Real-Time Measurement of Multi-Component Velocity Vectors Within Abdominal Aortic Aneurysms Using Echo PIV: Comparison of In Vitro and Computational Results

Author(s):  
Lingli Liu ◽  
Fuxing Zhang ◽  
Rui Wang ◽  
Robin Shandas

Abdominal aortic aneurysms (AAAs) are localized balloon-shaped expansions commonly found in the infrarenal segment of the abdominal aorta, between the renal arteries and the iliac bifurcation. Abdominal aortic aneurysm rupture has been estimated to occur in as much as 3%–9% of the population, and represents the 13th leading cause of death in the United States, producing more than 10,000 deaths annually [1]. Thus, determining the significant factors for aneurysm growth and rupture has become an important clinical goal. From a biomechanical standpoint, AAA rupture risk is related to certain mechanical and hemodynamic factors such as localized flow fields and velocity patterns, and flow-induced stresses within the fluid and in the aneurysm structure [2]. Disturbed flow patterns at different levels have also been found to trigger responses within medial and adventitial layers by altering intercellular communication mechanisms. Thus, localized hemodynamics proximal, within and distal to AAA formations play an important role in modulating the disease process, and non-invasive and easy-to-implement methods to characterize and quantify these complex hemodynamics would be tremendously useful.

2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Kiana M Samadzadeh ◽  
Anthony Nguyen ◽  
Kevin C Chun ◽  
Eugene S Lee

Purpose: The pleiotropic effects of statin drugs on reducing inflammation have been well regarded in decreasing AAA expansion. We hypothesize that increased monocyte activity plays a central role in AAA formation and expansion. This study examines whether statins can prevent monocyte cell adhesion, transmigration, and matrix metalloproteinase (MMP) and inhibitor (TIMP) concentrations in AAA patients compared to non-AAA patients. Methods: Peripheral blood was collected for monocyte and serum isolation from control (n=4) and AAA (n=8) patients. Monocyte adhesion and transmigration were assessed under untreated, statin treated, and statin + mevalonate (statin inhibitor) treated conditions in vitro. Luminex assays determined MMP and TIMP concentrations from cell culture and patient serum. Results: Untreated AAA patient monocytes showed higher levels of adhesion (p=0.05) and transmigration (p=0.04) compared to control subjects (Figure 1A & 1B). Statin treatment caused a decrease in AAA monocyte adherence to the endothelium (p=0.03) and high concentrations of mevalonate reversed statin treatment effects (p=0.04) (Figure 1A). A similar trend was noted in monocyte transmigration (Figure 1B). Higher concentrations of MMP-9 were found in AAA patient serum compared to controls (p=0.01) (Figure 1C). TIMP-4 concentration were decreased in AAA patients compared to controls (p=0.02) (Figure 1D). Conclusions: Statins reduce monocyte interaction with the endothelium in vitro, leading to decreased levels of MMP-9 and increased levels of TIMP-4, implying a possible mechanism by which statins reduce AAA expansion.


Author(s):  
Jeffrey N. Kinkaid ◽  
Steven P. Marra ◽  
Francis E. Kennedy ◽  
Mark F. Fillinger

Abdominal Aortic Aneurysms (AAAs) are localized enlargements of the aorta. If untreated, AAAs will grow irreversibly until rupture occurs. Ruptured AAAs are usually fatal and are a leading cause of death in the United States, killing 15,000 per year (National Center for Health Statistics, 2001). Surgery to repair AAAs also carries mortality risks, so surgeons desire a reliable tool to evaluate the risk of rupture versus the risk of surgery.


2008 ◽  
Vol 15 (4) ◽  
pp. 468-484 ◽  
Author(s):  
Timothy J. Corbett ◽  
Anthony Callanan ◽  
Liam G. Morris ◽  
Barry J. Doyle ◽  
Pierce A. Grace ◽  
...  

2015 ◽  
Author(s):  
John P. Davis ◽  
Gilbert R Upchurch Jr

Abdominal aortic aneurysms (AAAs) are characterized by dilation of the abdominal aorta at least 1.5 times the normal diameter of the average adult, which is approximately 2 cm in men and 1.5 cm in women. Although the incidence is relatively low, this disease can be devastating, with AAAs accounting for roughly 15,000 deaths annually in the United States. This review covers the focused history and physical examination of a patient with a known AAA, evaluation of small and large AAAs, and surveillance of AAAs. Tables highlight recommendations for best medical management of small AAAs during the surveillance period, and information on nicotine replacement and nonnicotinic pharmacotherapy. Figures show a calcific rim consistent with the atherosclerotic rim of an AAA, a small AAA, a small inflammatory AAA, and age-adjusted effects of lifestyle characteristics and risk of AAA. An algorithm provides an approach to nonoperative management of stable AAAs. This review contains 5 figures, 3 tables, and 86 references.


Vascular ◽  
2004 ◽  
Vol 12 (04) ◽  
pp. 218 ◽  
Author(s):  
Reid M. Wainess ◽  
Justin B. Dimick ◽  
John A. Cowan ◽  
Peter K. Henke ◽  
James C. Stanley ◽  
...  

2007 ◽  
Vol 98 (08) ◽  
pp. 427-433 ◽  
Author(s):  
Chaoyong Zhu ◽  
Angela Silveira ◽  
Anne-Louise Hemdahl ◽  
Anders Hamsten ◽  
Ulf Hedin ◽  
...  

SummaryIt has been suggested that the intraluminal thrombus of abdominal aortic aneurysms (AAAs) predisposes for AAA enlargement and rupture.The growth of theAAA is dependent on proteolytic degradation of elastin. Here, we analysed whether the neutrophil gelatinase-associated lipocalin (NGAL) is expressed within the thrombus and the aneurysm wall. NGAL can bind to metalloproteinase- 9 (MMP-9) and inhibit its degradation,thereby preserving enzymatic activity. Biopsies were obtained from thrombus- free and thrombus-covered aneurysm wall and the intraluminal thrombus from patients undergoing elective surgery for AAA. Immunohistochemistry and real-time PCR were used to study NGAL and MMP-9 expression. Immunoprecipitation, gel zymography,Western blot and ELISA were used to detect and quantify NGAL/MMP-9 complexes. NGAL was detected in the thrombus, the interface between the thrombus and the underlying wall and in the wall itself.Double staining showed that neutrophils are the major source of NGAL expression. Immunoprecipitation of MMP-9 with antibody against NGAL showed that complexes of NGAL and active MMP-9 were present in thrombus, the interface fluid and the aneurysm wall.Western blot analyses using non-reducing conditions and gel zymography demonstrated that high-molecular-weight complexes of NGAL/MMP-9 were present within the different regions.The concentration of the NGAL/MMP-9 complex was highest in the luminal part of the thrombus. In conclusion, NGAL in complex with activated MMP-9 is present in AAA wall and thrombus. Neutrophil-derived NGAL could enhance the proteolytic activity associated with AAA, but the importance of this mechanism for aneurysm growth remains to be shown.


Author(s):  
Ender A. Finol ◽  
Shoreh Hajiloo ◽  
Keyvan Keyhani ◽  
David A. Vorp ◽  
Cristina H. Amon

Abdominal Aortic Aneurysms (AAAs) are characterized by a continuous dilation of the infrarenal segment of the abdominal aorta. Despite significant improvements in surgical procedures and imaging techniques, the mortality and morbidity rates associated with untreated ruptured AAAs are still outrageously high. AAA disease is a health risk of significant importance since this kind of aneurysm is mostly asymptomatic until its rupture, which is frequently a lethal event with an overall mortality rate in the 80% to 90% range. From a purely biomechanical viewpoint, aneurysm rupture is a phenomenon that occurs when the mechanical stress acting on the dilating inner wall exceeds its failure strength. Since the internal mechanical forces are maintained by the dynamic action of blood flowing in the aorta, the quantification of the hemodynamics of AAAs is essential for the characterization of their biomechanical environment.


Author(s):  
Ron Layman ◽  
Samy Missoum ◽  
Jonathan Vande Geest

The local dilation of the infrarenal aorta, termed an abdominal aortic aneurysm (AAA), occurs over several years and may eventually lead to rupture, an event currently ranked the 15th leading cause of death in the United States [1, 2]. AAA can often remain quiescent and asymptomatic, making the diagnosis and treatment of AAA patients a clinical challenge. For patients whose AAAs dilate to a critical diameter there are two standard treatments: open surgical resection and endovascular repair (EVAR). EVAR involves inserting an endovascular graft into the aneurysm to prevent pressurization of the AAA cavity.


2021 ◽  
Vol 73 (1) ◽  
pp. 61-68 ◽  
Author(s):  
Kelli L. Summers ◽  
Edmund K. Kerut ◽  
Claudie M. Sheahan ◽  
Malachi G. Sheahan

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