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Review
. 2010 Jul-Aug;53(1-2):11-21.
doi: 10.1016/j.vph.2010.03.004. Epub 2010 Mar 25.

Hemodynamic influences on abdominal aortic aneurysm disease: Application of biomechanics to aneurysm pathophysiology

Affiliations
Review

Hemodynamic influences on abdominal aortic aneurysm disease: Application of biomechanics to aneurysm pathophysiology

Monica M Dua et al. Vascul Pharmacol. 2010 Jul-Aug.

Abstract

"Atherosclerotic" abdominal aortic aneurysms (AAAs) occur with the greatest frequency in the distal aorta. The unique hemodynamic environment of this area predisposes it to site-specific degenerative changes. In this review, we summarize the differential hemodynamic influences present along the length of the abdominal aorta, and demonstrate how alterations in aortic flow and wall shear stress modify AAA progression in experimental models. Improved understanding of aortic hemodynamic risk profiles provides an opportunity to modify patient activity patterns to minimize the risk of aneurysmal degeneration.

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Figures

Figure 1
Figure 1
Hemodynamic forces relevant to AAA pathogenesis; hydrostatic pressure, the perpendicular force acting on the vascular wall (A), wall shear stress, the tangential force exerted by moving blood along the axis of flow (B), and tensile hoop stress, the stress in the aortic wall acting circumferentially and produced by the resulting pressure (C).
Figure 2
Figure 2
Magnetic resonance angiography of the abdominal aorta in spinal cord injury (SCI) patients showing characteristic vascular phenotypes of ectatic distal aortic segments adjacent to diminished iliac arteries. Adapted from Yeung et al., 2006, J. Vasc. Surg. 44, 1254–1265 with permission.
Figure 3
Figure 3
Geometric modeling of resting WSS estimates at peak systole of normal aorta, SCI aorta and 4cm AAA from left to right, respectively. Adapted from Dalman et al., 2006, Ann. N. Y. Acad. Sci. 1085, 92–109 with permission.
Figure 4
Figure 4
Maximum aortic diameter at day 0, 7, or 14 days after PPE infusion (POD indicated postoperative day) as a function of normal flow (sham) or flow loading (AVF) applied either before (experiment 1) or after (experiment 2) PPE infusion (*p<0.05 against normal flow group). Reprinted from Nakahashi et al., 2002, Arterioscler. Thromb. Vasc. Biol. 22, 2017–2022 with permission.
Figure 5
Figure 5
Changes in aortic diameter after PPE infusion with iliac artery ligation (low-flow) or femoral arteriovenous fistula creation (high-flow). (*p<0.05 against preoperative diameter, †p<0.01 compared with low-flow AAA). Reprinted from Hoshina et al., 2003, J. Vasc. Surg. 37, 1067–1074 with permission.
Figure 6
Figure 6
Flow-dependent expression of relevant cell markers, cytokines, growth factors and growth factor receptors. AAA mRNA expression analysis determined by real time PCR. Data reported as the ratio of target molecules versus normal control aortic tissue. Reprinted from Sho et al., 2004b, Arterioscler. Thromb. Vasc. Biol. 24, 1916–1921 with permission.
Figure 7
Figure 7
Schematic of the human aorta with imaging planes at the supraceliac and infrarenal levels and flow data from a representative healthy subject, aged 59, at rest and during cycling exercise. Blood flow rate waveforms (top) show significant increases in flow at both the supraceliac and infrarenal levels from rest (left) to exercise (right) throughout the cardiac cycle. Also note that reversal of flow at the infrarenal level at rest is eliminated during exercise. Velocity surface plots are shown for the supraceliac and infrarenal levels of the aorta at rest (left) and during exercise (right) at peak systole (A), end systole (B), and end diastole (C). Blood velocities increase from rest to exercise for all cardiac phases, and most of the negative blood velocities near the walls of the supraceliac and infrarenal levels at end systole (B) at rest (left) become positive during exercise (right). Wall shear stress plots (bottom) reveal that nearly all of the negative wall shear stress present in the infrarenal aorta during diastole at rest is eliminated with exercise. Reprinted from Cheng et al., 2003b, Atherosclerosis. 168, 323–331 with permission.
Figure 8
Figure 8
Custom software was used to convert magnetic resonance data (left) to a three-dimensional geometric model of the flow domain (center left). The three-dimensional model, in combination with patient-specific blood flow information, was used to simulate blood flow in an aneurysm during rest and exercise. During resting conditions, areas of low flow and flow stagnation exist within the aneurysm even at peak systole (center right); these regions are decreased during simulated exercise (right). Reprinted from White and Dalman, 2008, The Permanente Journal. 12, 10–14, with permission from The Permanente Press.

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