Towards patient specific models of cardiac mechanics : a sensitivity study

In the design of patient specific mathematical models of cardiac mechanics, the lack of patient specific input data leads to default settings of various model parameters. To estimate the potential errors thus introduced, we evaluated changes in predicted mechanics in a model of the left ventricle (LV) induced by changes in geometry, fiber orientation, heterogeneity of passive material behavior and triaxial active stress development. Incorporation of measured heterogeneity of passive stiffness did not affect systolic mechanics. Incorporation of triaxial active stress development did significantly affect systolic mechanics, but knowledge on this mechanism is too limited to draw conclusions. LV geometry variations covering the biological range changed the equatorial distribution of active myofiber stress and shortening by about 10 to 15%. Similar changes were found by variation of fiber orientation by 8° at maximum. Since this change in orientation is at the edge of the accuracy, with which myofiber orientation can be measured in vitro, and far below the accuracy, obtainable for in vivo measurements, we conclude that the benefit of accounting for patient specific geometry is questionable when using experimental data on fiber orientation. We propose to select myofiber orientation such, that myofiber load is distributed homogeneously across the cardiac wall

Intra- and interventricular asynchrony of electromechanics in the ventricularly paced heart

The degree of restoration of pump function by ventricular pacing depends on the pacing site and timing of pacing. Numerical models of cardiac electromechanics could be used to investigate the relation between the ventricular pacing site and timing on the one side, and pump function on the other. In patient-specific models, these numerical models could be used to optimize location and timing for best pump function. The aim of this study was to demonstrate the potential for modeling patient-specific electromechanic during ventricular pacing by means of the extension of an existing three-dimensional finite-element model of LV electromechanics with the right ventricle. A parametrized geometry of the LV and RV was made from canine (non-invasively obtained) cine-MR short axis images. Depolarization was modeled using the eikonal-diffusion equation. Mechanics was computed from balance of momentum, with nonlinear anisotropic passive and time-, strain-, and strainrate-dependent uniaxial active behavior. Simulations of complete cardiac cycles were performed for a normal heart beat with synchronous activation and ventricular pacing at the right ventricular apex and left ventricular free wall. We focused on timing of LV and RV hemodynamics, asynchrony in depolarization and myofiber shortening, regional stroke work, and systolic septal motion. In the simulation of sinus rhytm, ventricular ejection was found to start earlier for the right side than for the left side, which is in agreement with experimental data. In simulations with ventricular pacing, results agreed with experimental findings in the following aspects: 1) depolarization sequence; 2) the spatial distributions of sarcomere length and stroke work density depended mainly on timing of depolarization; 3) maximum pressure and maximum increase of pressure were lower than during sinus rhythm; 4) the earliest activated ventricle had the earliest start of ejection, and 5) the septum moved towards the last activated ventricle at the onset of systole. As a first step, the potential of patient-specific modeling in simulating conduction disturbances has been demonstrated by inserting a ventricular geometry, obtained from non-invasively measured short axis MR images. Later steps would include the implementation of adaptation models to estimate patient myofiber orientation and to assess the effects of pacing in the long term

Cardiac fiber orientation and the left-right asymmetry determining mechanism

The invariant nature of body situs within and across vertebrate species implies that a highly conserved pathway controls the specification of the left-right (L/R) axis. Situs-specific morphogenesis begins at the end of this pathway and leads to normal organ arrangement, also known as situs solitus. Occasionally, individuals have a complete, mirror image reversal of this asymmetry, called situs inversus totalis (SIT). In these individuals, gross anatomy is mirror imaged. However, the helical myofiber pattern within the left ventricle (LV) wall is only partially mirror imaged: apical and superficial basal fiber orientation are as in normal persons, whereas the deeper basal layers have an inverted fiber orientation. Because of this bivalent fiber orientation pattern, LV deformation in humans with SIT is mirror imaged only near the base, but near the apex it is as in normal subjects. 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 LV wall

Biomechanical analysis of abdominal aortic aneurysms

The aorta is the largest artery in the human body, transporting oxygenized blood directly from the left ventricle of the heart to the rest of the body. An aortic aneurysm is a local dilation in the aorta of more than 1.5 times the original diameter [27]. Although aneurysms can be present in every part of the aorta, the majority of the aortic aneurysms are situated in the abdominal aorta (AAA, Fig. 6.1), below the level of the renal arteries and above the aortic bifurcation to the common iliac arteries [7]. A diameter of 3 cm or more is generally used as indication for an AAA (abdominal aortic aneurysm). In most AAAs, thrombus is found between the perfused flow lumen and the aortic wall. Thrombus is a fibrin structure with mainly blood cells, platelets, and blood proteins, which is deposited onto the vessel wall [21]

Biomechanical analysis of abdominal aortic aneurysms

The aorta is the largest artery in the human body, transporting oxygenized blood directly from the left ventricle of the heart to the rest of the body. An aortic aneurysm is a local dilation in the aorta of more than 1.5 times the original diameter [27]. Although aneurysms can be present in every part of the aorta, the majority of the aortic aneurysms are situated in the abdominal aorta (AAA, Fig. 6.1), below the level of the renal arteries and above the aortic bifurcation to the common iliac arteries [7]. A diameter of 3 cm or more is generally used as indication for an AAA (abdominal aortic aneurysm). In most AAAs, thrombus is found between the perfused flow lumen and the aortic wall. Thrombus is a fibrin structure with mainly blood cells, platelets, and blood proteins, which is deposited onto the vessel wall [21]