Comparative study of wall shear stress at the ascending aorta for different mechanical heart valve prostheses

An experimental study is reported which investigates the wall shear stress (WSS) distribution in a transparent model of the human aorta comparing a bileaflet mechanical heart valve (BMHV) with a trileaflet mechanical heart valve (TMHV) in physiological pulsatile flow. Elastic micro-pillar WSS sensors, calibrated by micro-Particle-Image-Velocimetry measurement, are applied to the wall along the ascending aorta. Peak WSS values are observed almost twice in BMHV compared to TMHV. Flow field analyses illuminate that these peaks are linked to the jet-like flows generated in the valves interacting with the aortic wall. Not only the magnitude but also the impact regions are specific for the different valve designs. The side-orifice jets generated by BMHV travel along the aortic wall in the ascending aorta and cause a whole range impact, while the jets generated by TMHV impact further downstream in the ascending aortic generating less severe WSS

Aortic Wave Dynamics and Its Influence on Left Ventricular Workload

The pumping mechanism of the heart is pulsatile, so the heart generates pulsatile flow that enters into the compliant aorta in the form of pressure and flow waves. We hypothesized that there exists a specific heart rate at which the external left ventricular (LV) power is minimized. To test this hypothesis, we used a computational model to explore the effects of heart rate (HR) and aortic rigidity on left ventricular (LV) power requirement. While both mean and pulsatile parts of the pressure play an important role in LV power requirement elevation, at higher rigidities the effect of pulsatility becomes more dominant. For any given aortic rigidity, there exists an optimum HR that minimizes the LV power requirement at a given cardiac output. The optimum HR shifts to higher values as the aorta becomes more rigid. To conclude, there is an optimum condition for aortic waves that minimizes the LV pulsatile load and consequently the total LV workload

Evolution and rupture of vulnerable plaques: a review of mechanical effects

Atherosclerosis occurs as a result of the buildup and infiltration of lipid streaks in artery walls, leading to plaques. Understanding the development of atherosclerosis and plaque vulnerability is of critical importance, since plaque rupture can result in heart attack or stroke. Plaques can be divided into two distinct types: those that rupture (vulnerable) and those that are less likely to rupture (stable). In the last few decades, researchers have been interested in studying the influence of the mechanical effects (blood shear stress, pressure forces, and structural stress) on the plaque formation and rupture processes. In the literature, physiological experimental studies are limited by the complexity of in vivo experiments to study such effects, whereas the numerical approach often uses simplified models compared with realistic conditions, so that no general agreement of the mechanisms responsible for plaque formation has yet been reached. In addition, in a large number of cases, the presence of plaques in arteries is asymptomatic. The prediction of plaque rupture remains a complex question to elucidate, not only because of the interaction of numerous phenomena involved in this process (biological, chemical, and mechanical) but also because of the large time scale on which plaques develop. The purpose of the present article is to review the current mechanical models used to describe the blood flow in arteries in the presence of plaques, as well as reviewing the literature treating the influence of mechanical effects on plaque formation, development, and rupture. Finally, some directions of research, including those being undertaken by the authors, are described

Vascular Hemodynamics CFD Modeling

Three dimensional pulsatile blood flow CFD simulations in geometrically genuine normal and non-normal (aneurysm) human neck-head vascular systems nominally spanning the aortic arch to the circle of Willis has been performed and studied. CT scans of the human aortic arch and the carotid arteries were interpreted to obtain geometric data defining the boundary for a vascular CFD simulation. This was accomplished by reconstructing the surface from the anatomical slices and by imposing pertinent boundary conditions at the various artery termini. Following automated formation of a non-conformal CFD mesh, steady and unsteady laminar and low turbulent simulations were performed both for the normal and aneurysm models. Atherosclerosis and atherosclerotic induced aneurysms can occur in the ascending aorta. The results showed marked differences in the flow dynamics for the two models. Secondary flow is induced in both of the models due to the curvature of the aortic arch which is distorted in three dimensions. Counter clockwise rotating vortex formation was seen at the aneurysm segment in the ascending aorta for the aneurysm model which was absent for the normal case. The effect of the aneurysm bulge was seen in regions proximal to it at peak reverse flow causing secondary flow. These secondary aortic blood flows are though to have an effect on the wall shear stress distribution. Maximum pressure regions for the aneurysm were observed at regions distal to it indicating the possible location for rupture. Wall shear force (WSF) values for the normal case at the aortic bend were low indicating the possible reason for the formation of the aneurysm in the first place. The WSF values at the aneurysm segment for the aneurysm case were also low supporting the low shear stress induced atherosclerotic aneurysms theory. These results may act as a precursor for a multiscale Large eddy simulation model (LES) for pulsatile blood flow eliminating the need for a priori definition of the flow as laminar or turbulent

Study of the relation between blood flow and the age-dependent localisation of early atherosclerosis

Atherosclerosis develops non-uniformly within the arterial system and the distribution of lesions has been observed to change with age. This thesis investigates the concept that the patchiness of the disease is related to local variations in blood flow. Based on the insights from a systematic literature review, a novel study was designed to analyse the relation between haemodynamic factors and age-dependent atherogenesis in the thoracic aorta of rabbits. Arterial geometries were reconstructed by micro-Computed Tomography of vascular corrosion casts, with particular attention to the anatomical accuracy of the dataset. Blood flow was simulated in these geometries using a spectral/hp element method. Distributions of traditional shear-related metrics were calculated and both qualitatively and quantitatively compared to maps of lesion prevalence. In addition, a time-averaged transverse wall shear stress was introduced. A geometric analysis of the dataset of rabbit thoracic aortas revealed a significant change with age in the degree of aortic taper. The geometric changes could explain age-related differences in flow characteristics, in particular in the extent of Dean-type vortical structures into the descending aorta and the strength of a dorsal streak of high shear. The comparative analysis of shear and lesion distributions did not unequivocally support the theory that lesions occur in regions of low shear. The novel haemodynamic metric, in combination with current metrics, enabled an improved identification of zones of multi-directional disturbed flow. In conclusion, this thesis adds to the understanding of the relation between blood flow and early atherosclerosis, and provides tools for use in future studies

Evolution of the wall shear stresses during the progressive enlargement of symmetric abdominal aortic aneurysms.

The changes in the evolution of the spatial and temporal distribution of the wall shear stresses (WSS) and gradients of wall shear stresses (GWSS) at different stages of the enlargement of an abdominal aortic aneurysm (AAA) are important in understanding the aetiology and progression of this vascular disease since they affect the wall structural integrity, primarily via the changes induced on the shape, functions and metabolism of the endothelial cells. Particle image velocimetry (PIV) measurements were performed in in vitro aneurysm models, while changing their geometric parameters systematically. It has been shown that, even at the very early stages of the disease, i.e. increase in the diameter ≤ 50%, the flow separates from the wall and a large vortex ring, usually followed by internal shear layers, is created. These lead to the generation of WSS that drastically differ in mean and fluctuating components from the healthy vessel. Inside the AAA, the mean WSS becomes negative along most of the aneurysmal wall and the magnitude of the WSS can be as low as 26% of the value in a healthy abdominal aorta. Two regions with distinct patterns of WSS were identified inside the AAA: the proximal region of flow detachment, characterized by oscillatory WSS of very low mean, and the region of flow reattachment, located distally, where large, negative WSS and sustained GWSS are produced as a result of the impact of the vortex ring on the wall. Comparison of the measured values of WSS and GWSS to an analytical solution, calculated for slowly expanding aneurysms shows a very good agreement, thus providing a validation of the PIV measurements

Abnormal wave reflections and left ventricular hypertrophy late after coarctation of the aorta repair

Patients with repaired coarctation of the aorta are thought to have increased afterload due to abnormalities in vessel structure and function. We have developed a novel cardiovascular magnetic resonance protocol that allows assessment of central hemodynamics, including central aortic systolic blood pressure, resistance, total arterial compliance, pulse wave velocity, and wave reflections. The main study aims were to (1) characterize group differences in central aortic systolic blood pressure and peripheral systolic blood pressure, (2) comprehensively evaluate afterload (including wave reflections) in the 2 groups, and (3) identify possible biomarkers among covariates associated with elevated left ventricular mass (LVM). Fifty adult patients with repaired coarctation and 25 age- and sex-matched controls were recruited. Ascending aorta area and flow waveforms were obtained using a high temporal-resolution spiral phase-contrast cardiovascular magnetic resonance flow sequence. These data were used to derive central hemodynamics and to perform wave intensity analysis noninvasively. Covariates associated with LVM were assessed using multivariable linear regression analysis. There were no significant group differences (P≥0.1) in brachial systolic, mean, or diastolic BP. However central aortic systolic blood pressure was significantly higher in patients compared with controls (113 versus 107 mm Hg, P=0.002). Patients had reduced total arterial compliance, increased pulse wave velocity, and larger backward compression waves compared with controls. LVM index was significantly higher in patients than controls (72 versus 59 g/m(2), P<0.0005). The magnitude of the backward compression waves was independently associated with variation in LVM (P=0.01). Using a novel, noninvasive hemodynamic assessment, we have shown abnormal conduit vessel function after coarctation of the aorta repair, including abnormal wave reflections that are associated with elevated LVM

Computational studies of blood flow at arterial branches in relation to the localisation of atherosclerosis

Atherosclerotic lesions are non-uniformly distributed at arterial bends and branch sites, suggesting an important role for haemodynamic factors, particularly wall shear stress (WSS), in their development. Using computational flow simulations in idealised and anatomically realistic models of aortic branches, this thesis investigates the role of haemodynamics in the localisation of atherosclerosis. The pattern of atherosclerotic lesions is different between species and ages. Such differences have been most completely documented for the origins of intercostal arteries within the descending thoracic aorta. The first part of the thesis deals with the analysis of wall shear stresses and flow field near the wall in the vicinity of model intercostal branch ostia using high-order spectral/hp element methods. An idealised model of an intercostal artery emerging perpendicularly from the thoracic aorta was developed, initially, to study effects of Reynolds number and flow division under steady flow conditions. Patterns of flow and WSS were strikingly dependent on these haemodynamic parameters. Incorporation of more realistic geometrical features had only minor effects. The WSS distribution in an anatomically correct geometry of a pair of intercostal arteries resembled in character the pattern seen in the idealised geometry. Under unsteady and non-reversing flow conditions, the effect of pulsatility was small. However, significantly different patterns were generated for reversing aortic near-wall flow and reversing side branch flow. The work was extended to study the wall shear stress distribution within the aortic arch and proximal branches of mice, in comparison to that of men. Mice are increasingly used as models to study atherosclerosis and it has been shown that, in knockout mice lacking the low density lipoprotein receptor and apolipoprotein E, lesions develop in vivo at the proximal wall of the entrance to the brachiocephalic artery. Three aortic arch geometries from wild-type mice were reconstructed from MRI images using in-house and commercial software, and the WSS distribution was calculated under steady flow conditions to establish the mouse haemodynamic environment and mouse-to-mouse variability. Approximated human aortic arch geometries were further considered to enable comparison of the flow and WSS fields with that of mice. The haemodynamic environment of the aortic arch varied between the two species. The overall distribution of wall shear stress was more heterogeneous in the human aortic arch than in the mouse arch, although some features were similar. Intraspecies differences in mice were small and influenced primarily by the detailed anatomical geometry and the Reynolds number. A number of simplifications were made in the above flow analyses, and clearly, relaxing these assumptions would increase complexity. Nonetheless, this thesis demonstrates the fundamental features of flow, which underlie the disparate patterns of WSS in different species and/or ages, for simplified cases, and the results are expected to be relevant to more complex ones. Aspects of the observed WSS patterns in the simplified model of intercostal artery correlate with, and may explain, some of the lesion patterns in human, rabbit and mouse aortas. WSS distributions in the aortic arch of wild-type mice associate with lesion locations seen in diseased mice.Open acces