Modelling whole heart electrical activity for ischemia and cardiac pacing simulation

2020 ◽  
Vol 10 (4) ◽  
pp. 837-850 ◽  
Author(s):  
Niccoló Biasi ◽  
Alessandro Tognetti
Keyword(s):  
Electrical Activity ◽  
Cardiac Pacing ◽  
Heart Electrical Activity ◽  
Whole Heart

scholarly journals A Simplified 3D Model of Whole Heart Electrical Activity and 12-Lead ECG Generation

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Siniša Sovilj ◽  
Ratko Magjarević ◽  
Nigel H. Lovell ◽  
Socrates Dokos
Keyword(s):  
Electrical Activity ◽  
Three Dimensional ◽  
Model Complexity ◽  
Bidomain Model ◽  
Computationally Efficient ◽  
Lead System ◽  
Heart Electrical Activity ◽  
Cell Tissue ◽  
Whole Heart ◽  
Electrocardiogram Ecg

We present a computationally efficient three-dimensional bidomain model of torso-embedded whole heart electrical activity, with spontaneous initiation of activation in the sinoatrial node, incorporating a specialized conduction system with heterogeneous action potential morphologies throughout the heart. The simplified geometry incorporates the whole heart as a volume source, with heart cavities, lungs, and torso as passive volume conductors. We placed four surface electrodes at the limbs of the torso: , , and and six electrodes on the chest to simulate the Einthoven, Goldberger-augmented and precordial leads of a standard 12-lead system. By placing additional seven electrodes at the appropriate torso positions, we were also able to calculate the vectorcardiogram of the Frank lead system. Themodel was able to simulate realistic electrocardiogram (ECG) morphologies for the 12 standard leads, orthogonal , , and leads, as well as the vectorcardiogram under normal and pathological heart states. Thus, simplified and easy replicable 3D cardiac bidomain model offers a compromise between computational load and model complexity and can be used as an investigative tool to adjust cell, tissue, and whole heart properties, such as setting ischemic lesions or regions of myocardial infarction, to readily investigate their effects on whole ECG morphology.

scholarly journals Simplified 2D Bidomain Model of Whole Heart Electrical Activity and ECG Generation

2014 ◽  
Vol 14 (3) ◽  
pp. 136-143 ◽  
Author(s):  
Siniša Sovilj ◽  
Ratko Magjarević ◽  
Amr Al Abed ◽  
Nigel H. Lovell ◽  
Socrates Dokos
Keyword(s):  
Electrical Activity ◽  
Sinoatrial Node ◽  
Biophysical Model ◽  
Model Complexity ◽  
Lead System ◽  
Heart Electrical Activity ◽  
Cardiac Model ◽  
Surface Ecg ◽  
Whole Heart ◽  
Ecg Morphology

Abstract The aim of this study was the development of a geometrically simple and highly computationally-efficient two dimensional (2D) biophysical model of whole heart electrical activity, incorporating spontaneous activation of the sinoatrial node (SAN), the specialized conduction system, and realistic surface ECG morphology computed on the torso. The FitzHugh-Nagumo (FHN) equations were incorporated into a bidomain finite element model of cardiac electrical activity, which was comprised of a simplified geometry of the whole heart with the blood cavities, the lungs and the torso as an extracellular volume conductor. To model the ECG, we placed four electrodes on the surface of the torso to simulate three Einthoven leads VI, VII and VIII from the standard 12-lead system. The 2D model was able to reconstruct ECG morphology on the torso from action potentials generated at various regions of the heart, including the sinoatrial node, atria, atrioventricular node, His bundle, bundle branches, Purkinje fibers, and ventricles. Our 2D cardiac model offers a good compromise between computational load and model complexity, and can be used as a first step towards three dimensional (3D) ECG models with more complex, precise and accurate geometry of anatomical structures, to investigate the effect of various cardiac electrophysiological parameters on ECG morphology.

Effect of Drugs on the Heart Electrical Activity of Man

1970 ◽  
Vol 10 (2) ◽  
pp. 95-102 ◽  
Author(s):  
CARL C. PFEIFFER ◽  
MOHINDER SINGH ◽  
LEONIDE GOLDSTEIN
Keyword(s):  
Electrical Activity ◽  
Heart Electrical Activity

scholarly journals Computational approaches to understand cardiac electrophysiology and arrhythmias

2012 ◽  
Vol 303 (7) ◽  
pp. H766-H783 ◽  
Author(s):  
Byron N. Roberts ◽  
Pei-Chi Yang ◽  
Steven B. Behrens ◽  
Jonathan D. Moreno ◽  
Colleen E. Clancy
Keyword(s):  
Ion Channels ◽  
Electrical Activity ◽  
Cardiac Electrophysiology ◽  
Cardiac Activity ◽  
Computational Approaches ◽  
Cardiac Electrical Activity ◽  
Whole Heart ◽  
Arrhythmia Therapy ◽  
Emergent Behaviors ◽  
The Brain

Cardiac rhythms arise from electrical activity generated by precisely timed opening and closing of ion channels in individual cardiac myocytes. These impulses spread throughout the cardiac muscle to manifest as electrical waves in the whole heart. Regularity of electrical waves is critically important since they signal the heart muscle to contract, driving the primary function of the heart to act as a pump and deliver blood to the brain and vital organs. When electrical activity goes awry during a cardiac arrhythmia, the pump does not function, the brain does not receive oxygenated blood, and death ensues. For more than 50 years, mathematically based models of cardiac electrical activity have been used to improve understanding of basic mechanisms of normal and abnormal cardiac electrical function. Computer-based modeling approaches to understand cardiac activity are uniquely helpful because they allow for distillation of complex emergent behaviors into the key contributing components underlying them. Here we review the latest advances and novel concepts in the field as they relate to understanding the complex interplay between electrical, mechanical, structural, and genetic mechanisms during arrhythmia development at the level of ion channels, cells, and tissues. We also discuss the latest computational approaches to guiding arrhythmia therapy.

The Persistence and Regularity of Electrical Activity in Whole Heart Explants

1961 ◽  
Vol 52 (2) ◽  
pp. 101-107 ◽  
Author(s):  
A. W. B. Cunningham ◽  
N. O. Lunell ◽  
B. J. Rylander
Keyword(s):  
Electrical Activity ◽  
Whole Heart

scholarly journals Vitamin E administration attenuates the tri-iodothyronine-induced modification of heart electrical activity in the rat.

1997 ◽  
Vol 200 (5) ◽  
pp. 909-914
Author(s):  
P Venditti ◽  
T De Leo ◽  
S Di Meo
Keyword(s):  
Lipid Peroxidation ◽  
Heart Rate ◽  
Free Radical ◽  
Vitamin E ◽  
Thyroid Hormone ◽  
Action Potential ◽  
Electrical Activity ◽  
Radical Mechanism ◽  
Antioxidant Systems ◽  
Heart Electrical Activity

This work was designed to determine whether the thyroid-hormone-induced modifications of heart electrical activity are, at least in part, due to increased free radical production. For this study, 60-day-old euthyroid, hyperthyroid and hyperthyroid vitamin-E-treated rats were used. Hyperthyroidism, elicited by a 10 day treatment with tri-iodothyronine, induced an increase in lipid peroxidation without changing the level of antioxidants. Intraperitoneal vitamin administration to hyperthyroid rats led to a reduction in lipid peroxidation and a non-significant increase in antioxidant level. The hyperthyroid state was also associated with an increase in heart rate measured in vivo and a decrease in the duration of the ventricular action potential recorded in vitro. Administration of vitamin E attenuated the thyroid-hormone-induced changes in heart rate and action potential duration, which were, however, significantly different from those of the control euthyroid rats. These results suggest that vitamin E protects hyperthyroid heart against lipid peroxidation by mechanisms that may be independent of the changes in antioxidant systems. Moreover, the reduction in the tri-iodothyronine effects on heart electrophysiological properties indicates that such effects are mediated, at least in part, through a membrane modification, probably related to increased lipid peroxidation, involving a free radical mechanism.

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