@article {23999,
	title = {High-order finite element methods for cardiac monodomain simulations},
	journal = {Frontiers in Physiology},
	year = {2015},
	month = {08/2015},
	publisher = {Frontiers Media S.A.},
	abstract = {Computational modeling of tissue-scale cardiac electrophysiology requires numerically converged solutions to avoid spurious artifacts. The steep gradients inherent to cardiac action potential propagation necessitate fine spatial scales and therefore a substantial computational burden. The use of high-order interpolation methods has previously been proposed for these simulations due to their theoretical convergence advantage. In this study, we compare the convergence behavior of linear Lagrange, cubic Hermite, and the newly proposed cubic Hermite-style serendipity interpolation methods for finite element simulations of the cardiac monodomain equation. The high-order methods reach converged solutions with fewer degrees of freedom and longer element edge lengths than traditional linear elements. Additionally, we propose a dimensionless number, the cell Thiele modulus, as a more useful metric for determining solution convergence than element size alone. Finally, we use the cell Thiele modulus to examine convergence criteria for obtaining clinically useful activation patterns for applications such as patient-specific modeling where the total activation time is known a priori.},
	doi = {10.3389/fphys.2015.00217},
	url = {http://journal.frontiersin.org/article/10.3389/fphys.2015.00217/abstract},
	author = {K. P. {Vincent} and M. J. {Gonzales} and Andrew K. {Gillette} and C. T. {Villongco} and Pezzuto, Simone and J. H. {Omens} and M. J. {Holst} and Andrew D. {McCulloch}}
}
@article {Simula.simula.66,
	title = {Ventricular Dilation and Electrical Dyssynchrony Synergistically Increase Regional Mechanical Non-Uniformity But Not Mechanical Dyssynchrony; a Computational Model},
	journal = {Circulation: Heart Failure},
	volume = {3},
	number = {4},
	year = {2010},
	month = {May},
	pages = {528-536},
	abstract = {Background Heart failure (HF) in combination with mechanical dyssynchrony is associated with a high mortality rate. To quantify contractile dysfunction in patients with HF, investigators have proposed several indices of mechanical dyssynchrony, including percentile range of time to peak shortening (WTpeak), circumferential uniformity ratio estimate (CURE), and internal stretch fraction (ISF). The goal of this study was to compare the sensitivity of these indices to 4 major abnormalities responsible for cardiac dysfunction in dyssynchronous HF: dilation, negative inotropy, negative lusitropy, and dyssynchronous activation. Methods and Results All combinations of these 4 major abnormalities were included in 3D computational models of ventricular electromechanics. Compared with a nonfailing heart model, ventricles were dilated, inotropy was reduced, twitch duration was prolonged, and activation sequence was changed from normal to left bundle branch block. In the nonfailing heart, CURE, ISF, and WTpeak were 0.97\pm0.004, 0.010\pm0.002, and 78\pm1 milliseconds, respectively. With dilation alone, CURE decreased 2.0\pm0.07\%, ISF increased 58\pm47\%, and WTpeak increased 31\pm3\%. With dyssynchronous activation alone, CURE decreased 15\pm0.6\%, ISF increased 14-fold (\pm3), and WTpeak increased 121\pm4\%. With the combination of dilation and dyssynchronous activation, CURE decreased 23\pm0.8\%, ISF increased 20-fold (\pm5), and WTpeak increased 147\pm5\%. Conclusions Dilation and left bundle branch block combined synergistically decreased regional cardiac function. CURE and ISF were sensitive to this combination, but WTpeak was not. CURE and ISF also reflected the relative nonuniform distribution of regional work better than WTpeak. These findings might explain why CURE and ISF are better predictors of reverse remodeling in cardiac resynchronization therapy.},
	author = {J. H. {Omens} and Andrew D. {McCulloch} and L. J. {Mulligan}}
}
@article {Simula.sc.1198,
	title = {Effect of Transmurally Heterogeneous Myocyte Excitation-contraction Coupling on Canine Left Ventricular Electromechanics},
	journal = {Experimental Physiology},
	volume = {94},
	number = {5},
	year = {2009},
	pages = {541-552},
	publisher = {BioMedCentral},
	doi = {10.1113/expphysiol.2008.044057},
	author = {S. G. {Campbell} and Howard, E. and Aguado-Sierra, Jazmin and B. A. {Coppola} and J. H. {Omens} and L. J. {Mulligan} and Andrew D. {McCulloch}}
}
@article {Simula.sc.1196,
	title = {Hypertrophic Gene Expression Induced by Chronic Stretch of Excised Mouse Heart Muscle},
	journal = {Mol Cell Biomech.},
	volume = {6},
	number = {3},
	year = {2009},
	pages = {145-159},
	publisher = {PubMed Central},
	author = {A. M. {Raskin} and Hoshijima, M. and Swanson, E. and Andrew D. {McCulloch} and J. H. {Omens}}
}
@article {Simula.sc.934,
	title = {Cardiac Resynchronization: Insight From Experimental and Computational Models},
	journal = {Progress in Biophysics and Molecular Biology},
	volume = {97},
	number = {2-3},
	year = {2008},
	month = {June-July},
	pages = {543-561},
	abstract = {Cardiac resynchronization therapy (CRT) is a promising therapy for heart failure patients with a conduction disturbance, such as left bundle branch block. The aim of CRT is to resynchronize contraction between and within ventricles. However, about 30\% of patients do not respond to this therapy. Therefore, a better understanding is needed for the relation between electrical and mechanical activation. In this paper, we focus on to what extent animal experiments and mathematical models can help in order to understand the pathophysiology of asynchrony to further improve CRT.},
	doi = {10.1016/j.pbiomolbio.2008.02.024},
	author = {Lumens, J. and Vernooy, K. and J. H. {Omens} and L. J. {Mulligan} and Delhaas, T. and Arts, Thomas and Andrew D. {McCulloch} and F. W. {Prinzen}}
}
@article {Simula.sc.1216,
	title = {Substrate Stiffness Affects the Functional Maturation of Neonatal Rat Ventricular Myocytes},
	journal = {Biophysiology Journal},
	volume = {95},
	number = {7},
	year = {2008},
	pages = {3479-3487},
	author = {J. J. {Jacot} and Andrew D. {McCulloch} and J. H. {Omens}}
}
@article {Simula.sc.1202,
	title = {Coupling of a 3D Finite Element Model of Cardiac Ventricular Mechanics to Lumped Systems Models of the Systemic and Pulmonic Circulation},
	journal = {Ann. Biomed. Eng.},
	volume = {35},
	number = {1},
	year = {2007},
	pages = {1-18},
	author = {M. L. {Neal} and J. B. {Bassingthwaighte} and J. H. {Omens} and Andrew D. {McCulloch}}
}
@article {Simula.sc.1240,
	title = {Myocyte Shearing, Myocardial Sheets, and Microtubules},
	journal = {Circulation Research},
	volume = {98},
	number = {1},
	year = {2006},
	pages = {1-3},
	author = {J. H. {Omens} and Andrew D. {McCulloch}}
}
@article {Simula.sc.1238,
	title = {Role of Diastolic Properties in the Transition to Failure in a Mouse Model of Cardiac Dilatation},
	journal = {American Journal of Physiology - Heart and Circulatory Physiology},
	volume = {291},
	number = {6},
	year = {2006},
	pages = {H2971-2979},
	author = {P. N. {Costandi} and L. R. {Frank} and Andrew D. {McCulloch} and J. H. {Omens}}
}
