Hemodynamic Forces as a Stimulus for Arteriogenesis

Abstract

Ischemic heart diseases put a heavy economical burden on Western society. They remain one of the major causes of morbidity, and preventive or postoperative treatments are lengthy and expensive. In some patients of ischemic heart diseases, there is not a direct correlation between the degree of occlusion of major arteries and the development of medical symptoms or damage to the heart function. Interestingly, these patients develop well-formed collateral vessels that compensate for the decrease in blood supply to the heart wall. Clearly, the ability to understand why and how these patients develop collateral vessels may serve as a base for a new strategy to treat ischemic heart diseases by promoting collateral formation. The current article summarizes recent advances in the understanding of how collateral vessels develop and offers the authors' point of view on the central role of biomechanical forces in this process and the molecular mechanisms that underline it.

Role of ephrinB2 expression in endothelial cells during arteriogenesis: impact on smooth muscle cell migration and monocyte recruitment

“…Both shear stress and circumferential wall strain have been proposed as important "molding forces" for arteriogenic remodeling. 29,30 Because VEGF expression, which could easily explain the up-regulation of ephrinB2, is not affected at sites of collateral vessel growth 31 and increased shear stress down-regulates rather than up-regulates endothelial cell ephrinB2 abundance, 11 we focused on the effects of cyclic stretch, which corresponds to the rhythmic changes in circumferential wall strain in the arterial vessel wall. In contrast to shear stress, this biomechanical force affects endothelial cells and SMCs alike.…”

CFD analysis in an anatomically realistic coronary artery model based on non-invasive 3D imaging: comparison of magnetic resonance imaging with computed tomography

“…Hemodynamic parameters and their link to biological aspects A large body of evidence demonstrates the influence of wall shear stress on vascular endothelial cells as well as on vascular smooth muscle cells [3][4][5][6][7] resulting in as different events as flow mediated vasodilatation, atherosclerosis, thrombus formation and vascular remodelling. Additionally to the timeaveraged WSS, other hemodynamic parameters of the near wall flow have been proposed for clinicallyoriented flow studies: the oscillatory shear index (OSI), the time-averaged wall shear stress gradient (both spatial (WSSG s ) and temporal (WSSG t )), the wall shear stress angle deviation (WSSAD) and the wall shear stress angle gradient (WSSAG) [15].…”

“…A large body of evidence demonstrates the influence of wall shear stress (WSS) on vascular endothelial cells as well as on vascular smooth muscle cells [3][4][5][6][7], resulting in different events such as flow mediated vasodilatation, atherosclerosis and vascular remodelling. Therefore three-dimensional reconstruction of the geometry and the prediction of biofluidmechanical properties based on CFD modelling may help to assess the local risk in coronary artery segments prone to early atherosclerosis.…”

Formation of cardiovascular tubes in invertebrates and vertebrates

“…In the adult, hemodynamic stimuli caused by shear stress also induce lumen diameter expansion as seen for example during the growth of collateral arteries in arteriogenesis [103]. However, the embryonic aorta at early stages of lumen expansion lacks mural cells and blood flow [12,104], showing that alternative mechanisms of vascular lumen expansion must be in place.…”