1,720,982 research outputs found
A protective device for monorenal subjects or subjects with renal disease
There is described a protective device (1) for monorenal subjects or subjects with renal disease comprising : - a garment (2) wearable by a subject (P) at least at a lumbar region (L) of the subject (P) - at least one protective element (4) installed on said garment (2) at a portion thereof configured to be positioned at the lumbar region (L) of the subject (P) when the garment (2) is worn by the subject (P) - a belt element (6) configured to at least partially encircle the torso of the subject (P) in the lumbar region (L) and to exert a compressive action of the at least one protective element (4) against the lumbar region (L) of the subject (P)
In silico approaches for transcatheter aortic valve replacement inspection
Introduction: Increasing applications of transcatheter aortic valve replacement (TAVR) to treat high- or medium-risk patients with aortic diseases have been proposed in recent years. Despite its increasing use, many influential factors are still to be understood. Furthermore, innovative applications of TAVR such as in bicuspid aortic valves or in low-risk patients are emerging in clinical use. Numerical analyses are increasingly used to reproduce clinical treatments. The future trends in this area are foreseen for in silico trials and personalized medicine. Areas covered: This review paper analyzes the recent years (Jan 2018–Aug 2020) of in silico studies simulating the behavior of transcatheter aortic valves with emphasis on the addressed clinical question and the used modeling strategies. The manuscripts are firstly classified based on their clinical hypothesis. A second classification is based on the adopted modeling approach in terms of patient domain, device modeling, and inclusion or exclusion of the fluid domain. Expert opinion: The TAVR can be virtually performed in numerous vessel geometries and with different devices. This versatility allows a rapid evaluation of the feasibility of different implantation approaches for specific patients, and patient populations, resulting in faster and safer introduction or optimization of new treatments or devices
An electrophysiologic computational model of the zebrafish heart
In recent years there has been a growing interest in the zebrafish thanks to its physiological characteristics similar to humans '. The following work aims to create a full electrophysiological computational model of the zebrafish heart with the ultimate purpose of assessing the influence of pathologies and drug administration. The model considers a full body and the two-chambers of a 3 days post fertilization zebrafish. A four-variable phenomenological Action Potential model is used to describe the action potential of different regions of the heart. Tissue conductivity has been calibrated in order to reproduce the activation sequence described in literature. This model allows the evaluation of the main electrophysiological parameters in terms of activation sequence and timing, AP morphology (i.e., APD{90}, AP amplitude, maximum and minimum AP derivatives), and ECG morphology (i.e., P-wave, T-wave, and QRS-complex amplitudes and durations)
Influence of the Stimulation Current on the Differences between Cell and Tissue Electrophysiological Simulations
This study compares stimulation waveforms for single-cell simulations. The alternatives include monophasic and biphasic current pulses, and a new waveform that resembles the transmembrane current responsible for conduction in tissue. Results indicate that the new stimulation produces the lowest mismatch between action potential markers simulated in cell and in tissue. In comparison with the monophasic stimulation, the new stimulation reduced cell-fiber differences by 99% for triangulation, by 95% for maximum transmembrane voltage, and by 76% for the maximum voltage slope. In conclusion, the new stimulation waveform could help to improve the trustworthiness of single-cell simulations in studies involving tissue-derived markers
Effect of myofibril architecture on the active contraction of dystrophic muscle. A mathematical model
Duchenne muscular dystrophy (DMD) is a muscle degenerative disease caused by a mutation in the dystrophin gene. The lack of dystrophin leads to persistent inflammation, degeneration/regeneration cycles of muscle fibers, Ca2+ dysregulation, incompletely regenerated fibers, necrosis, fibrotic tissue replacement, and alterations in the fiber ultrastructure i.e., myofibril misalignment and branched fibers. This work aims to develop a comprehensive chemo-mechanical model of muscle-skeletal tissue accounting for dispersion in myofibrillar orientations, in addition to the disorders in sarcomere pattern and the fiber branching. The model results confirm a significant correlation between the myofibrillar dispersion and the reduction of isometric force in the dystrophic muscle and indicate that the reduction of contraction velocity in the dystrophic muscle seems to be associated with the local disorders in the sarcomere patterns of the myofibrils. Also, the implemented model can predict the force–velocity response to both concentric and eccentric loading. The resulting model represents an original approach to account for defects in the muscle ultrastructure caused by pathologies as DMD
Analysis of vulnerability to reentry in acute myocardial ischemia using a realistic human heart model
Electrophysiological alterations of the myocardium caused by acute ischemia constitute a pro-arrhythmic substrate for the generation of potentially lethal arrhythmias. Experimental evidence has shown that the main components of acute ischemia that induce these electrophysiological alterations are hyperkalemia, hypoxia (or anoxia in complete artery occlusion), and acidosis. However, the influence of each ischemic component on the likelihood of reentry is not completely established. Moreover, the role of the His-Purkinje system (HPS) in the initiation and maintenance of arrhythmias is not completely understood. In the present work, we investigate how the three components of ischemia affect the vulnerable window (VW) for reentry using computational simulations. In addition, we analyze the role of the HPS on arrhythmogenesis. A 3D biventricular/torso human model that includes a realistic geometry of the central and border ischemic zones with one of the most electrophysiologically detailed model of ischemia to date, as well as a realistic cardiac conduction system, were used to assess the VW for reentry. Four scenarios of ischemic severity corresponding to different minutes after coronary artery occlusion were simulated. Our results suggest that ischemic severity plays an important role in the generation of reentries. Indeed, this is the first 3D simulation study to show that ventricular arrhythmias could be generated under moderate ischemic conditions, but not in mild and severe ischemia. Moreover, our results show that anoxia is the ischemic component with the most significant effect on the width of the VW. Thus, a change in the level of anoxia from moderate to severe leads to a greater increment in the VW (40 ms), in comparison with the increment of 20 ms and 35 ms produced by the individual change in the level of hyperkalemia and acidosis, respectively. Finally, the HPS was a necessary element for the generation of approximately 17% of reentries obtained. The retrograde conduction from the myocardium to HPS in the ischemic region, conduction blocks in discrete sections of the HPS, and the degree of ischemia affecting Purkinje cells, are suggested as mechanisms that favor the generation of ventricular arrhythmias
Why Does Extracellular Potassium Rise in Acute Ischemia? Insights from Computational Simulations
Hyperkalemia, acidosis and hypoxia are the three main components of acute myocardial ischemia. In particular, the increase of extracellular K+ concentration (hyperkalemia), has been proved to be very proarrhythmic because it sets the stage for ventricular fibrillation. However, the intimate mechanisms remain partially unknown. The aim of this work was to investigate, using computational simulation, the relationship between the different phases of hiperkalemia, the activity of the ion channels and the changes related to the action potential in the absence of coronary flow. Our results show that the partial inhibition of the sodium-potassium pump is the main cause of extracellular potassium accumulation. However, the cause of the plateau phase could be due to the appearance of action potential alternans, which reduces the net potassium efflux and limits the increase of extracellular potassium concentration
A Novel Model of Acute Myocardial Ischemia in Human Ventricular Cardiomyocytes
Acute myocardial ischemia is known to be a pathology with a high mortality worldwide. In the last decades, computational simulation has been a widely used tool to study the electrophysiological effects of ischemia. In this work, we present an up-to-date model of the effects of myocardial ischemia in the action potential which includes more ischemia-affected current alterations than any other previously published model. The model was used to simulate action potentials during a 10-minute period of dynamic ischemia, and the main biomarkers of the action potential were monitored, as well as the extracellular potassium elevation. The results agree with those obtained experimentally, suggesting that the model can be useful for 3D simulations of acute myocardial ischemia
A comparison of regional classification strategies implemented for the population based approach to modelling atrial fibrillation
(1) Background: in silico models are increasingly relied upon to study the mechanisms of atrial fibrillation. Due to the complexity associated with atrial models, cellular variability is often ignored. Recent studies have shown that cellular variability may have a larger impact on electrophysiological behaviour than previously expected. This paper compares two methods for AF remodelling using regional populations. (2) Methods: using 200,000 action potentials, experimental data was used to calibrate healthy atrial regional populations with two cellular models. AF remodelling was applied by directly adjusting maximum channel conductances. AF remodelling was also applied through adjusting biomarkers. The methods were compared upon replication of experimental data. (3) Results: compared to the percentage method, the biomarker approach resulted in smaller changes. RMP, APD20, APD50, and APD90 were changed in the percentage method by up to 11%, 500%, 50%, and 60%, respectively. In the biomarker approach, RMP, APD20, APD50, and APD90 were changed by up to 4.5%, 132%, 50%, and 35%, respectively. (4) Conclusion: applying AF remodelling through biomarker-based clustering resulted in channel conductance changes that were consistent with experimental data, while maintaining the highly non-linear relationships between channel conductances and biomarkers. Directly changing conductances in the healthy regional populations impacted the non-linear relationships and resulted in non-physiological APD20 and APD50 values
The impact of calcification patterns in transcatheter aortic valve performance: a fluid-structure interaction analysis
Transcatheter aortic valve replacement (TAVR) strongly depends on the calcification patterns, which may lead to a malapposition of the stented valve and complication onsets in terms of structure kinematics and paravalvular leakage (PVL). From one anatomical-resembling model of the aortic root, six configurations with different calcific deposits were built. TAVR fluid-structure interaction simulations predicted different outcomes for the different calcifications patterns in terms of the final valve configuration in the implantation site and the PVL estimations. In particular models with deposits along the cups coaptation resulted in mild PVL, while those with deposits along the attachment line in moderate PVL
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