Length-dependent tension in the failing heart and the efficacy of cardiac resynchronization therapy

Niederer, Steven A.; Plank, Gernot; Chinchapatnam, Phani; Ginks, Matthew; Lamata, Pablo; Rhode, Kawal; Rinaldi, Christopher Aldo; Razavi, Reza; Smith, Nicolas P.

doi:10.1093/cvr/cvq318

Cited by 142 publications

(171 citation statements)

References 30 publications

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“…The resulting equation set has been widely implemented across the cardiac electrophysiology modelling community and is relatively computationally inexpensive to solve. At the same time, these equations can be used to perform physiologically [29] and clinically relevant simulations [6].…”

Section: (A) Models Of Cardiac Electrophysiologymentioning

confidence: 99%

Verification of cardiac tissue electrophysiology simulators using an N -version benchmark

Niederer

Kerfoot

Benson

et al. 2011

Phil. Trans. R. Soc. A.

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253

311

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One contribution of 11 to a Theme Issue 'Towards the virtual physiological human: mathematical and computational case studies'. 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.

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Section: (A) Models Of Cardiac Electrophysiologymentioning

confidence: 99%

Verification of cardiac tissue electrophysiology simulators using an N -version benchmark

Niederer

Kerfoot

Benson

et al. 2011

Phil. Trans. R. Soc. A.

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253

311

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“…Owing to the close relationship between myocardium electrical and mechanical activities, cardiaccoupled electromechanical models were developed, in from one to three dimensions, for both normal and pathological situations (Usyk and McCulloch, 2003a;2003b;Nash and Panfilov, 2004;Nickerson et al, 2005;Niederer and Smith, 2008;Kerckhoffs et al, 2010;Niederer et al, 2011;Trayanova, 2011;Trayanova et al, 2011;Kuijpers et al, 2012). These coupled models fall mainly into two categories, namely, weak and strong coupling models (Kerckhoffs et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Fibroblast proliferation alters cardiac excitation conduction and contraction: a computational study

Zhan

Xia

Shou

et al. 2014

J. Zhejiang Univ. Sci. B

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Abstract:In this study, the effects of cardiac fibroblast proliferation on cardiac electric excitation conduction and mechanical contraction were investigated using a proposed integrated myocardial-fibroblastic electromechanical model. At the cellular level, models of the human ventricular myocyte and fibroblast were modified to incorporate a model of cardiac mechanical contraction and cooperativity mechanisms. Cellular electromechanical coupling was realized with a calcium buffer. At the tissue level, electrical excitation conduction was coupled to an elastic mechanics model in which the finite difference method (FDM) was used to solve electrical excitation equations, and the finite element method (FEM) was used to solve mechanics equations. The electromechanical properties of the proposed integrated model were investigated in one or two dimensions under normal and ischemic pathological conditions. Fibroblast proliferation slowed wave propagation, induced a conduction block, decreased strains in the fibroblast proliferous tissue, and increased dispersions in depolarization, repolarization, and action potential duration (APD). It also distorted the wave-front, leading to the initiation and maintenance of re-entry, and resulted in a sustained contraction in the proliferous areas. This study demonstrated the important role that fibroblast proliferation plays in modulating cardiac electromechanical behaviour and which should be considered in planning future heart-modeling studies.

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“…Regions of scar tissue were segmented from gadolinium enhanced MR images and mapped to the meshes [9]. Rulebased fiber orientations, based on cadaveric and canine data, varying along the transmural, apical-basal and between the left and right ventricles were assigned to the meshes as previously described in [10]. The electrical activation of the heart was simulated using CARP [11].…”

Section: Methodsmentioning

confidence: 99%

“…The active mechanics of the heart were modeled using a lengthdependent model [10]. The systemic blood flow and boundary conditions were modeled using a three element Windkessel model.…”

Section: Methodsmentioning

confidence: 99%

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Personalised Biophysical Model to Optimise Left Ventricle Pacing Location for Cardiac Resynchronisation Therapy Over Time

Lee

Sohal

Behar

et al. 2016

2016 Computing in Cardiology Conference (CinC)

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Cardiac Resynchronisation Therapy (CRT) causes changes in cardiac anatomy, electrophysiology and mechanics of the heart after 3-6 months of treatment. Multi-pole pacing (MPP) and multi-vein pacing (MVP) (AHR). After sustained CRT treatment the heart remodels and the models predict that the optimal region for pacing the LV would expand by 46% after this remodeling. The expansion in the optimal LV pacing region after remodeling predicts that if LV lead location was placed within the optimal region prior to CRT treatment, it will remain within the optimal region after sustained pacing. IntroductionCardiac Resynchronisation Therapy (CRT) is one of the few effective treatments for patients with drug refractory dyssynchronous heart failure, however 30% of patients fail to respond to this treatment [1]. Many factors can lead to non-response, including suboptimal LV pacing lead location [2].In CRT, the heart is implanted with pacing leads in the right and left ventricles with the aim to resynchronise the ventricular contraction of the heart [3]. The left ventricular (LV) lead is typically implanted via the venous branches of the coronary sinus to electrically stimulate the LV epicardium. To improve the response rate of patients, the optimal location from which to pace the LV free wall has therefore received some interest. In earlier studies, it was found that the optimal location from which to pace the LV is in the non-ischemic, non-apical, postero-lateral/lateral regions of the LV epicardium, or the latest point of mechanical or electrical activation [4][5][6].The heart remodels in response to sustained pacing with regards to the anatomy, mechanics and electrophysiology properties [7,8]. New pacing catheter technologies such as multipole pacing (MPP) and multi-vein pacing (MVP) allow for the LV lead position to be altered post implant without further surgery. The long term benefits of MVP and MPP depend on whether the optimal location for LV pacing changes after remodeling due to CRT. MethodsA male patient with standard indication for CRT (NYHA class III, QRSd≥120ms, LBBB on surface ECG, LV EF≤35%) was recruited and clinical data was acquired before and after six months of sustained CRT. The heart was implanted with three leads, one at the high right atria to regulate the heart rate, one at the RV apex and with a MPP LV lead in the posterior/lateral regions of the heart to synchronize ventricular contraction.Prior to CRT implantation, 3D whole heart MR images were acquired and after device implantation, the heart anatomy was captured using 2D and 3D echocardiography. Gadolinium enhanced MR images were also acquired prior to implantation to determine the regions of infarcted tissues in the heart. Electrical activation of the heart was measured using 12-lead ECG and invasive electroanatomical mapping of the left ventricle. At time of implant and after at least six months of sustained pacing, invasive pressure measurements were taken from the left ventricle cavity under biventricular pacing (DDD-BiV) and with ...

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Length-dependent tension in the failing heart and the efficacy of cardiac resynchronization therapy

Cited by 142 publications

References 30 publications

Verification of cardiac tissue electrophysiology simulators using an N -version benchmark

Verification of cardiac tissue electrophysiology simulators using an N -version benchmark

Fibroblast proliferation alters cardiac excitation conduction and contraction: a computational study

Personalised Biophysical Model to Optimise Left Ventricle Pacing Location for Cardiac Resynchronisation Therapy Over Time

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