Optimizing ventricular fibers : uniform strain or stress, but not ATP consumption, leads to high efficiency

The aim of this work is to investigate the influence of fiber orientation in the left ventricular (LV) wall on the ejection fraction, efficiency and the heterogeneity of the distributions of developed fiber stress, strain and ATP consumption. A finite element model of LV mechanics was used with active properties of the cardiac muscle described by the Huxley-type cross-bridge model. The computed variances of sarcomere length (VarSL), developed stress (VarDS) and ATP consumption (VarATP) have several minima at different transmural courses of helix fiber angle. We identified only one region in the used design space with high ejection fraction, high efficiency of the LV and relatively small VarSL, VarDS, and VarATP. This region corresponds to the physiological distribution of the helix fiber angle in the LV wall. Tra! nsmural fiber angle can be predicted by minimizing VarSL and VarDS, but not VarATP. If VarATP was minimized then the transverse fiber angle was considerably underestimated. The results suggest that ATP consumption distribution is not regulating the fiber orientation in the heart

Left ventricular apical torsion and architecture are not inverted in situs inversus totalis

Occasionally, individuals have a complete, mirror-image reversal of their internal organ position, called situs inversus totalis (SIT). Whereas gross anatomy is mirror-imaged in SIT, this might not be the case for the internal architecture of organs, e.g. the myofiber pattern in the left cardiac ventricle. We performed a Magnetic Resonance Tagging study in 9 controls and in 8 subjects with SIT to assess the deformation pattern in the apical half of the LV wall. It appeared that both groups had the same LV apical deformation pattern. This implies that not only the superficial LV apical layers in SIT follow a normal, not inverted pattern, but the deeper layers as well. Apparently, the embryonic L/R controlling genetic pathway does determine situs-specific gross anatomy morphogenesis but it is not the only factor regulating fiber architecture within the apical part of the LV wall. We propose that mechanical forces generated in the not-inverted molecular structure of the basic right-handed helical contractile components of the sarcomere play a role in shaping the LV apex

Cardiac mechanoenergetics replicated by cross-bridge model

The aim of this work is to reproduce the experimentally measured linear dependence of cardiac muscle oxygen consumption on stress–strain area using a model, composed of a three-state Huxley-type model for cross-bridge interaction and a phenomenological model of Ca2+-induced activation. By selecting particular cross-bridge cycling rate constants and modifying the cross-bridge activation model, we replicated the linear dependence between oxygen consumption and stress–strain area together with other important mechanical properties of cardiac muscle such as developed stress dependence on the sarcomere length and force-velocity relationship. The model predicts that (1) the amount of the passenger cross bridges, i.e., cross bridges that detach without hydrolyzing ATP molecule, is relatively small and (2) ATP consumption rate profile within a beat and the amount of the passenger cross bridges depend on the contraction protocol

Biomechanics of the heart muscle

In this paper the mechanics of the beating left ventricle is investigated using finite element modelling. Important aspects considered in the modelling of the mechanical behaviour are: (1) influence of muscle fibre orientation on ventricular mechanics, (2) redistribution of intracoronary blood in the ventricular wall during the cardiac cycle, (3) viscoelastic behaviour of myocardial tissue, and regional decrease of myocardial perfusion, resulting in an ischemic region

Adaptation to mechanical load determines shape and properties of heart and circulation : the CircAdapt model

With circulatory pathology, patient-specific simulation of hemodynamics is required to minimize invasiveness for diagnosis, treatment planning, and followup. We investigated the advantages of a smart combination of often already known hemodynamic principles. The CircAdapt model was designed to simulate beat-to-beat dynamics of the four-chamber heart with systemic and pulmonary circulation while incorporating a realistic relation between pressure-volume load and tissue mechanics and adaptation of tissues to mechanical load. Adaptation was modeled by rules, where a locally sensed signal results in a local action of the tissue. The applied rules were as follows: For blood vessel walls, 1) flow shear stress dilates the wall and 2) tensile stress thickens the wall; for myocardial tissue, 3) strain dilates the wall material, 4) larger maximum sarcomere length increases contractility, and 5) contractility increases wall mass. The circulation was composed of active and passive compliances and inertias. A realistic circulation developed by self-structuring through adaptation provided mean levels of systemic pressure and flow. Ability to simulate a wide variety of patient-specific circumstances was demonstrated by application of the same adaptation rules to the conditions of fetal circulation followed by a switch to the newborn circulation around birth. It was concluded that a few adaptation rules, directed to normalize mechanical load of the tissue, were sufficient to develop and maintain a realistic circulation automatically. Adaptation rules appear to be the key to reduce dramatically the number of input parameters for simulating circulation dynamics. The model may be used to simulate circulation pathology and to predict effects of treatment