BackgroundThe use of telehealth steadily increases as it has become a viable modality to patient care. Early adopters attempt to use telehealth to deliver high-quality care. Patient satisfaction is a key indicator of how well the telemedicine modality met patient expectations.ObjectiveThe objective of this systematic review and narrative analysis is to explore the association of telehealth and patient satisfaction in regards to effectiveness and efficiency.MethodsBoolean expressions between keywords created a complex search string. Variations of this string were used in Cumulative Index of Nursing and Allied Health Literature and MEDLINE.Results2193 articles were filtered and assessed for suitability (n=44). Factors relating to effectiveness and efficiency were identified using consensus. The factors listed most often were improved outcomes (20%), preferred modality (10%), ease of use (9%), low cost 8%), improved communication (8%) and decreased travel time (7%), which in total accounted for 61% of occurrences.ConclusionThis review identified a variety of factors of association between telehealth and patient satisfaction. Knowledge of these factors could help implementers to match interventions as solutions to specific problems.

Chaste ('Cancer, heart and soft-tissue environment') is a software library and a set of test suites for computational simulations in the domain of biology. Current functionality has arisen from modelling in the fields of cancer, cardiac physiology and soft-tissue mechanics. It is released under the LGPL 2.1 licence. Chaste has been developed using agile programming methods. The project began in 2005 when it was reasoned that the modelling of a variety of physiological phenomena required both a generic mathematical modelling framework, and a generic computational/simulation framework. The Chaste project evolved from the Integrative Biology (IB) e-Science Project, an inter-institutional project aimed at developing a suitable IT infrastructure to support physiome-level computational modelling, with a primary focus on cardiac and cancer modelling. Program summaryProgram title: Chaste Catalogue identifier: AEFD_v1_0 Program summary URL:

Abstract-Although effects of shock strength and waveform on cardiac vulnerability to electric shocks have been extensively documented, the contribution of ventricular anatomy to shock-induced polarization and postshock propagation and thus, to shock outcome, has never been quantified; this is caused by lack of experimental methodology capable of mapping 3-D electrical activity. The goal of this study was to use optical imaging experiments and 3-D bidomain simulations to investigate the role of structural differences between left and right ventricles in vulnerability to electric shocks in rabbit hearts. The ventricles were paced apically, and uniform-field, truncated-exponential, monophasic shocks of reversed polarity were applied over a range of coupling intervals (CIs) in experiment and model. Experiments and simulations revealed that reversing the direction of externally-applied field (RVϪ or LVϪ shocks) alters the shape of the vulnerability area (VA), the 2-D grid encompassing episodes of arrhythmia induction. For RVϪ shocks, VA was nearly rectangular indicating little dependence of postshock arrhythmogenesis on CI. For LVϪ shocks, the probability of arrhythmia induction was higher for longer than for shorter CIs. The 3-D simulations demonstrated that these effects stem from the fact that reversal of field direction results in relocation of the main postshock excitable area from LV wall (RVϪ shocks) to septum (LVϪ shocks). Furthermore, the effect of septal (but not LV) excitable area in postshock propagation was found to strongly depend on preshock state. Knowledge regarding the location of the main postshock excitable area within the 3-D ventricular volume could be important for improving defibrillation efficacy. Key Words: ventricles Ⅲ virtual electrode polarization Ⅲ reentry Ⅲ excitable area Ⅲ arrhythmia induction D efibrillation and cardiac vulnerability to electric shocks are strongly linked. A large body of research has demonstrated that ventricular fibrillation induction with an electric shock in sinus rhythm and defibrillation are driven by the same mechanisms. 1-3 Furthermore, it has become a standard in the clinical practice of defibrillation to use the upper limit of vulnerability (ULV), which approximates the defibrillation threshold, 4 -8 in programming the implantable cardioverter/defibrillator. Therefore, complete understanding of the mechanisms by which a defibrillation shock fails in terminating lethal arrhythmias and subsequent optimization of the clinical procedure of defibrillation benefits from the knowledge regarding the factors that contribute to and alter cardiac vulnerability to electric shocks.Strength of the shock and its waveform are important factors affecting ventricular vulnerability to electric shocks. Equally important is the multifaceted ventricular structure with its convoluted geometry and complex fiber architecture. It provides a pathway through which the shock current flows; it also channels the propagation of the postshock activations. Whereas the effects of shock wavefo...

Enhanced temporal and spatial variability in cardiac repolarization has been related to increased arrhythmic risk both clinically and experimentally. Causes and modulators of variability in repolarization and their implications in arrhythmogenesis are however not well understood. At the ionic level, the slow component of the delayed rectifier potassium current (I(Ks)) is an important determinant of ventricular repolarization. In this study, a combination of experimental and computational multiscale studies is used to investigate the role of intrinsic and extrinsic noise in I(Ks) in modulating temporal and spatial variability in ventricular repolarization in human and guinea pig. Results show that under physiological conditions: i), stochastic fluctuations in I(Ks) gating properties (i.e., intrinsic noise) cause significant beat-to-beat variability in action potential duration (APD) in isolated cells, whereas cell-to-cell differences in channel numbers (i.e., extrinsic noise) also contribute to cell-to-cell APD differences; ii), in tissue, electrotonic interactions mask the effect of I(Ks) noise, resulting in a significant decrease in APD temporal and spatial variability compared to isolated cells. Pathological conditions resulting in gap junctional uncoupling or a decrease in repolarization reserve uncover the manifestation of I(Ks) noise at cellular and tissue level, resulting in enhanced ventricular variability and abnormalities in repolarization such as afterdepolarizations and alternans.

Abnormalities in repolarization and its rate dependence are known to be related to increased proarrhythmic risk. A number of repolarization-related electrophysiological properties are commonly used as preclinical biomarkers of arrhythmic risk. However, the variability and complexity of repolarization mechanisms make the use of cellular biomarkers to predict arrhythmic risk preclinically challenging. Our goal is to investigate the role of ionic current properties and their variability in modulating cellular biomarkers of arrhythmic risk to improve risk stratification and identification in humans. A systematic investigation into the sensitivity of the main preclinical biomarkers of arrhythmic risk to changes in ionic current conductances and kinetics was performed using computer simulations. Four stimulation protocols were applied to the ten Tusscher and Panfilov human ventricular model to quantify the impact of +/-15 and +/-30% variations in key model parameters on action potential (AP) properties, Ca(2+) and Na(+) dynamics, and their rate dependence. Simulations show that, in humans, AP duration is moderately sensitive to changes in all repolarization current conductances and in L-type Ca(2+) current (I(CaL)) and slow component of the delayed rectifier current (I(Ks)) inactivation kinetics. AP triangulation, however, is strongly dependent only on inward rectifier K(+) current (I(K1)) and delayed rectifier current (I(Kr)) conductances. Furthermore, AP rate dependence (i.e., AP duration rate adaptation and restitution properties) and intracellular Ca(2+) and Na(+) levels are highly sensitive to both I(CaL) and Na(+)/K(+) pump current (I(NaK)) properties. This study provides quantitative insights into the sensitivity of preclinical biomarkers of arrhythmic risk to variations in ionic current properties in humans. The results show the importance of sensitivity analysis as a powerful method for the in-depth validation of mathematical models in cardiac electrophysiology.

Carusi A, Burrage K, Rodríguez B. Bridging experiments, models and simulations: an integrative approach to validation in computational cardiac electrophysiology. Am J Physiol Heart Circ Physiol 303: H144 -H155, 2012. First published May 11, 2012; doi:10.1152/ajpheart.01151.2011.-Computational models in physiology often integrate functional and structural information from a large range of spatiotemporal scales from the ionic to the whole organ level. Their sophistication raises both expectations and skepticism concerning how computational methods can improve our understanding of living organisms and also how they can reduce, replace, and refine animal experiments. A fundamental requirement to fulfill these expectations and achieve the full potential of computational physiology is a clear understanding of what models represent and how they can be validated. The present study aims at informing strategies for validation by elucidating the complex interrelations among experiments, models, and simulations in cardiac electrophysiology. We describe the processes, data, and knowledge involved in the construction of whole ventricular multiscale models of cardiac electrophysiology. Our analysis reveals that models, simulations, and experiments are intertwined, in an assemblage that is a system itself, namely the model-simulation-experiment (MSE) system. We argue that validation is part of the whole MSE system and is contingent upon 1) understanding and coping with sources of biovariability; 2) testing and developing robust techniques and tools as a prerequisite to conducting physiological investigations; 3) defining and adopting standards to facilitate the interoperability of experiments, models, and simulations; 4) and understanding physiological validation as an iterative process that contributes to defining the specific aspects of cardiac electrophysiology the MSE system targets, rather than being only an external test, and that this is driven by advances in experimental and computational methods and the combination of both. computational physiology; systems biology; computer simulations; whole ventricular models; cardiac electrophysiology COMPUTATIONAL PHYSIOLOGY belongs to the broad family of research in the life sciences referred to as systems biology. As with other domains of systems biology, it considers biological processes as systems of interacting components, and draws upon mathematical and computational modeling to bring these into new configurations with experimentation. It shares the basic commitments of systems biology to nonreductionist or integrative principles, geared towards the exploration of emergence and nonlinear interactions among components and between levels (12,16,41,49,53,71,88). From a sociological point of view, it is also a mode of research that depends on a high degree of interdisciplinary collaboration, where the increased sophistication of computational modeling in the life sciences can elicit high expectations but also skepticism sometimes, thus making collaboration more difficult (19,20,...

Chaste (Cancer, Heart And Soft Tissue Environment) is an open source simulation package for the numerical solution of mathematical models arising in physiology and biology.To date, Chaste development has been driven primarily by applications that include continuum modelling of cardiac electrophysiology ('Cardiac Chaste'), discrete cell-based modelling of soft tissues ('Cell-based Chaste'), and modelling of ventilation in lungs ('Lung Chaste'). Cardiac Chaste addresses the need for a high-performance, generic, and verified simulation framework for cardiac electrophysiology that is freely available to the scientific community. Cardiac chaste provides a software package capable of realistic heart simulations that is efficient, rigorously tested, and runs on HPC platforms. Cell-based Chaste addresses the need for efficient and verified implementations of cell-based modelling frameworks, providing a set of extensible tools for simulating biological tissues. Computational modelling, along with live imaging techniques, plays an important role in understanding the processes of tissue growth and repair. A wide range of cell-based modelling frameworks have been developed that have each been successfully applied in a range of biological applications. Cell-based Chaste includes implementations of the cellular automaton model, the cellular Potts model, cell-centre models with cell representations as overlapping spheres or Voronoi tessellations, and the vertex model. Lung Chaste addresses the need for a novel, generic and efficient lung modelling software package that is both tested and verified. It aims to couple biophysically-detailed models of airway mechanics with organ-scale ventilation models in a package that is freely available to the scientific community.

In this work, the authors use computer modeling to theoretically investigate the mechanisms involved in figure-of-eight reentry during acute regional myocardial ischemia, a pattern of excitation which may lead to ventricular fibrillation and sudden cardiac death. For this purpose, a modified version of the Luo-Rudy dynamic model for the action potential and ionic currents has been used, together with a two-dimensional model of the regionally ischemic ventricle. The virtual tissue comprises several realistically dimensioned and located transitional border zones for hyperkalemia, hypoxia and acidosis, simulating the substrate heterogeneity created by acute ischemia. Different types of patterns of excitation following the delivery of a premature stimulus were obtained, including figure-of-eight reentry. Action potentials and selected ionic currents which explain the reentry process are analyzed. The effect of the degree of ATP-sensitive current activation in the vulnerability to reentry is also studied. The results are in accordance with experimental observations, and demonstrate the ability of second-generation mathematical models to analyze and explain the mechanisms involved in ischemic reentry.