Abstract
Hemodynamics have been linked to the genesis and progress of vascular disease in humans and animals1. Disturbed flow patterns such as stagnant flow or flow reversal lead to low or oscillating wall shear stress (WSS). Several in-vivo studies have correlated these types of WSS with disease formation1, 2. The desire to find correlations between markers of vascular disease and mechanical stimuli and because of their easier availability has led to an increasing number of animal model studies. The mouse, in particular, is a commonly used animal for investigating vascular disease formation and progression. Suo et al., were one of the first to relate findings on the molecular level with WSS1. They found increased VCAM and ICAM expression in areas of low WSS. More recently Hoi et al.2, have shown a correlation between atherosclerotic plaque development and hemodynamic parameters such as low time averaged wall shear stress (TAWSS) and Oscillatory Shear Index (OSI).
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