@article {Land:2015dq,
	title = {Verification of cardiac mechanics software: benchmark problems and solutions for testing active and passive material behaviour},
	journal = {Proceedings of the Royal Society A},
	volume = {471},
	year = {2015},
	month = {12/2015},
	publisher = {The Royal Society},
	abstract = {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.},
	author = {Land, Sander and Arens, Sander and Christoph M {Augustin} and Baron, Lukas and Castro, Sebastian and Crozier, Andrew and Favino, Marco and Thomas E {Fastl} and Fritz, Thomas and Gao, Hao and Gizzi, Alessio and Boyce E {Griffith} and Daniel E {Hurtado} and Krause, Rolf and Luo, Xiaoyu and Martyn P {Nash} and Pezzuto, Simone and Plank, Gernot and Rossi, Simone and Ruprecht, Daniel and Seemann, Gunnar and Nicolas P. {Smith} and Sundnes, Joakim and Rice, Jeremy and Natalia A. {Trayanova} and Wang, Dafang and Zhinuo Jenny {Wang} and Steven A {Niederer}}
}
@article {Simula.simula.2200,
	title = {In Silico Screening of the Key Cellular Remodeling Targets in Chronic Atrial Fibrillation},
	journal = {PLoS Computational Biology},
	volume = {10(5)},
	number = {e1003620},
	year = {2014},
	month = {May},
	publisher = { },
	abstract = {Background - Chronic atrial fibrillation (AF) is a complex disease, with underlying changes in electrophysiology, calcium signaling and the structure of atrial myocytes. How these individual remodeling targets and their emergent interactions contribute to cell physiology in chronic AF is not well understood. Methodology/Principal Findings - In silico experiments were performed in a computational model of the human atrial myocyte. Remodeled function of cellular components was based on a broad review of the literature of in vitro findings in chronic AF, and these were integrated into the model to define a cohort of virtual cells. Simulation results indicate that while the altered function of calcium and potassium ion channels alone causes a pronounced decrease in action potential duration, remodeling of calcium handling has a substantial impact on the chronic AF phenotype as well. We also found that the reduction of intracellular calcium transient amplitude in chronic AF in comparison to normal sinus rhythm is mostly due to remodeling of calcium channel function, calcium handling and cellular geometry. Finally, we found that decreased electrical resistance of the membrane together with remodeled calcium handling synergistically decrease cellular excitability and inducibility of repolarization abnormalities in the human atrial myocyte in chronic AF. Conclusions/Significance - The results highlight the complexity of both intrinsic cellular interactions and emergent properties of human atrial myocytes in chronic AF. Therefore, reversing the remodeling for a single remodeled component does very little to restore the normal sinus rhythm phenotype. These findings may have important implications for developing novel therapeutic approaches for chronic AF.},
	author = {Koivum{\"a}ki, Jussi and Seemann, Gunnar and Maleckar, Molly and Tavi, Pasi}
}
@article {Simula.simula.1704,
	title = {Benchmarking Electrophysiological Models of Human Atrial Myocytes},
	journal = {Frontiers in Computational Physiology and Medicine},
	volume = {3},
	number = {487},
	year = {2013},
	month = {January},
	author = {Wilhelms, Mathias and Hettmann, Hanne and Maleckar, Molly and Koivum{\"a}ki, Jussi and D{\"o}ssel, Olaf and Seemann, Gunnar}
}
@inproceedings {Simula.simula.1708,
	title = {Divergent Action Potential Morphology in Human Atrial Cells Vs. Tissue: Underlying Ionic Mechanisms},
	journal = {Computing in Cardiology},
	volume = {39},
	year = {2012},
	pages = {121-124},
	publisher = {Alan Murray},
	type = {Conference},
	isbn = {978-1-4673-2076-4},
	author = {Koivum{\"a}ki, Jussi and Seemann, Gunnar and Maleckar, Molly},
	editor = {Murray, Alan}
}
@misc {Simula.simula.1712,
	title = {Divergent Action Potential Morphology in Human Atrial Cells Vs. Tissue: Underlying Ionic Mechanisms},
	howpublished = {Computing in Cardiology conference},
	year = {2012},
	month = {September},
	author = {Koivum{\"a}ki, Jussi and Seemann, Gunnar and Maleckar, Molly}
}
@misc {Simula.simula.1716,
	title = {Divergent Action Potential Morphology in Human Atrial Cells Vs. Tissue: Underlying Ionic Mechanisms},
	year = {2012},
	month = {September},
	keywords = {Conference},
	author = {Koivum{\"a}ki, Jussi and Seemann, Gunnar and Maleckar, Molly}
}
@article {Simula.simula.230,
	title = {N-Version Benchmark Evaluation of Cardiac Tissue Electrophysiology Simulators},
	journal = {Philosophical Transactions of the Royal Society A},
	volume = {369},
	number = {1954},
	year = {2011},
	month = {November},
	pages = {4331-51},
	abstract = {Ongoing developments in cardiac modelling have resulted, in particular, in the development of advanced and increasingly complex computational frameworks for simulating cardiac tissue electrophysiology. The goal of these simulations is often to represent the detailed physiology and pathologies of the heart using codes that exploit the computational potential of high-performance computing architectures. These developments have rapidly progressed the simulation capacity of cardiac virtual physiological human style models; however, they have also made it increasingly challenging to verify that a given code provides a faithful representation of the purported governing equations and corresponding solution techniques. This study provides the first cardiac tissue electrophysiology simulation benchmark to allow these codes to be verified. The benchmark was successfully evaluated on 11 simulation platforms to generate a consensus gold-standard converged solution. The benchmark definition in combination with the gold-standard solution can now be used to verify new simulation codes and numerical methods in the future.},
	doi = {10.1098/rsta.2011.0139},
	author = {Steven A {Niederer} and Kerfoot, Eric and Benson, Alana and Bernabeu, Miguel and Bernus, Olivier and Cherry, Elizabeth and Clayton, Richard and Fenton, Flavio and Garny, Alan and Heidenreich, Elvio and Land, Sander and Maleckar, Molly and Pathmanathan, Pras and Plank, Gernot and Rodriguez, Jose and Roy, Ishani and Sachse, Frank and Seemann, Gunnar and Skavhaug, Ola and Nicolas P. {Smith}}
}
