LES of non-Newtonian physiological blood flow in a model of arterial stenosis

Large Eddy Simulation (LES) is performed to study the physiological pulsatile transition-to-turbulent non-Newtonian blood flow through a 3D model of arterial stenosis by using five different blood viscosity models: (i) Power-law, (ii) Carreau, (iii) Quemada, (iv) Cross and (v) modified-Casson. The computational domain has been chosen is a simple channel with a biological type stenosis formed eccentrically on the top wall. The physiological pulsation is generated at the inlet of the model using the first four harmonic series of the physiological pressure pulse (Loudon and Tordesillas [1]). The effects of the various viscosity models are investigated in terms of the global maximum shear rate, post-stenotic re-circulation zone, mean shear stress, mean pressure, and turbulent kinetic energy. We find that the non-Newtonian viscosity models enlarge the length of the post-stenotic re-circulation region by moving the reattachment point of the shear layer separating from the upper wall further downstream. But the turbulent kinetic energy at the immediate post-lip of the stenosis drops due to the effects of the non-Newtonian viscosity. The importance of using LES in modelling the non-Newtonian physiological pulsatile blood flow is also assessed for the different viscosity models in terms of the results of the dynamic subgrid-scale (SGS) stress Smagorinsky model constant, C<sub>s</sub>, and the corresponding SGS normalised viscosity

The role of biomechanics in the assessment of carotid atherosclerosis severity: a numerical approach

Numerical fluid biomechanics has been proved to be an efficient tool for understanding vascular diseases including atherosclerosis. There are many evidences that atherosclerosis plaque formation and rupture are associated with blood flow behavior. In fact, zones of low wall shear stress are vivid areas of proliferation of atherosclerosis, and in particular, in the carotid artery. In this paper a model is presented for investigating how the presence of the plaque influences the distribution of the wall shear stress. In complement to a first approach with rigid walls, an FSI model is developed as well to simulate the coupling between the blood flow and the carotid artery deformation. The results show that the presence of the plaque causes an attenuation of the WSS in the after-plaque region as well as the emergence of recirculation areas

Roles of fibrin α- and γ-chain specific cross-linking by FXIIIa in fibrin structure and function

Factor XIII is responsible for the cross-linking of fibrin γ-chains in the early stages of clot formation, whilst α-chain cross-linking occurs at a slower rate. Although γ- and α-chain cross-linking was previously shown to contribute to clot stiffness, the role of cross-linking of both chains in determining clot structure is currently unknown. Therefore, the aim of this study was to determine the role of individual α- and γ-chain cross-linking during clot formation, and its effects on clot structure. We made use of a recombinant fibrinogen (γQ398N/Q399N/K406R), which does not allow for γ-chain cross-linking. In the absence of cross-linking, intact D-D interface was shown to play a potential role in fibre appearance time, clot stiffness and elasticity. Cross-linking of the fibrin α-chain played a role in the thickening of the fibrin fibres over time, and decreased lysis rate in the absence of α2-antiplasmin. We also showed that α-chain cross-linking played a role in the timing of fibre appearance, straightening fibres, increasing clot stiffness and reducing clot deformation. Cross-linking of the γ-chain played a role in fibrin fibre appearance time and fibre density. Our results show that α- and γ-chain cross-linking play independent and specific roles in fibrin clot formation and structure

Influence of lipids and obesity on haemorheological parameters in patients with deep vein thrombosis

It is not well established whether haemorheological alterations constitute independent risk factors for deep vein thrombosis (DVT).We have determined in 149 DVT patients and in 185 control subjects the body mass index (BMI), the haemorheological profile: blood viscosity (BV), plasma viscosity (PV), fibrinogen (Fg), erythrocyte aggregation (EA), erythrocyte deformability (ED) and plasma lipids. In the crude analysis BMI, Fg, PV, EA, triglycerides (TG) and ApoB were statistically higher and HDL cholesterol (HDL-Chol) statistically lower in DVT patients than in controls. No differences in BV and ED were observed.After BMI adjustment, Fg, PV and EA remained statistically higher in DVT cases than in controls (P=0.013; P=0.012; P=0.013; P=0.028, respectively). When the risk of DVT associated with these variables (using cut-offs that corresponded to the mean plus one SD of the control group) was estimated, EA>8.2 and PV>1.28 mPa.s were significantly associated with DVT even further adjustment for lipids and obesity (OR=2.78, P=0.004; OR=1.91, P=0.024, respectively). However, PV did not remain statistically significant after additional adjustment for Fg.When we consider together all the analyzed variables in order to control every variable for each other,TG>175 mg/dl (OR=3,2,P=0.004) and BMI>30 kg/m2 (OR=3.5, P=0.003), were also independently associated with a greater risk of DVT. Our results suggest that increased EA constitute an independent risk factor for DVT. However, when associated to hyperlipidaemia and obesity it further increases thrombotic [email protected]

Effects of unidirectional flow shear stresses on the formation, fractal microstructure and rigidity of incipient whole blood clots and fibrin gels

Incipient clot formation in whole blood and fibrin gels was studied by the rheometric techniques of controlled stress parallel superposition (CSPS) and small amplitude oscillatory shear (SAOS). The effects of unidirectional shear stress on incipient clot microstructure, formation kinetics and elasticity are reported in terms of the fractal dimension (df) of the fibrin network, the gel network formation time (TGP) and the shear elastic modulus, respectively. The results of this first haemorheological application of CSPS reveal the marked sensitivity of incipient clot microstructure to physiologically relevant levels of shear stress, these being an order of magnitude lower than have previously been studied by SAOS. CSPS tests revealed that exposure of forming clots to increasing levels of shear stress produces a corresponding elevation in df, consistent with the formation of tighter, more compact clot microstructures under unidirectional flow. A corresponding increase in shear elasticity was recorded. The scaling relationship established between shear elasticity and df for fibrin clots and whole blood confirms the fibrin network as the dominant microstructural component of the incipient clot in terms of its response to imposed stress. Supplementary studies of fibrin clot formation by rheometry and microscopy revealed the substantial additional network mass required to increase df and provide evidence to support the hypothesis that microstructural changes in blood clotted under unidirectional shear may be attributed to flow enhanced thrombin generation and activation. CSPS also identified a threshold value of unidirectional shear stress above which no incipient clot formation could be detected. CSPS was shown to be a valuable haemorheological tool for the study of the effects of physiological and pathological levels of shear on clot properties

Biophysical Mechanisms Mediating Fibrin Fiber Lysis

The formation and dissolution of blood clots is both a biochemical and a biomechanical process. While much of the chemistry has been worked out for both processes, the influence of biophysical properties is less well understood. This review considers the impact of several structural and mechanical parameters on lytic rates of fibrin fibers. The influences of fiber and network architecture, fiber strain, FXIIIa cross-linking, and particle transport phenomena will be assessed. The importance of the mechanical aspects of fibrinolysis is emphasized, and future research avenues are discussed.ECU Open Access Fun

Microscale flow dynamics of red blood cells in microchannels: an experimental and numerical analysis

Approximately, the half volume of the blood is composed of red blood cells (RBCs) which is believed to strongly influence its flow properties. Blood flow in microvessels depends strongly on the motion, deformation and interaction of RBCs. Several experimental studies on both individual and concentrated RBCs have already been performed in the past (Goldsmith 1971, Goldsmith and Marlow 1979, Chien et al. 1984, Goldsmith and Turitto 1986). However, all studies used conventional microscopes and also ghost cells to obtain visible trace RBCs through the microchannel. Recently, considerable progress in the development of confocal microscopy and consequent advantages of this microscope over the conventional microscopes have led to a new technique known as confocal micro-PIV (Tanaami et al. 2002, Park et al. 2004, Lima et al. 2006, 2007a). This technique combines the conventional PIV system with a spinning disk confocal microscope (SDCM). Due to its outstanding spatial filtering technique together with the multiple point light illumination system, this technique has the ability to obtain in-focus images with optical thickness less than 1 mm. In a numerical context, blood flow in large arteries is usually modeled as a continuum however this assumption is not valid in small vessels such as arterioles and capillaries. In this way, we are developing an integrative multi-scale model to simulate the blood flow at mesoscopic level. This computational approach may provide important information on the rheology of blood in small vasculatures where non-Newtonian property of blood is not negligible. The main purpose of this paper is to measure flow behavior of individual RBCs at different haematocrits (Hct) through a 75mm circular polydimethysiloxane (PDMS) microchannel by means of confocal micro-PTV system. Moreover we introduce an integrative multi-scale model to simulate the blood flow behavior through microvessels in order to obtain more detailed insights about the blood rhelogical properties at cellular level.This study was supported in part by the following grants: International Doctoral Program in Engineering from the Ministry of Education, Culture, Sports, Science and Technology of Japan (MEXT), “Revolutionary Simulation Software (RSS21)” next-generation IT program of MEXT; Grants-in-Aid for Scientific Research from MEXT and JSPS Scientific Research in Priority Areas (768) “Biomechanics at Micro- and Nanoscale Levels,” Scientific Research (A) No.16200031 “Mechanism of the formation, destruction, and movement of thrombi responsible for ischemia of vital organs”, Grant-in-Aid for Young Scientists (A) 19680024

Behaviour of the neutrophil to lymphocyte ratio in young subjects with acute myocardial infarction

In the last years the neutrophil to lymphocyte ratio (NLR) has been examined in cardiovascular disorders and in particular in coronary artery disease and acute myocardial infarction (AMI). Now we examined this parameter in subjects with juvenile myocardial infarction at the initial stage and after 3 and 12 months. We enrolled 123 young subjects (112 men and 11 women, mean age 39.4\ub15.8 yrs) with AMI. The time interval between the AMI onset and the investigation was 13\ub17 days. The mean value of NLR observed in young AMI subjects was significantly increased compared to normal controls (N = 1.817\ub10.711; young AMI subjects = 2.376\ub10.873, p < 0.0001). NLR does not discriminate STEMI (2.427\ub10.878) and non STEMI (2.392\ub10.868) or diabetics (2.604\ub11.000) and non diabetics (2.324\ub10.853), but it differentiates smokers (2.276\ub10.853) and non smokers (2.837\ub11.072). NLR at the initial stage is not correlated with the number of cardiovascular risk factors or with the extent of the coronary disease. In this study we found a significant decrease of neutrophil count at 3 and 12 months later AMI without any significant variation of lymphocyte and consequently we observed a decrease in NLR at these two intervals of time in comparison with the initial stage. Despite some limitations present in this study, it is interesting to underline that also in juvenile myocardial infarction this low-cost haematological marker may be considered together with other inflammatory indicators

Analysis of the Blood Viscosity Behavior in the Sicilian Study on Juvenile Myocardial Infarction

Considering the role of hemorheology in coronary circulation, we studied blood viscosity in patients with juvenile myocardial infarction. We examined whole blood viscosity at high shear rate using the cone-on-plate viscosimeter Wells-Brookfield \ubd LVT and at low shear rate employing a viscometer Contraves LS30 in 120 patients (aged <46 years) with myocardial infarction, at the initial stage and subsequently 3 and 12 months after. At the initial stage, patients had an increased whole blood viscosity in comparison to normal controls. This hemorheological profile was not influenced by the cardiovascular risk factors, nor by the extent of coronary lesions, even if some differences were evident between patients with ST-segment elevation myocardial infarction (STEMI) and non-STEMI (NSTEMI). The blood viscosity pattern at the initial stage did not influence recurring ischemic events or the onset of heart failure during an 18 months\u2019 follow-up. The neutrophil to lymphocyte ratio did not affect the blood viscosity pattern. We reevaluated 83 patients 3 months after and 70 patients 12 months after the acute coronary syndrome, and we found that the hemorheological parameters were still altered in comparison to normal controls at both times. We observed an impairment of the hemorheological pattern in young patients with myocardial infarction, partially influenced by the infarction type (STEMI and NSTEMI) and persisting in the long term