Atherosclerosis is the main cause of death in Western societies.1 Myocardial infarction or stroke is, in the majority of cases, caused by rupture or erosion of an atherosclerotic plaque, in either the coronary or carotid circulation. Often, people are unaware of their risk for cardiovascular events, because plaques prone to rupture do not necessarily limit the blood flow and thus do not cause any symptoms. These plaques, called vulnerable plaques, are characterized by their specific morphology and composition: a large lipid pool covered by a thin fibrous cap (<65 µm)2 infiltrated by macrophages3 and expansive remodeling.2,4 In the presence of risk factors, which are systemic in nature, atherosclerotic plaques develop predominantly at specific locations in the arterial tree, including bifurcations and inner curves of arteries.5 As these predilection sites are associated with deviations of the normal velocity field, flow-induced shear stress, acting on the endothelial cells (ECs), has been recognized as a key player in plaque localization and plaque growth.6-9 The influence of shear stress on the generation and destabilization of vulnerable plaques is discussed in this chapter.

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Wentzel, J.J, Gijsen, F.J.H, Krams, R, de Crom, M.P.G, Cheng, C, Groen, H.C, … Serruys, P.W.J.C. (2007). Shear stress and the vulnerable plaque. In Handbook of the Vulnerable Plaque, Second Edition (pp. 233–244). Retrieved from