The distribution of atherosclerotic lesions within the coronary arteries is highly localized, despite the fact that risk factors (e.g., dyslipidemia) are systemic nature. The biomechanical milieu of the coronary arteries is unique in that in addition to cyclic pressure, circumferential distension and shear stress, they experience mechanical deformations of twisting, bending, and longitudinal stretching due to their tethering to the dynamic epicardial surface [1]. Biplane cineangiographic reconstruction studies have demonstrated that the coronary arteries experience as much as 20° of torsion during a cardiac cycle [2]. Spatial variations in shear and mural stresses caused by this deformation could account for the heterogeneity of atherosclerotic plaques.

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