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CHA PTE R

Impact of the Fluid-Structure Interaction

Modeling on the Human Vessel Hemodynamics

§
Mauro Malve ` * ,†,‡ , Myriam Cilla , Estefanı ´a Pen ˜a †,‡,¶ ,
Miguel Angel Martı ´nez †,‡,¶
†
*Department of Engineering, Public University of Navarra, Pamplona, Spain Centro de Investigacio ´n en Red
‡
en Bioingenierı ´a, Biomaterialesy Nanomedicina, CIBER-BBN, Zaragoza, Spain Arago ´n Institute of Engineering
§
Research (I3A), University of Zaragoza, Zaragoza, Spain Centro Universitario de la Defensa, Academia General Militar,
¶
Zaragoza, Spain Department of Mechanical Engineering, University of Zaragoza, Zaragoza, Spain

5.1 CLINICAL BACKGROUND

It is estimated that approximately 60% of all human deaths are caused by cardiovascular disorders [1]. The most
relevant disease in this sense is atherosclerosis, due to the increasing number of affected persons [1]. Atherosclerosis is
a pathological obstruction of blood vessels consisting of the formation, growth, and development of a plaque that is
deposited from different origins. The narrowing caused by this progressive deposit on the artery limits the oxygen-rich
blood flow to the heart and other vessels, promoting heart attack and stroke among other pathologies and leading
even to death. The lesion begins with some accumulation in the intima layer and progresses, forming a fatty cap
that can eventually become calcified. There is much evidence that atherosclerosis is nonuniformly distributed in
the human body. On the contrary, it occurs at certain specific locations of the cardiovascular system, especially the
arterial bifurcations [2, 3].
It is known that many factors affecting the whole body such as smoking, high cholesterol, hypertension, and life-
style, among others, promote cardiovascular diseases. In recent years, it has been suggested that perturbed blood flow
and/or abnormal stresses and strains of the artery may play a considerable role in atherogenesis. Extensive numerical
studies centered on the modeling of human and animal hemodynamics have shown that bifurcations are peculiar
geometrical regions submitted to highly perturbed flows. The latter promotes complex flow patterns characterized
by unsteadiness, high local Reynolds numbers, flow recirculation with a variety of flow structures, and local peaks
of high and low endothelial shear stress. In some arteries such as the aorta, blood flow may even become locally tur-
bulent. In this context, it is clear that near the bifurcation, the endothelium is loaded with nonuniform forces generated
by the complexity of the aforementioned flow patterns. The smooth muscle cells of the artery are certainly influenced
and stimulated by the blood flow acting on the vessel walls by means of the shear stress. For this reason, many inves-
tigations into atherosclerosis have been focused on searching for a surrogate marker for atherogenesis in the compu-
tational hemodynamics. The most accepted theory in respect to this is that the oscillating or low average shear stress is
responsible for the appearance of the plaque. However, there are a few studies that propose high shear stress as an
important factor for atherogenesis, and there is no agreement in this sense. Due to the intervariability of the arterial
morphology among patients, perturbed flow and nonuniform wall shear stress (WSS) have often been correlated with
geometrical factors that may considerably change among the different parts of the blood vessels [4–6].
Atherogenesis has been associated with arterial bifurcation, also considering the vessel walls. Geometrically speak-
ing, arteries are compliant cylindrical tubes that at the bifurcation, due to the changes promoted by stretch and dila-
tation, may show important changes and complex morphologies. An increase or decrease of curvature as well as
changes of diameter and of shape and variations of wall thickness are shown to promote the concentration of stresses

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