Modeling of heterogeneous electrophysiology in the human heart with respect to ECG genesis

Weiß, Daniel L.; Seemann, Gunnar; Keller, D. U. J.; Farina, D.; Sachse, Frank B.; Dössel, Olaf

doi:10.1109/cic.2007.4745418

Cited by 17 publications

(9 citation statements)

References 13 publications

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“…In addition to computational modeling studies requiring accurate fiber orientation, it is becoming increasingly important to model spatial heterogeneity in ion channel density and conductivity throughout the myocardium. 38 Assigning such properties throughout models with complex cardiac geometries poses the same challenges as encountered when assigning fiber orientation. From the results presented in this study, it is evident that the LDRB algorithm provides the accurate parameterization of the myocardium that is necessary to easily perform this otherwise daunting task.…”

Section: Discussionmentioning

confidence: 99%

A Novel Rule-Based Algorithm for Assigning Myocardial Fiber Orientation to Computational Heart Models

et al. 2012

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Electrical waves traveling throughout the myocardium elicit muscle contractions responsible for pumping blood throughout the body. The shape and direction of these waves depend on the spatial arrangement of ventricular myocytes, termed fiber orientation. In computational studies simulating electrical wave propagation or mechanical contraction in the heart, accurately representing fiber orientation is critical so that model predictions corroborate with experimental data. Typically, fiber orientation is assigned to heart models based on Diffusion Tensor Imaging (DTI) data, yet few alternative methodologies exist if DTI data is noisy or absent. Here we present a novel Laplace–Dirichlet Rule-Based (LDRB) algorithm to perform this task with speed, precision, and high usability. We demonstrate the application of the LDRB algorithm in an image-based computational model of the canine ventricles. Simulations of electrical activation in this model are compared to those in the same geometrical model but with DTI-derived fiber orientation. The results demonstrate that activation patterns from simulations with LDRB and DTI-derived fiber orientations are nearly indistinguishable, with relative differences ≤6%, absolute mean differences in activation times ≤3.15 ms, and positive correlations ≥0.99. These results convincingly show that the LDRB algorithm is a robust alternative to DTI for assigning fiber orientation to computational heart models.

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Section: Discussionmentioning

confidence: 99%

A Novel Rule-Based Algorithm for Assigning Myocardial Fiber Orientation to Computational Heart Models

et al. 2012

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“…Since no significant change was found in the density of connexin-43, the gap junction protein responsible for cell-to-cell electrical communication, in non-infarcted myocardium of infarcted hearts 37 , we used the conductivities of normal tissue 38 39 in these regions. These conductivities were further adjusted using a systematic approach 40 to match human myocardium conduction velocity measured in experimental studies 41 42 43 44 . The values of the non-infarcted tissue conductivities used in this study were 0.255 and 0.0775 S m −1 in the longitudinal and transverse directions, respectively.…”

Section: Methodsmentioning

confidence: 99%

Arrhythmia risk stratification of patients after myocardial infarction using personalized heart models

et al. 2016

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Sudden cardiac death (SCD) from arrhythmias is a leading cause of mortality. For patients at high SCD risk, prophylactic insertion of implantable cardioverter defibrillators (ICDs) reduces mortality. Current approaches to identify patients at risk for arrhythmia are, however, of low sensitivity and specificity, which results in a low rate of appropriate ICD therapy. Here, we develop a personalized approach to assess SCD risk in post-infarction patients based on cardiac imaging and computational modelling. We construct personalized three-dimensional computer models of post-infarction hearts from patients' clinical magnetic resonance imaging data and assess the propensity of each model to develop arrhythmia. In a proof-of-concept retrospective study, the virtual heart test significantly outperformed several existing clinical metrics in predicting future arrhythmic events. The robust and non-invasive personalized virtual heart risk assessment may have the potential to prevent SCD and avoid unnecessary ICD implantations.

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“…Membrane kinetics were represented by the Ten Tusscher-Panfilov (TTP) model of human ventricular tissue (14). Transmural heterogeneity in ion channel expression between the three cell layers was modeled according to Table 1 of Weiss et al (21). Intra- and extracellular components were coupled in 3D using a bidomain formulation and assigned conductivity values to produce transmural conduction velocities of 0.4m/s in endocardial and M-cell layers, and 0.28m/s in epicardium (22).…”

Section: Methodsmentioning

confidence: 99%

Action Potential Dynamics Explain Arrhythmic Vulnerability in Human Heart Failure

Narayan

Bayer

Lalani

et al. 2008

Journal of the American College of Cardiology

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Objective To determine whether abnormalities of calcium cycling explain ventricular action potential (AP) oscillations and cause ECG T-wave Alternans (TWA). Background Mechanisms explaining why heart failure patients are at risk for malignant ventricular arrhythmias (VT/VF) are unclear. We studied whether oscillations in human ventricular AP explain TWA and predict VT/VF, and used computer modeling to suggest potential cellular mechanisms. Methods We studied 53 patients with LV ejection fraction 28±8% and 18 control subjects. Monophasic AP were recorded in the right (RV, n=62) and/or left (LV, n=9) ventricle at 109 beats/min. Results Alternans of AP amplitude, computed spectrally, had higher magnitude in study patients than controls (p=0.03), particularly in AP phase II (p=0.02) rather than phase III (p=0.10). APD and activation restitution (n=11 patients) were flat at 109 beats/min and did not explain TWA. In computer simulations, only reduced sarcoplasmic reticulum calcium uptake explained our results, causing causing calcium oscillations, AP amplitude alternans and TWA that were all abolished by calcium clamping. On prospective follow-up for 949±553 days, 17 patients suffered VT/VF. AP amplitude alternans predicted VT/VF (p=0.04), and was 78% concordant with simultaneous TWA (p=0.003). Conclusions Patients with systolic dysfunction show ventricular AP amplitude alternans that prospectively predicted VT/VF. Alternans in AP amplitude, but not variations in APD or conduction, explained TWA at ≤109 beats/min. In computer models, these findings were best explained by reduced sarcoplasmic reticulum calcium uptake. In heart failure patients, in vivo AP alternans may reflect cellular calcium abnormalities and provide a mechanistic link with VT/VF.

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Modeling of heterogeneous electrophysiology in the human heart with respect to ECG genesis

Cited by 17 publications

References 13 publications

A Novel Rule-Based Algorithm for Assigning Myocardial Fiber Orientation to Computational Heart Models

A Novel Rule-Based Algorithm for Assigning Myocardial Fiber Orientation to Computational Heart Models

Arrhythmia risk stratification of patients after myocardial infarction using personalized heart models

Action Potential Dynamics Explain Arrhythmic Vulnerability in Human Heart Failure

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