Non-Newtonian Rheology in Blood Circulation

Blood is a complex suspension that demonstrates several non-Newtonian rheological characteristics such as deformation-rate dependency, viscoelasticity and yield stress. In this paper we outline some issues related to the non-Newtonian effects in blood circulation system and present modeling approaches based mostly on the past work in this field.Comment: 26 pages, 5 figures, 2 table

A theoretical model of the endothelial cell morphology due to different waveforms

Endothelial cells are key units in the regulatory biological process of blood vessels. They represent an interface to transmit variations on the fluid dynamic changes. They are able to adapt its cytoskeleton, by means of microtubules reorientation and F-actin reorganization, due to new mechanical environments. Moreover, they are responsible for initiating a huge cascade of biological processes, such as the release of endothelins (ET-1), in charge of the constriction of the vessel and growth factors such as TGF-ß and PDGF. Although a huge efforts have been made in the experimental characterization and description of these two issues the computational modeling has not gained such an attention. In this work we study the 3D remodeling of endothelial cells based on the main features of blood flow. In particular we study how different oscillatory shear index and the time average wall shear stresses modify the endothelial cell shape. We found our model fitted the experimental works presented before in in vitro studies. We also include our model within a computational fluid dynamics simulation of a carotid artery to evaluate endothelial cell shape index which is a key predictor of atheroma plaque formation. Moreover, our approach can be coupled with models of collagen and smooth muscle cell growth, where remodeling and the associated release of chemical substance are involved.Peer ReviewedPostprint (author's final draft

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

Mathematical modeling of collagen turnover in biological tissue

The final publication is available at Springer via http://dx.doi.org/10.1007/s00285-012-0613-yWe present a theoretical and computational model for collagen turnover in soft biological tissues. Driven by alterations in the mechanical environment, collagen fiber bundles may undergo important chronic changes, characterized primarily by alterations in collagen synthesis and degradation rates. In particular, hypertension triggers an increase in tropocollagen synthesis and a decrease in collagen degradation, which lead to the well-documented overall increase in collagen content. These changes are the result of a cascade of events, initiated mainly by the endothelial and smooth muscle cells. Here, we represent these events collectively in terms of two internal variables, the concentration of growth factor TGF-$\beta$ and tissue inhibitors of metalloproteinases TIMP. The upregulation of TGF-$\beta$ increases the collagen density. The upregulation of TIMP also increases the collagen density through decreasing matrix metalloproteinase MMP. We establish a mathematical theory for mechanically-induced collagen turnover and introduce a computational algorithm for its robust and efficient solution. We demonstrate that our model can accurately predict the experimentally observed collagen increase in response to hypertension reported in literature. Ultimately, the model can serve as a valuable tool to predict the chronic adaptation of collagen content to restore the homeostatic equilibrium state in vessels with arbitrary micro-structure and geometry.Peer ReviewedPostprint (author's final draft

The Role of Biofluid Mechanics in the Assessment of Clinical and Pathological Observations: Sixth International Bio-Fluid Mechanics Symposium and Workshop, March 28–30, 2008 Pasadena, California

Biofluid mechanics is increasingly applied in support of diagnosis and decision-making for treatment of clinical pathologies. Exploring the relationship between blood flow phenomena and pathophysiological observations is enhanced by continuing advances in the imaging modalities, measurement techniques, and capabilities of computational models. When combined with underlying physiological models, a powerful set of tools becomes available to address unmet clinical needs, predominantly in the direction of enhanced diagnosis, as well as assessment and prediction of treatment outcomes. This position paper presents an overview of current approaches and future developments along this theme that were discussed at the 5th International Biofluid Symposium and Workshop held at the California Institute of Technology in 2008. The introduction of novel mechanical biomarkers in device design and optimization, and applications in the characterization of more specific and focal conditions such as aneurysms, are at the center of attention. Further advances in integrative modeling, incorporating multiscale and multiphysics techniques are also discussed

Advancements in blood rheology and hemodynamics simulation with a brief history

Blood rheology is a complex field of study that investigates blood flow behavior, vital for understanding its role in physiological and pathological conditions. This article delves into various rheological models that describe blood behavior, ranging from Generalized Newtonian models to more sophisticated thixotropic and elastoviscoplastic models. One such model, the Horner-Armstrong-Wagner-Beris (HAWB) model, offers valuable insights into the dynamic interplay of reversible and irreversible phenomena in blood flow. Recent advancements, such as the mHAWB framework, provide enhanced accuracy and versatility in modeling blood rheology, holding great potential for diagnostic and therapeutic applications. Moreover, microscopic and mesoscopic simulations have paved the way for deeper insights into blood behavior, bridging the gap between theory and experiment. Multiscale models offer a promising approach to capturing the complexities of blood rheology at various length scales. Finally, we explore the clinical implications of blood rheology, including its significance in conditions like polycythemia, neonatal respiratory distress, and circulatory inadequacy. By understanding blood rheology comprehensively, we can advance our knowledge of complex blood flow dynamics and its potential applications in healthcare