Vladimir S. Markhasin

Mathematical model of the anatomy and fibre orientation field of the left ventricle of the heart

BackgroundOne of the main factors affecting propagation of electrical waves and contraction in ventricles of the heart is anisotropy of cardiac tissue. Anisotropy is determined by orientation of myocardial fibres. Determining fibre orientation field and shape of the heart is important for anatomically accurate modelling of electrical and mechanical function of the heart. The aim of this paper is to introduce a theoretical rule-based model for anatomy and fibre orientation of the left ventricle (LV) of the heart and to compare it with experimental data. We suggest explicit analytical formulae that allow us to obtain the left ventricle form and its fibre direction field. The ventricle band concept of cardiac architecture given by Torrent-Guasp is chosen as the model postulate.MethodsIn our approach, anisotropy of the heart is derived from some general principles. The LV is considered as a set of identical spiral surfaces, each of which can be produced from the other by rotation around one vertical axis. Each spiral surface is filled with non-intersecting curves which represent myocardial fibres.For model verification, we use experimental data on fibre orientation in human and canine hearts.ResultsLV shape and anisotropy are represented by explicit analytical expressions in a curvilinear 3-D coordinate system. The derived fibre orientation field shows good qualitative agreement with experimental data. The model reveals the most thorough quantitative simulation of fibre angles at the LV middle zone.ConclusionsOur analysis shows that the band concept can generate realistic anisotropy of the LV. Our model shows good qualitative agreement between the simulated fibre orientation field and the experimental data on LV anisotropy, and the model can be used for various numerical simulations to study the effects of anisotropy on cardiac excitation and mechanical function.

Electrical Wave Propagation in an Anisotropic Model of the Left Ventricle Based on Analytical Description of Cardiac Architecture

We develop a numerical approach based on our recent analytical model of fiber structure in the left ventricle of the human heart. A special curvilinear coordinate system is proposed to analytically include realistic ventricular shape and myofiber directions. With this anatomical model, electrophysiological simulations can be performed on a rectangular coordinate grid. We apply our method to study the effect of fiber rotation and electrical anisotropy of cardiac tissue (i.e., the ratio of the conductivity coefficients along and across the myocardial fibers) on wave propagation using the ten Tusscher–Panfilov (2006) ionic model for human ventricular cells. We show that fiber rotation increases the speed of cardiac activation and attenuates the effects of anisotropy. Our results show that the fiber rotation in the heart is an important factor underlying cardiac excitation. We also study scroll wave dynamics in our model and show the drift of a scroll wave filament whose velocity depends non-monotonically on the fiber rotation angle; the period of scroll wave rotation decreases with an increase of the fiber rotation angle; an increase in anisotropy may cause the breakup of a scroll wave, similar to the mother rotor mechanism of ventricular fibrillation.

Drift of scroll wave filaments in an anisotropic model of the left ventricle of the human heart

Scroll waves are three-dimensional vortices which occur in excitable media. Their formation in the heart results in the onset of cardiac arrhythmias, and the dynamics of their filaments determine the arrhythmia type. Most studies of filament dynamics were performed in domains with simple geometries and generic description of the anisotropy of cardiac tissue. Recently, we developed an analytical model of fibre structure and anatomy of the left ventricle (LV) of the human heart. Here, we perform a systematic study of the dynamics of scroll wave filaments for the cases of positive and negative tension in this anatomical model. We study the various possible shapes of LV and different degree of anisotropy of cardiac tissue. We show that, for positive filament tension, the final position of scroll wave filament is mainly determined by the thickness of the myocardial wall but, however, anisotropy attracts the filament to the LV apex. For negative filament tension, the filament buckles, and for most cases, tends to the apex of the heart with no or slight dependency on the thickness of the LV. We discuss the mechanisms of the observed phenomena and their implications for cardiac arrhythmias.

Mechano-electric feedback in one-dimensional model of myocardium.

We utilized our earlier developed 1D mathematical model of the heart muscle strand to study contribution of the bilateral interactions between excitation and contraction on the cellular and tissue levels to the local and global myocardium function. Numerical experiments on the model showed that an initially uniform strand, formed on the inherently identical cells, became functionally heterogeneous due to the asynchronous excitation via the electrical wave spread. Mechanical interactions between the cells and the mechano-electric feedback beat-to-beat affect the functional characteristics of coupled cardiomyocytes further, adjusting their electrical and mechanical heterogeneity to the activation timing. Model simulations showed that functional heterogeneity increases with an enlarged spatial extension of the myocardial strand (in terms of the longer slack length not a higher stretch of the strand), demonstrating a special role of the heart size in its function. Model analysis suggests that cooperative mechanisms of myofilament calcium activation contribute essentially to the generation of cellular functional heterogeneity in contracting cardiac tissue.

Role of Mechanics in Rhythm Disturbances in 1D Mathematical Model of Myocardial Tissue with Local Ca2+-Overload

Possible contribution of the mechanics to the arrhythmogenesis in Ca2+ overloaded cardiomyocytes has been under appreciated. Earlier developed mathematical model of cardiomyocyte electromechanical function predicted a significant role of intra- and extracellular mechanical factors in triggering rhythm abnormalities. We utilized the cellular model to study effects of the electromechanical coupling between cardiomyocytes in a 1D heterogeneous muscle strand comprised normal (N) and sub-critical (SC) cardiomyocytes with moderately decreased Na+-K+ pump activity. The single SC cardiomyocytes did not demonstrate spontaneous activity during isometric contractions at a reference length. In the tissue, excitation spreads via electro-diffusional cell coupling and activates cell contractions and force development. Mechanical interactions between Nand SC-cells in the tissue resulted in the spontaneous activity emerged in the SC zone between the regular stimuli. The results suggest that ectopic activity may emerge in a rather small SC-region and expand by capturing normal regions in myocardium due to the electromechanical coupling between cardiomyocytes.