Hemodynamic changes occurring during the progressive enlargement of abdominal aortic aneurysms.

Ann Vasc Surg

Laboratory of Biomedical Flows, Department of Mechanical and Aerospace Engineering, University of California, San Diego, La Jolla, CA 92093, USA.

Published: January 2004

The purpose of this study is to characterize the evolution of the hemodynamic forces acting on the arterial walls at progressive stages of enlargement of abdominal aortic aneurysms (AAA). The specific aims are twofold: first, to determine the magnitude of the "wall shear stresses" (WSS) and their spatial and temporal gradients at various stages of enlargement, and second, to identify the critical size at which the formation of regions of stasis and/or the transition to a turbulent state occur inside the AAA. A parametric in vitro study of the pulsatile blood flow was conducted in rigid models of AAA by systematically varying the hemodynamic conditions and the size of the aneurysm. The instantaneous flow characteristics inside the AAA models were measured along the cardiac cycle, using tomographic digital particle image velocimetry (TDPIV). The TDPIV measurements showed that even for the case of large dilatation ratios (internal diameter >4.5 mm), the flow inside the AAA remained fully attached to the walls during systole, but massively detached during diastole. A critical aneurysm aspect ratio (length-to-diameter ratio) was found, for which a transition to a turbulent state occurred. The formation of internal shear layers (internal jet) and slowly recirculating regions (stasis) generated large spatial gradients of WSS and regions of low and oscillating WSS. The formation of regions of flow stasis was observed even at very early stages in the aneurysm enlargement. These spatial and temporal variations in the hemodynamic forces, the formation of regions of stasis, and the transition to turbulence are postulated to play an important role in the etiology of the disease by activating endoluminar thrombus formation, lipid deposition, and certain inflammatory mechanisms.

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http://dx.doi.org/10.1007/s10016-003-0101-3DOI Listing

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