calcium release, the action potential could be shortened depending on the timing of the strain. This effect was highly model dependent, with a canine epicardial EP model being the most sensitive. These model results suggest that known mechanisms of mechano-electric coupling in cardiac myocyte may be sufficient to be pro-arrhythmic, but only in combination and under specific strain patterns. [ABSTRACT FROM AUTHOR]

Aim Investigate to what extent low-intensity swim training for six weeks counterbalances the adverse remodeling due to the advance of pathological hypertrophy in the left ventricle (LV) structural and mechanical properties in the early compensated phase of hypertension in male SHR. Main methods Four-month-old male SHR and Wistar rats were randomly divided into Sed (sedentary) and Ex (exercised) groups. The exercised rats were submitted to a swimming protocol (1 h/day, 5 times/week, no additional load) for six weeks. LV tissue and isolated myocytes were used to assess structural and mechanical properties. Myocytes were stimulted at frequencies (F) of 1 and 3 Hz at 37 °C. Key findings Exercised SHR showed improvement in cardiovascular parameters compared to sedentary SHR (mean arterial pressure: 13.22%; resting HR: 14.28.%). About structural and mechanical properties, swim training induced a decrease in LV myocyte thickness (10.85%), number of inflammatory cells (21.24%); collagen type III (74.23%) and type I (85.6%) fiber areas; amplitude of single myocyte shortening (47% to F1 and 28.46% to F3), timecourses of shortening (16.5% to F1 and 7.55% to F3) and relaxation (15.31% to F3) compared to sedentary SHR. Significance Six weeks of swim training attenuates the adverse remodeling of LV structural and mechanical properties in the early compensated phase of hypertension in male SHR. [ABSTRACT FROM AUTHOR]

The aim of this paper is to determine the influence of heating rate on the dynamic mechanical performance of coal measure rocks after heat treatment. Uniaxial compression tests were conducted using a split Hopkinson pressure bar system on coal measure rocks after heat treatment at 800°C at different heating rates. The results reveal that a high-temperature treatment changed the physical and mechanical properties of the sandstone. When the heating rate was increased, the natural and mechanical properties were reduced gradually. The failure mode of sandstone after heat treatment was tension destruction, and shear fracturing occurred locally only at high heating rates. Original cracks grew inside the sandstone after heat treatment, while the number of defects (including cracks and pores) increased gradually with an increased heating rate, which was the main reason for the change in the sandstone’s macromechanical properties. The energy dissipation during fracturing was correlated closely to the fracture characteristics and increased with increased heating rates. The results of this work can provide references for future engineering projects, such as underground coal gasification and coal-bed methane thermal exploitation. [ABSTRACT FROM AUTHOR]

The aortic wall is always loaded in vivo , which makes it challenging to estimate the material parameters of its nonlinear, anisotropic constitutive equation from in vivo image data. Previous approaches largely relied on either computationally expensive finite element models or simplifications of the geometry or material models. In this study, we investigated a new inverse method based on aortic wall stress computation. This approach consists of the following two steps: (1) computing an “almost true” stress field from the in vivo geometries and loading conditions, (2) building an objective function based on the “almost true” stress fields, constitutive equations and deformation relations, and estimating the material parameters by minimizing the objective function. The method was validated through numerical experiments by using the in vivo data from four ascending aortic aneurysm (AsAA) patients. The results demonstrated that the method is computationally efficient. This novel approach may facilitate the personalized biomechanical analysis of aortic tissues in clinical applications, such as in the rupture risk analysis of ascending aortic aneurysms. [ABSTRACT FROM AUTHOR]

Short-term exposure to ambient air pollution is linked with adverse cardiovascular effects. While previous research focused primarily on particulate matter-induced responses, gaseous air pollutants also contribute to cause short-term cardiovascular effects. Mechanisms underlying such effects have not been adequately described, however the immediate nature of the response suggests involvement of irritant neural activation and downstream autonomic dysfunction. Thus, this study examines the role of TRPA1, an irritant sensory receptor found in the airways, in the cardiac response of mice to acrolein and ozone. Conscious unrestrained wild-type C57BL/6 (WT) and TRPA1 knockout (KO) mice implanted with radiotelemeters were exposed once to 3 ppm acrolein, 0.3 ppm ozone, or filtered air. Heart rate (HR) and electrocardiogram (ECG) were recorded continuously before, during and after exposure. Analysis of ECG morphology, incidence of arrhythmia and heart rate variability (HRV) were performed. Cardiac mechanical function was assessed using a Langendorff perfusion preparation 24 h post-exposure. Acrolein exposure increased HRV independent of HR, as well as incidence of arrhythmia. Acrolein also increased left ventricular developed pressure in WT mice at 24 h post-exposure. Ozone did not produce any changes in cardiac function. Neither gas produced ECG effects, changes in HRV, arrhythmogenesis, or mechanical function in KO mice. These data demonstrate that a single exposure to acrolein causes cardiac dysfunction through TRPA1 activation and autonomic imbalance characterized by a shift toward parasympathetic modulation. Furthermore, it is clear from the lack of ozone effects that although gaseous irritants are capable of eliciting immediate cardiac changes, gas concentration and properties play important roles. [ABSTRACT FROM AUTHOR]

Tagged magnetic resonance imaging (tMRI) is a well-established method for evaluating regional mechanical function of the heart. Many techniques have been developed to compute 2D or 3D cardiac deformation and strain from tMRI images. In this paper, we present a new method for measuring 3D plus time biventricular myocardial strain from tMRI data. The method is composed of two parts. First, we use a Gabor filter bank to extract tag points along tag lines. Second, each tag point is classified to one of a set of indexed reference tag lines using a point classification with graph cuts (PCGC) algorithm and a motion compensation technique. 3D biventricular deformation and strain is computed at each image time frame from the classified tag points using a previously published finite difference method. The strain computation is fully automatic after myocardial contours are defined near end-diastole and end-systole. An in-vivo dataset composed of 30 human imaging studies with a range of pathologies was used for validation. Strains computed with the PCGC method with no manual corrections were compared to strains computed from both manually placed tag points and a manually-corrected unwrapped phase method. A typical cardiac imaging study with 10 short-axis slices and 6 long-axis slices required 30 min for contouring followed by 44 min of automated processing. The results demonstrate that the proposed method can reconstruct accurate 3D plus time cardiac strain maps with minimal user intervention. [ABSTRACT FROM AUTHOR]

In this research, a reduced order method (ROM) called the Proper Orthogonal Decomposition with Interpolation (PODI) is used to drastically reduce computation time of highly complex and non-linear problems as encountered in simulating the heart. The idea behind this method is to first construct a database of pre-computed full-scale solutions using the Element Free Galerkin method (EFG) and then project a selected subset of these solutions to a low dimensional space. Using the Moving Least Square method an interpolation is carried out for the problem at hand, before the resulting coefficients are projected back to the original high dimensional solution space. Computations are carried out on a bi-ventricle model to investigate the performance and accuracy varying the material parameters and to determine the sensitivity with respect to the parametric values. The PODI calculations are completed within 1.25 s on a normal desktop machine with the relative ℓ 2 error norm not exceeding 2.5 × 10 − 3 . Hence, it is demonstrated that real-time modelling of the heart can be successfully carried out at acceptable error levels. [ABSTRACT FROM AUTHOR]

Objective We attempted to test the hypothesis that preinduction of heat shock protein (HSP) 72 in the heart would improve left ventricular performance in rat heatstroke. Methods Cardiac expression of HSP 72 was quantitatively evaluated by western blot analysis in rats 0 h, 12 h, or 72 h after mild heat preconditioning (MHP; 43 °C for 30 min). They were subjected to severe heat stress (SHS; 43 °C for 70 min) to induce heatstroke. A 1.2 F catheter-tip pressure transducer was inserted into the left ventricle of these group rats under general anesthesia to record hemodynamic in the closed chest with a pressure–volume loop module data recording and analysis system. Results At the time point of heatstroke onset, compared with normothermic controls, group rats with 12 h post-MHP had significantly increased cardiac HSP 72, decreased hyperthermia, decreased hypotension, decreased bradycardia, increased end-systolic pressure, increased end-diastolic pressure, increased stroke volume, decreased end-systolic volume, decreased end-diastolic pressure, increased cardiac output, increased ejection fraction, increased stroke work, increased arterial elastance, and decreased time constant of fall in ventricular pressure by Glantz-methods. With the loss of cardiac HSP 72 expression observed at 72 h in post-MHP group rats, an insignificant protection against left ventricular performance was observed. Conclusion Preinduction of cardiac HSP 72 may improve hypotension in heatstroke rats by increasing both cardiac mechanical efficiency and arterial elastance. [ABSTRACT FROM AUTHOR]

Injectable hydrogels that resemble electromechanical properties of the myocardium are crucial for cardiac tissue engineering prospects. We have developed a facile approach that uses chitosan (CS) to generate a thermosensitive conductive hydrogel with a highly porous network of interconnected pores. Gold nanoparticles (GNPs) were evenly dispersed throughout the CS matrix in order to provide electrical cues. The gelation response and electrical conductivity of the hydrogel were controlled by different concentrations of GNPs. The CS-GNP hydrogels were seeded with mesenchymal stem cells (MSCs) and cultivated for up to 14 days in the absence of electrical stimulations. CS-GNP scaffolds supported viability, metabolism, migration and proliferation of MSCs along with the development of uniform cellular constructs. Immunohistochemistry for early and mature cardiac markers showed enhanced cardiomyogenic differentiation of MSCs within the CS-GNP compared to the CS matrix alone. The results of this study demonstrate that incorporation of nanoscale electro-conductive GNPs into CS hydrogels enhances the properties of myocardial constructs. These constructs could find utilization for regeneration of other electroactive tissues. [ABSTRACT FROM AUTHOR]

Alterations in energetic state of the myocardium are associated with decompensated heart failure in humans and in animal models. However, the functional consequences of the observed changes in energetic state on mechanical function are not known. The primary aim of the study was to quantify mechanical/energetic coupling in the heart and to determine if energetic dysfunction can contribute to mechanical failure. A secondary aim was to apply a quantitative systems pharmacology analysis to investigate the effects of drugs that target cross-bridge cycling kinetics in heart failure-associated energetic dysfunction. Herein, a model of metabolite- and calcium-dependent myocardial mechanics was developed from calcium concentration and tension time courses in rat cardiac muscle obtained at different lengths and stimulation frequencies. The muscle dynamics model accounting for the effect of metabolites was integrated into a model of the cardiac ventricles to simulate pressure-volume dynamics in the heart. This cardiac model was integrated into a simple model of the circulation to investigate the effects of metabolic state on whole-body function. Simulations predict that reductions in metabolite pools observed in canine models of heart failure can cause systolic dysfunction, blood volume expansion, venous congestion, and ventricular dilation. Simulations also predict that myosin-activating drugs may partially counteract the effects of energetic state on cross-bridge mechanics in heart failure while increasing myocardial oxygen consumption. Our model analysis demonstrates how metabolic changes observed in heart failure are alone sufficient to cause systolic dysfunction and whole-body heart failure symptoms. [ABSTRACT FROM AUTHOR]

Ascending thoracic aortic aneurysm (ATAA) can be a life threatening disease as it leads to a lack of function in most of the connective tissues. Marfan syndrome is a congenital connective tissue disorder that may have influence on the cardiovascular system. It has been shown that Marfan syndrome invokes a degradation of the elastin and collagen content of the aortic wall and, consequently, a remarkable weakness in the mechanical strength of the arterial wall. However, so far, the mechanical properties of the aortic wall due to Marfan syndrome have not been determined. Therefore, this study was aimed to perform a comparative experimental study to quantify the linear elastic and non-linear hyperelastic mechanical properties of the healthy and Marfan syndrome ATA. Eight healthy and Marfan aorta tissues were excised from the human body during invasive cardiac surgery and autopsy respectively. The tissue samples were subjected to the longitudinal and circumferential loadings until breakage occurred. The elastic modulus, maximum stress and strain of the ATA tissues were calculated. The non-linear mechanical behaviour of the ATA tissues was also computationally investigated using Mooney–Rivlin hyperelastic material model. The results showed that the healthy ATA tissues are stiffer in the longitudinal direction compared to the circumferential direction. The highest elastic modulus (764.10 N cm− 2) and maximum stress (298.18 N cm− 2) were observed for the Marfan ATA wall in the longitudinal direction, while the healthy ATA tissues showed the axial elastic modulus and maximum stress of 367.08 and 220.14 N cm− 2respectively. The hyperelastic material model also well defined the non-linear mechanical behaviour of the ATA tissues. These results may have implications not only for understanding the mechanical properties of the healthy and Marfan ATA tissues but also for a wide range of clinical applications, including valve repair or replacement. [ABSTRACT FROM AUTHOR]

Following myocardial infarction (MI), damaged myocytes are replaced by collagenous scar tissue, which serves an important mechanical function – maintaining integrity of the heart wall against enormous mechanical forces – but also disrupts electrical function as structural and electrical remodeling in the infarct and borderzone predispose to re-entry and ventricular tachycardia. Novel emerging regenerative approaches aim to replace this scar tissue with viable myocytes. Yet an alternative strategy of therapeutically modifying selected scar properties may also prove important, and in some cases may offer similar benefits with lower risk or regulatory complexity. Here, we review potential goals for such modifications as well as recent proof-of-concept studies employing specific modifications, including gene therapy to locally increase conduction velocity or prolong the refractory period in and around the infarct scar, and modification of scar anisotropy to improve regional mechanics and pump function. Another advantage of scar modification techniques is that they have applications well beyond MI. In particular, ablation treats electrical abnormalities of the heart by intentionally generating scar to block aberrant conduction pathways. Yet in diseases such as atrial fibrillation (AF) where ablation can be extensive, treating the electrical disorder can significantly impair mechanical function. Creating smaller, denser scars that more effectively block conduction, and choosing the location of those lesions by balancing their electrical and mechanical impacts, could significantly improve outcomes for AF patients. We review some recent advances in this area, including the use of computational models to predict the mechanical effects of specific lesion sets and gene therapy for functional ablation. Overall, emerging techniques for modifying scar properties represents a potentially important set of tools for improving patient outcomes across a range of heart diseases, whether used in place of or as an adjunct to regenerative approaches. [ABSTRACT FROM AUTHOR]

The article offers the author's insights on the role of nitrite (NO2) in mediating the protective effect of ischemic preconditioning (IPC) and remote ischemic preconditioning (RIPC) to heart. Topics mentioned include the technique for attenuating the ischemic reperfusion injury (IRI) severity, the protection to distant organs by the RIPC, and the diagram that show the mechanism on how generated nitrite attenuates cytokine production and inflammasomes activation in the heart.

Background: Disruption of pulmonary vasculogenesis occurs in bronchopulmonary dysplasia (BPD). Increased impedance to pulmonary flow secondary to abnormal vascular development may affect ventricular mechanics. Objectives: We aimed to test the hypothesis that cardiac mechanics are altered in prematurely born children with BPD. Methods: A cohort of 47 children was studied: 22 aged 48.9 ± 6.4 months born preterm with BPD (group I), 13 aged 46.3 ± 8.1 months born preterm without BPD (group II), and 12 healthy children aged 53.4 ± 12.2 months born at term (group III). Left (LV) and right ventricular (RV) strain and strain rate were assessed by speckle-tracking echocardiography. Results: The global RV systolic strain rate (p = 0.022) was significantly lower, while RV systolic strain (p = 0.05) and early diastolic strain rate (p = 0.05) and LV longitudinal systolic strain rate (p = 0.06) also tended to be lower in group I than group III. Group I also tended to have lower RV systolic strain (p = 0.09) and early diastolic strain rate (p = 0.049) and LV longitudinal systolic strain rate (p = 0.08) than group II. An increasing trend from group I to III was observed for RV lateral wall and septal systolic strain and strain rate (all p < 0.05). The LV but not RV size was significantly smaller in group I compared with group III (p < 0.05). Multiple regression identified duration of invasive ventilation (β = -0.66, p = 0.032) as an independent determinant of RV systolic strain after adjustment for perinatal risk factors. Conclusion: Impairment of RV myocardial deformation occurs in children with BPD, the magnitude of which is associated negatively with the duration of invasive ventilation. © 2015 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Models of cardiac mechanics are increasingly used to investigate cardiac physiology. These models are characterized by a high level of complexity, including the particular anisotropic material properties of biological tissue and the actively contracting material. A large number of independent simulation codes have been developed, but a consistent way of verifying the accuracy and replicability of simulations is lacking. To aid in the verification of current and future cardiac mechanics solvers, this study provides three benchmark problems for cardiac mechanics. These benchmark problems test the ability to accurately simulate pressure-type forces that depend on the deformed objects geometry, anisotropic and spatially varying material properties similar to those seen in the left ventricle and active contractile forces. The benchmark was solved by 11 different groups to generate consensus solutions, with typical differences in higher-resolution solutions at approximately 0.5%, and consistent results between linear, quadratic and cubic finite elements as well as different approaches to simulating incompressible materials. Online tools and solutions are made available to allow these tests to be effectively used in verification of future cardiac mechanics software. [ABSTRACT FROM AUTHOR]

Objective: The aim of this study was to evaluate the relationship between atrial electromechanical delay (EMD) measured with tissue Doppler imaging (TDI) and left atrial (LA) mechanical functions in patients with ischemic stroke and compare them with healthy controls. Methods: Thirty patients with ischemic stroke were enrolled into this cross-sectional, observational study. The control group consisted of 35 age- and gender-matched apparently healthy individuals patients. Acute cerebral infarcts of probable embolic origin were diagnosed via imaging and were confirmed by a neurologist. Echocardiographically, time intervals from the beginning of P wave to beginning of A wave from the lateral and septal mitral and right ventricular tricuspid annuli in TDI were recorded. The differences between these intervals gave the mechanical delays (inter- and intra-atrial). Left atrial (LA) volumes were measured using the biplane area-length method, and LA mechanical function parameters were calculated. Statistical analysis was performed using student's t-test, chi-squared test, and Pearson's test. Results: The laboratory and clinical characteristics were similar in the two groups. Increased left atrial EMD (21.36±10.38 ms versus 11.74±6.06 ms, p<0.001), right atrial EMD (13.66±8.62 ms versus 9.66±6.81 ms, p=0.040), and interatrial EMD (35.03±9.95 ms versus 21.40±8.47 ms, p<0.001) were observed in stroke patients as compared to controls. Active LA emptying volume and fraction and passive LA emptying volumes and fraction were similar between controls and stroke patients. Total LA emptying volumes were significantly increased in stroke patients as compared to healthy controls (33.19±11.99 mL/m2 versus 27.48±7.08 mL/m2, p=0.021). Conclusion: According to the results of our study, interatrial electromechanical delay may be a new predictor for ischemic stroke. [ABSTRACT FROM AUTHOR]

Myocardial infarction (MI) triggers a series of maladaptive events that lead to structural and functional changes in the left ventricle. It is crucial to better understand the progression of adverse remodeling, in order to develop effective treatment. In addition, being able to assess changes in vivo would be a powerful tool in the clinic. The goal of the current study is to quantify the in vivo material properties of infarcted and remote myocardium 1 week after MI, as well as the orientation of collagen fibers in the infarct. This will be accomplished by using a combination of magnetic resonance imaging (MRI), catheterization, finite element modeling, and numerical optimization to analyze a porcine model ( $$N = 4$$ ) of posterolateral myocardial infarction. Specifically, properties will be determined by minimizing the difference between in vivo strains and volume calculated from MRI and finite element model predicted strains and volume. The results indicate that the infarct region is stiffer than the remote region and that the infarct collagen fibers become more circumferentially oriented 1 week post-MI. These findings are consistent with previous studies, which employed ex vivo techniques. The proposed methodology will ultimately provide a means of predicting remote and infarct mechanical properties in vivo at any time point post-MI. [ABSTRACT FROM AUTHOR]

This paper is concerned with the mathematical analysis of a coupled elliptic-parabolic system modeling the interaction between the propagation of electric potential and subsequent deformation of the cardiac tissue. The problem consists in a reaction-diffusion system governing the dynamics of ionic quantities, intra- and extra-cellular potentials, and the linearized elasticity equations are adopted to describe the motion of an incompressible material. The coupling between muscle contraction, biochemical reactions and electric activity is introduced with a so-called active strain decomposition framework, where the material gradient of deformation is split into an active (electrophysiology-dependent) part and an elastic (passive) one. Under the assumption of linearized elastic behavior and a truncation of the updated nonlinear diffusivities, we prove existence of weak solutions to the underlying coupled reaction-diffusion system and uniqueness of regular solutions. The proof of existence is based on a combination of parabolic regularization, the Faedo-Galerkin method, and the monotonicity-compactness method of Lions. A finite element formulation is also introduced, for which we establish existence of discrete solutions and show convergence to a weak solution of the original problem. We close with a numerical example illustrating the convergence of the method and some features of the model. [ABSTRACT FROM AUTHOR]

Background Rewarming from hypothermia is often complicated by cardiac dysfunction, characterized by substantial reduction in stroke volume. Previously we have reported that inotropic agents, working via cardiac β-receptor agonism may exert serious side effects when applied to treat cardiac contractile dysfunction during rewarming. In this study we tested whether Milrinone, a phosphodiesterase III inhibitor, is able to ameliorate such dysfunction when given during rewarming. Methods A rat model designed for circulatory studies during experimental hypothermia with cooling to a core temperature of 15 °C, stable hypothermia at this temperature for 3 h and subsequent rewarming was used, with a total of 3 groups: (1) a normothermic group receiving Milrinone, (2) a hypothermic group receiving Milrinone the last hour of hypothermia and during rewarming, and (3) a hypothermic saline control group. Hemodynamic function was monitored using a conductance catheter introduced to the left ventricle. Results After rewarming from 15 °C, stroke volume and cardiac output returned to within baseline values in Milrinone treated animals, while these variables were significantly reduced in saline controls. Conclusions Milrinone ameliorated cardiac dysfunction during rewarming from 15 °C. The present results suggest that at low core temperatures and during rewarming from such temperatures, pharmacologic efforts to support cardiovascular function is better achieved by substances preventing cyclic AMP breakdown rather than increasing its formation via β-receptor stimulation. [ABSTRACT FROM AUTHOR]

In the wide literature devoted to the cardiac structural mechanics, the strain energy proposed by Holzapfel and Ogden exhibits a number of interesting features: it has suitable mathematical properties and it is based on few material parameters that can, in principle, be identified by standard laboratory tests. In this work we illustrate the implementation of a numerical solver based on such a model for both the passive and active mechanics of the heart. Moreover we discuss its performance on a few tests that can be regarded as preliminary to the adoption of the Holzapfel–Ogden model for a real cardiac simulation. While the passive behavior of the cardiac muscle is modeled as an orthotropic hyperelastic material, the active contraction is here accounted for a multiplicative decomposition of the deformation gradient, yielding the so–called “active strain” approach, a formulation that automatically preserves the ellipticity of the stress tensor and introduces just one extra parameter in the model. We adopt the usual volumetric–isochoric decomposition of the stress tensor to obtain a mathematically consistent quasi–incompressible version of the material, then the numerical approximation applies to a classical Hu–Washizu three fields formulation. After introduction of the tangent problem, we select suitable finite element spaces for the representation of the physical fields. Boundary conditions are prescribed by introduction of a Lagrange multiplier. The robustness and performance of the numerical solver are tested versus a novel benchmark test, for which an exact solution is provided. The curvature data obtained from the free contraction of muscular thin films are used to fit the active contraction parameter. [ABSTRACT FROM AUTHOR]

The complex phenomena underlying mechanical contraction of cardiac cells and their influence in the dynamics of ventricular contraction are extremely important in understanding the overall function of the heart. In this paper we generalize previous contributions on the active strain formulation and propose a new model for the excitation-contraction coupling process. We derive an evolution equation for the active fiber contraction based on configurational forces, which is thermodynamically consistent. Geometrically, we link microscopic and macroscopic deformations giving rise to an orthotropic contraction mechanism that is able to represent physiologically correct thickening of the ventricular wall. A series of numerical tests highlights the importance of considering orthotropic mechanical activation in the heart and illustrates the main features of the proposed model. [ABSTRACT FROM AUTHOR]

The heart is not only our most vital, but also our most complex organ: Precisely controlled by the interplay of electrical and mechanical fields, it consists of four chambers and four valves, which act in concert to regulate its filling, ejection, and overall pump function. While numerous computational models exist to study either the electrical or the mechanical response of its individual chambers, the integrative electro-mechanical response of the whole heart remains poorly understood. Here we present a proof-of-concept simulator for a four-chamber human heart model created from computer topography and magnetic resonance images. We illustrate the governing equations of excitation–contraction coupling and discretize them using a single, unified finite element environment. To illustrate the basic features of our model, we visualize the electrical potential and the mechanical deformation across the human heart throughout its cardiac cycle. To compare our simulation against common metrics of cardiac function, we extract the pressure–volume relationship and show that it agrees well with clinical observations. Our prototype model allows us to explore and understand the key features, physics, and technologies to create an integrative, predictive model of the living human heart. Ultimately, our simulator will open opportunities to probe landscapes of clinical parameters, and guide device design and treatment planning in cardiac diseases such as stenosis, regurgitation, or prolapse of the aortic, pulmonary, tricuspid, or mitral valve. [ABSTRACT FROM AUTHOR]

Computational models have huge potential to improve our understanding of the coupled biological, electrical, and mechanical underpinning mechanisms of cardiac function and diseases. This contribution is concerned with the computational modeling of different cardiac dysfunctions related to the excitation–contraction coupling in the heart. To this end, the coupled problem of cardiac electromechanics is formulated through the conservation of linear momentum equation and the excitation equation formulated in the Eulerian setting and solved monolithically through an entirely finite element-based implicit algorithm. To model the electromechanical coupling, we use the recently proposed, novel generalized Hill model that is based on the multiplicative decomposition of the deformation gradient into the active and passive parts and on the additive split of the free energy function. This framework enables us to combine the advantageous features of the active-stress and the active-strain models suggested in literature. The proposed coupled approach is further supplemented by the Windkesel-based model to account for the pressure evolution within the ventricular chambers during the cardiac cycle. This allows us to generate the pressure–volume curves as a diagnostic tool to detect possible cardiac dysfunctions and to assess the efficiency of the heart function. The proposed model is employed to investigate different pathological cases that include infarction, eccentric hypertrophy, and concentric hypertrophy. The effects of these distinct cardiac dysfunctions on the pressure–volume curves and on the overall excitation–contraction of the heart are computationally examined and compared to the clinical observations reported in literature. [ABSTRACT FROM AUTHOR]

Abstract: In the past few years, a considerable amount of effort has been devoted toward the development of biomimetic scaffolds for cardiac tissue engineering. However, most of the previous scaffolds have been electrically insulating or lacked the structural and mechanical robustness to engineer cardiac tissue constructs with suitable electrophysiological functions. Here, we developed tough and flexible hybrid scaffolds with enhanced electrical properties composed of carbon nanotubes (CNTs) embedded aligned poly(glycerol sebacate):gelatin (PG) electrospun nanofibers. Incorporation of varying concentrations of CNTs from 0 to 1.5% within the PG nanofibrous scaffolds (CNT–PG scaffolds) notably enhanced fiber alignment and improved the electrical conductivity and toughness of the scaffolds while maintaining the viability, retention, alignment, and contractile activities of cardiomyocytes (CMs) seeded on the scaffolds. The resulting CNT–PG scaffolds resulted in stronger spontaneous and synchronous beating behavior (3.5-fold lower excitation threshold and 2.8-fold higher maximum capture rate) compared to those cultured on PG scaffold. Overall, our findings demonstrated that aligned CNT–PG scaffold exhibited superior mechanical properties with enhanced CM beating properties. It is envisioned that the proposed hybrid scaffolds can be useful for generating cardiac tissue constructs with improved organization and maturation. [Copyright &y& Elsevier]

Following myocardial infarction, damaged muscle is gradually replaced by collagenous scar tissue. The structural and mechanical properties of the scar are critical determinants of heart function, as well as the risk of serious post-infarction complications such as infarct rupture, infarct expansion, and progression to dilated heart failure. A number of therapeutic approaches currently under development aim to alter infarct mechanics in order to reduce complications, such as implantation of mechanical restraint devices, polymer injection, and peri-infarct pacing. Because mechanical stimuli regulate scar remodeling, the long-term consequences of therapies that alter infarct mechanics must be carefully considered. Computational models have the potential to greatly improve our ability to understand and predict how such therapies alter heart structure, mechanics, and function over time. Toward this end, we developed a straightforward method for coupling an agent-based model of scar formation to a finite-element model of tissue mechanics, creating a multi-scale model that captures the dynamic interplay between mechanical loading, scar deformation, and scar material properties. The agent-based component of the coupled model predicts how fibroblasts integrate local chemical, structural, and mechanical cues as they deposit and remodel collagen, while the finite-element component predicts local mechanics at any time point given the current collagen fiber structure and applied loads. We used the coupled model to explore the balance between increasing stiffness due to collagen deposition and increasing wall stress due to infarct thinning and left ventricular dilation during the normal time course of healing in myocardial infarcts, as well as the negative feedback between strain anisotropy and the structural anisotropy it promotes in healing scar. The coupled model reproduced the observed evolution of both collagen fiber structure and regional deformation following coronary ligation in the rat, and suggests that fibroblast alignment in the direction of greatest stretch provides negative feedback on the level of anisotropy in a scar forming under load. In the future, this coupled model may prove useful in computational design and screening of novel therapies to influence scar formation in mechanically loaded tissues. [ABSTRACT FROM AUTHOR]

Advances in material science techniques and pioneering circuit designs have led to the development of electronic membranes that can form intimate contacts with biological tissues. In this review, we present the range of geometries, sensors, and actuators available for custom configurations of electronic membranes in cardiac applications. Additionally, we highlight the desirable mechanics achieved by such devices that allow the circuits and substrates to deform with the beating heart. These devices unlock opportunities to collect continuous data on the electrical, metabolic, and mechanical state of the heart as well as a platform on which to develop high definition therapeutics. [ABSTRACT FROM AUTHOR]

Stretch-induced arrhythmias are multi-scale phenomena in which alterations in channel activities and/or calcium handling lead to the organ level derangement of the heart rhythm. To understand how cellular mechano-electric coupling (MEC) leads to stretch-induced arrhythmias at the organ level, we developed stretching devices and optical voltage/calcium measurement techniques optimized to each cardiac level. This review introduces these experimental techniques of (1) optical voltage measurement coupled with a carbon-fiber technique for single isolated cardiomyocytes, (2) optical voltage mapping combined with motion tracking technique for myocardial tissue/whole heart preparations and (3) real-time calcium imaging coupled with a laser optical trap technique for cardiomyocytes. Following the overview of each methodology, results are presented. We conclude that individual MEC in cardiomyocytes can be heterogeneous at the ventricular level, especially when moderate amplitude mechanical stretches are applied to the heart, and that this heterogeneous MEC can evoke focal excitation that develops into re-entrant arrhythmias. [ABSTRACT FROM AUTHOR]

Aortic valve endothelial cells (ECs) function in vastly different levels of shear stress. The biomechanical characteristics of cells on each side of valve have not been investigated. We assessed the morphology and mechanical properties of cultured or native valve ECs on intact porcine aortic valve cusps using a scanning ion conductance microscope (SICM). The autocrine influence of several endothelial-derived mediators on cell compliance and the expression of actin were also examined. Cells on the aortic side of the valve are characterized by a more elongated shape and were aligned along a single axis. Measurement of EC membrane compliance using the SICM showed that the cells on the aortic side of intact valves were significantly softer than those on the ventricular side. A similar pattern was seen in cultured cells. Addition of 10~6 M of the nitric oxide donor sodium nitroprusside caused a significant reduction in the compliance of ventricular ECs but had no effect on cells on the aortic side of the valve. Conversely, endothelin-1 (10~10-10~8 M) caused an increase in the compliance of aortic cells but had no effect on cells on the ventricular side of the valve. Aortic side EC compliance was also increased by 10 ~4 M of the nitric oxide synthase inhibitor N°-nitro-L-arginine methyl ester. Immunofluorescent staining of actin filaments revealed a great density of staining in ECs on the ventricular surface. The expression of actin and the relative membrane compliance of ECs on both side of the valve were not affected by ventricular and aortic patterns of flow. This study has shown side-specific differences in the biomechanics of aortic valve ECs. These differences can have important implications for valve function. [ABSTRACT FROM AUTHOR]

Highlights: [•] A finite element displacement formulation stemming from the Perturbed Lagrangian. [•] The efficiency is enhanced with a Shamanskii–Newton–Raphson scheme. [•] Comparison with Perturbed Lagrangian, Lagrange Multiplier and penalty methods. [•] Presence of locking in the penalty method, for whole-cycle cardiac mechanics. [•] The presented form combines good convergence behavior with a simplified structure. [Copyright &y& Elsevier]

Ski boot quality is determined by mechanical properties and comfort. Comfort is strongly affected by cold feet. The purpose of this study was to determine the microclimate in ski boots. Climate chamber tests with five male subjects and field tests with two male subjects were conducted. Temperature and relative humidity were measured using four sensors placed on the foot and one on the liner. Absorbed water in liners and socks was measured with a precision balance. The subjects gave subjective ratings for comfort. The toe sensor temperature dropped below 20 °C at an ambient temperature of 0 °C, −10 °C, and −20 °C. Relative humidity values at the foot were as high as 78% in the climate chamber and 93% in the field. Water absorption in socks and liners ranged from 4 to 10 g in the climate chamber and 19 to 45.5 g in the field. The results reveal the importance of keeping the feet and in particular the toes warm during skiing. One possible improvement may be to construct the liner so that sweat and melted snow are kept as far away as possible from the foot. Liner material with high water absorption capacity and hydrophobic socks were suggested to prevent wet feet. [ABSTRACT FROM AUTHOR]

The major risks of pacemaker and implantable cardioverter defibrillator extraction are attributable to the fibrotic tissue that encases them in situ, yet little is known about the cellular and functional properties of this response. In the present research, we performed a histological and mechanical analysis of human tissue collected from the lead–tissue interface to better understand this process and provide insights for the improvement of lead design and extraction. The lead–tissue interface consisted of a thin cellular layer underlying a smooth, acellular surface, followed by a circumferentially organized collagen-rich matrix. 51.8±4.9% of cells were myofibroblasts via immunohistochemistry, with these cells displaying a similar circumferential organization. Upon mechanical testing, samples exhibited a triphasic force–displacement response consisting of a toe region during initial tensioning, a linear elastic region and a yield and failure region. Mean fracture load was 5.6±2.1N, and mean circumferential stress at failure was 9.5±4.1MPa. While the low cellularity and fibrotic composition of tissue observed herein is consistent with a foreign body reaction to an implanted material, the significant myofibroblast response provides a mechanical explanation for the contractile forces complicating extractions. Moreover, the tensile properties of this tissue suggest the feasibility of circumferential mechanical tissue disruption, similar to balloon angioplasty devices, as a novel approach to assist with lead extraction. [ABSTRACT FROM AUTHOR]

Objectives: Using cardiac magnetic resonance (CMR), we sought to evaluate the relative influences of mechanical, electrical, and scar properties at the left ventricular lead position (LVLP) on cardiac resynchronization therapy (CRT) response and clinical events. Background: CMR cine displacement encoding with stimulated echoes (DENSE) provides high-quality strain for overall dyssynchrony (circumferential uniformity ratio estimate [CURE] 0 to 1) and timing of onset of circumferential contraction at the LVLP. CMR DENSE, late gadolinium enhancement, and electrical timing together could improve upon other imaging modalities for evaluating the optimal LVLP. Methods: Patients had complete CMR studies and echocardiography before CRT. CRT response was defined as a 15% reduction in left ventricular end-systolic volume. Electrical activation was assessed as the time from QRS onset to LVLP electrogram (QLV). Patients were then followed for clinical events. Results: In 75 patients, multivariable logistic modeling accurately identified the 40 patients (53%) with CRT response (area under the curve: 0.95 [p < 0.0001]) based on CURE (odds ratio [OR]: 2.59/0.1 decrease), delayed circumferential contraction onset at LVLP (OR: 6.55), absent LVLP scar (OR: 14.9), and QLV (OR: 1.31/10 ms increase). The 33% of patients with CURE <0.70, absence of LVLP scar, and delayed LVLP contraction onset had a 100% response rate, whereas those with CURE ≥0.70 had a 0% CRT response rate and a 12-fold increased risk of death; the remaining patients had a mixed response profile. Conclusions: Mechanical, electrical, and scar properties at the LVLP together with CMR mechanical dyssynchrony are strongly associated with echocardiographic CRT response and clinical events after CRT. Modeling these findings holds promise for improving CRT outcomes. [Copyright &y& Elsevier]

It has been hypothesized that myofiber orientation adapts to achieve a preferred mechanical loading state in the myocardial tissue. Earlier studies tested this hypothesis in a combined model of left ventricular (LV) mechanics and remodeling of myofiber orientation in response to fiber cross-fiber shear, assuming synchronous timing of activation and uniaxial active stress development. Differences between computed and measured patterns of circumferential-radial shear strain Ecr were assumed to be caused by limitations in either the LV mechanics model or the myofiber reorientation model. Therefore, we extended the LV mechanics model with a physiological transmural and longitudinal gradient in activation pattern and with triaxial active stress development. We investigated the effects on myofiber reorientation, LV function, and deformation. The effect on the developed pattern of the transverse fiber angle βt,0 and the effect on global pump function were minor. Triaxial active stress development decreased amplitudes of Ecr towards values within the experimental range and resulted in a similar base-to-apex gradient during ejection in model computed and measured Ecr. The physiological pattern of mechanical activation resulted in better agreement between computed and measured strain in myofiber direction, especially during isovolumic contraction phase and first half of ejection. In addition, remodeling was favorable for LV pump and myofiber function. In conclusion, the outcome of the combined model of LV mechanics and remodeling of myofiber orientation is found to become more physiologic by extending the mechanics model with triaxial active stress development and physiological activation pattern. [ABSTRACT FROM AUTHOR]