scholarly journals Numerical Simulations of Dynamics Behaviour of the Action Potential of the Human Heart's Conduction System

10.5772/63017 ◽  
2016 ◽  
Author(s):  
Beata Jackowska-Zduniak
Keyword(s):  
Action Potential ◽  
Numerical Simulations ◽  
Conduction System

Sodium channel kinetic changes that produce Brugada syndrome or progressive cardiac conduction system disease

2007 ◽  
Vol 292 (1) ◽  
pp. H399-H407 ◽  
Author(s):  
Zhu-Shan Zhang ◽  
Joseph Tranquillo ◽  
Valentina Neplioueva ◽  
Nenad Bursac ◽  
Augustus O. Grant
Keyword(s):  
Action Potential ◽  
Sodium Channel ◽  
Brugada Syndrome ◽  
Sodium Current ◽  
Conduction System ◽  
Cardiac Conduction ◽  
Cardiac Conduction System ◽  
Wild Type ◽  
System Disease ◽  
Conduction System Disease

Some mutations of the sodium channel gene NaV1.5 are multifunctional, causing combinations of LQTS, Brugada syndrome and progressive cardiac conduction system disease (PCCD). The combination of Brugada syndrome and PCCD is uncommon, although they both result from a reduction in the sodium current. We hypothesize that slow conduction is sufficient to cause S-T segment elevation and undertook a combined experimental and theoretical study to determine whether conduction slowing alone can produce the Brugada phenotype. Deletion of lysine 1479 in one of two positively charged clusters in the III/IV inter-domain linker causes both syndromes. We have examined the functional effects of this mutation using heterologous expression of the wild-type and mutant sodium channel in HEK-293-EBNA cells. We show that ΔK1479 shifts the potential of half-activation, V1/2m, to more positive potentials ( V1/2m = −36.8 ± 0.8 and −24.5 ± 1.3 mV for the wild-type and ΔK1479 mutant respectively, n = 11, 10). The depolarizing shift increases the extent of depolarization required for activation. The potential of half-inactivation, V1/2h, is also shifted to more positive potentials ( V1/2h = −85 ± 1.1 and −79.4 ± 1.2 mV for wild-type and ΔK1479 mutant respectively), increasing the fraction of channels available for activation. These shifts are quantitatively the same as a mutation that produces PCCD only, G514C. We incorporated experimentally derived parameters into a model of the cardiac action potential and its propagation in a one dimensional cable (simulating endo-, mid-myocardial and epicardial regions). The simulations show that action potential and ECG changes consistent with Brugada syndrome may result from conduction slowing alone; marked repolarization heterogeneity is not required. The findings also suggest how Brugada syndrome and PCCD which both result from loss of sodium channel function are sometimes present alone and at other times in combination.

DYNAMICAL EFFECTS OF MYOCARDIAL ISCHEMIA IN ANISOTROPIC CARDIAC MODELS IN THREE DIMENSIONS

2007 ◽  
Vol 17 (12) ◽  
pp. 1965-2008 ◽  
Author(s):  
PIERO COLLI FRANZONE ◽  
LUCA F. PAVARINO ◽  
SIMONE SCACCHI
Keyword(s):  
Myocardial Ischemia ◽  
Action Potential ◽  
Numerical Simulations ◽  
Cardiac Muscle ◽  
Action Potential Duration ◽  
Three Dimensions ◽  
Extracellular Potential ◽  
Anisotropic Structure ◽  
Orthogonal Components ◽  
Cardiac Excitation

The interaction between the presence of moderate or severe subendocardial ischemic regions and the anisotropic structure of the cardiac muscle is investigated here by means of numerical simulations based on anisotropic Bidomain and Monodomain models. The ischemic effects on cardiac excitation, recovery and distribution of action potential duration are discussed, showing the presence of ischemic epicardial markers. Extracellular potential distributions during the ST and TQ intervals are computed separately using non-stationary models. During the ST interval, the extracellular potential patterns differ from those simulated with stationary models used in the literature. These differences are explained by decomposing the cardiac current sources into conormal, axial and orthogonal components and by determining which component is dominant during the ST and TQ intervals.

Cardiac myocytes and the cardiac action potential

2010 ◽  
pp. 2603-2618
Author(s):  
Kenneth T. MacLeod ◽  
Steven B. Marston ◽  
Philip A. Poole-Wilson ◽  
Nicholas J. Severs ◽  
Peter H. Sugden
Keyword(s):  
Action Potential ◽  
Cardiac Myocytes ◽  
Ventricular Myocytes ◽  
Conduction System ◽  
Cardiac Action Potential ◽  
Contractile Apparatus ◽  
Atp Production ◽  
Cardiac Action ◽  
Heart Mass ◽  
Contractile Cells

Cardiac myocytes are the contractile cells of the heart and constitute the bulk of heart mass. There are differences between the myocytes of the ventricles, the atria, and the conduction system: ventricular myocytes are elongated cells and packed with myofibrils (the contractile apparatus) and mitochondria (for ATP production)....

scholarly journals Action Potential Characteristics and Arrhythmogenic Properties of the Cardiac Conduction System of the Murine Heart

2001 ◽  
Vol 89 (4) ◽  
pp. 329-335 ◽  
Author(s):  
Justus M.B. Anumonwo ◽  
Yvonne N. Tallini ◽  
Frederick J. Vetter ◽  
José Jalife
Keyword(s):  
Action Potential ◽  
Conduction System ◽  
Cardiac Conduction ◽  
Cardiac Conduction System

scholarly journals Action potential propagation and block in a model of atrial tissue with myocyte–fibroblast coupling

2021 ◽  
Vol 38 (1) ◽  
pp. 106-131
Author(s):  
Peter Mortensen ◽  
Hao Gao ◽  
Godfrey Smith ◽  
Radostin D Simitev
Keyword(s):  
Action Potential ◽  
Numerical Simulations ◽  
Asymptotic Theory ◽  
Numerical Solutions ◽  
Direct Numerical Simulations ◽  
Critical Values ◽  
Fast Time ◽  
Slow Time ◽  
Atrial Tissue ◽  
Time Problem

Abstract The electrical coupling between myocytes and fibroblasts and the spacial distribution of fibroblasts within myocardial tissues are significant factors in triggering and sustaining cardiac arrhythmias, but their roles are poorly understood. This article describes both direct numerical simulations and an asymptotic theory of propagation and block of electrical excitation in a model of atrial tissue with myocyte–fibroblast coupling. In particular, three idealized fibroblast distributions are introduced: uniform distribution, fibroblast barrier and myocyte strait—all believed to be constituent blocks of realistic fibroblast distributions. Primary action potential biomarkers including conduction velocity, peak potential and triangulation index are estimated from direct simulations in all cases. Propagation block is found to occur at certain critical values of the parameters defining each idealized fibroblast distribution, and these critical values are accurately determined. An asymptotic theory proposed earlier is extended and applied to the case of a uniform fibroblast distribution. Biomarker values are obtained from hybrid analytical-numerical solutions of coupled fast-time and slow-time periodic boundary value problems and compare well to direct numerical simulations. The boundary of absolute refractoriness is determined solely by the fast-time problem and is found to depend on the values of the myocyte potential and on the slow inactivation variable of the sodium current ahead of the propagating pulse. In turn, these quantities are estimated from the slow-time problem using a regular perturbation expansion to find the steady state of the coupled myocyte–fibroblast kinetics. The asymptotic theory gives a simple analytical expression that captures with remarkable accuracy the block of propagation in the presence of fibroblasts.

How to sample the entire length of a single muscle fiber quick-frozen after electrical point stimulation for high resolution EM

1992 ◽  
Vol 50 (1) ◽  
pp. 776-777
Author(s):  
Joachim R. Sommer ◽  
Teresa High ◽  
Betty Scherer ◽  
Isaiah Taylor ◽  
Rashid Nassar
Keyword(s):  
Skeletal Muscle ◽  
High Resolution ◽  
Action Potential ◽  
Muscle Fiber ◽  
Freeze Fracture ◽  
Freeze Substitution ◽  
Electrical Field Stimulation ◽  
Skeletal Muscle Fiber ◽  
Freeze Dried ◽  
Quick Freezing

We have developed a model that allows the quick-freezing at known time intervals following electrical field stimulation of a single, intact frog skeletal muscle fiber isolated by sharp dissection. The preparation is used for studying high resolution morphology by freeze-substitution and freeze-fracture and for electron probe x-ray microanlysis of sudden calcium displacement from intracellular stores in freeze-dried cryosections, all in the same fiber. We now show the feasibility and instrumentation of new methodology for stimulating a single, intact skeletal muscle fiber at a point resulting in the propagation of an action potential, followed by quick-freezing with sub-millisecond temporal resolution after electrical stimulation, followed by multiple sampling of the frozen muscle fiber for freeze-substitution, freeze-fracture (not shown) and cryosectionmg. This model, at once serving as its own control and obviating consideration of variances between different fibers, frogs etc., is useful to investigate structural and topochemical alterations occurring in the wake of an action potential.

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