To determine whether variations in aortic wall motion exist in mammalian species other than humans and to consider the potential implications of such variations.M-mode ultrasound was used to measure abdominal aortic wall motion in 4 animal species [mice (n=10), rats (n=8), rabbits (n=7), and pigs (n=5)], and humans (n=6). Anterior wall displacement, posterior wall displacement, and diastolic diameter were measured. The ratio of displacement to diameter and cyclic strain were calculated.Body mass varied from 24.1+/-2.4 g (mouse) to 61.8+/-13.4 kg (human); aortic diameter varied from 0.53+/-0.07 mm (mouse) to 1.2+/-1 mm (human). Anterior wall displacement was 2.5 to 4.0 times greater than posterior among the species studied. The ratios of wall displacement to diastolic diameter were similar for the anterior (range 9.40%-11.80%) and posterior (range 2.49%-3.91%) walls among species. The ratio of anterior to posterior displacement (range 2.47-4.03) and aortic wall circumferential cyclic strain (range 12.1%-15.7%) were also similar. An allometric scaling exponent was experimentally derived relating anterior wall (0.377+/-0.032, R2=0.94) and posterior wall (0.378+/-0.037, R2=0.93) displacement to body mass.Abdominal aortic wall dynamics are similar in animals and humans regardless of aortic size, wih more anterior than posterior wall motion. Wall displacement increases linearly with diameter, but allometrically with body mass. These data suggest increased dynamic strain of the anterior wall. Increased strain, corresponding to increased elastin fatigue, may help explain why human abdominal aortic aneurysms initially develop anteriorly. Aortic wall motion should be considered when developing endovascular devices, since asymmetric motion may affect device migration, fixation, and sealing.
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Intermittent pneumatic compression is part of the current standard of care model for preventing venous thromboembolic events (VTE) after total joint arthroplasty. Pneumatic motors limit the rate of inflation resulting in bulky devices with uncomfortable sleeves that inhibited patient compliance and mobility. Nonpneumatic mechanical devices are an alternative for providing mobile, graded, intermittent, sequential, rapid, and monitorable compression posthospitalization. Fifteen healthy volunteers underwent mechanical compression using the Cirvo (Radial Medical, Mountain View, CA) as well as pneumatic compression with four commercially available systems (VenaFlow Elite, Kendall SCD Compression System, ActiveCare DVT, Vasculaire Compression System) and manual calf compression. Peak flow velocity (PFV) was measured by ultrasound of the femoral vein during compression and at baseline. Mechanical compression for 1 second resulted in a significant increase in femoral venous PFV to 107.8 ± 38.2 cm/s from 17.1 ± 4.7 cm/s at baseline (P < .001). The change in femoral venous PFV with mechanical compression for 1 second (90.7 ± 34.9 cm/s) was not statistically different from pneumatic compression from VenaFlow system (106.0 ± 35.6 cm/s, P = .124) and statistically lower than manual calf compression (115.5 ± 26.8 cm/s, P = .015). Pneumatic compression from the VenaFlow system produced the largest change in femoral venous PFV of all commercial pneumatic systems tested. Mechanical compression replicates or exceeds femoral venous PFV available from currently available intermittent pneumatic compression.
Arterial wall biomechanics are thought to be important in aneurysm development and atherosclerotic plaque localization. Vessel wall dilation occurs because of pulsatile blood flow during the cardiac cycle. Until recently, it was commonly assumed that this dilation occurred concentrically about the center of the lumen. However, dynamic MR, CT, and ultrasound imaging techniques have now shown that aortic wall motion undergoes unequal circumferential deformation during the cardiac cycle. This phenomenon has been observed in both humans and pigs [1, 2]. The purpose of our study was to determine whether variations in circumferential aortic wall dilation persist across mammalian species.
Purpose: To present a unique demonstration of postoperative perigraft contrast masquerading as an endoleak following endovascular abdominal aortic aneurysm (AAA) repair. Case Report: A 66-year-old man underwent endovascular stent-graft repair of a 4.6-cm infrarenal AAA. The procedure was uncomplicated, and intraoperative completion angiography demonstrated good proximal and distal fixation of the stent-graft without an endoleak. A spiral computed tomographic (CT) angiogram obtained on postoperative day 2 revealed a large amount of extrastent contrast along the posterior aspect of the aneurysm sac. This defect had the appearance of an endoleak, but it was also present on the noncontrast images. A color-flow duplex examination performed on the same day showed a widely patent stent-graft with no evidence of extrastent flow. Conclusions: Contrast trapped in the aneurysm sac during endovascular aneurysm repair may be misinterpreted as an endoleak on postprocedural CT scans. “Pseudoendoleaks” can be distinguished from true endoleaks by examination of prebolus, noncontrast CT images, as well as by duplex ultrasound scanning.
To determine the significance of persistent type-II endoleaks and whether they can be predicted preoperatively in patients with abdominal aortic aneurysms (AAA).The charts of all AAA patients treated with the AneuRx stent-graft at a single center from 1996 to 1998 were reviewed. Patients with <12-month follow-up or type-I endoleaks were excluded. The presence or absence of type-II endoleaks was determined from duplex imaging and computed tomographic angiography. Three groups were identified and compared: 16 patients with persistent type-II endoleaks (PE), 14 patients with transient type-II endoleaks (TE), and 16 patients with no endoleak (NE).The groups did not differ with regard to age, preoperative comorbidities, follow-up time, and AAA neck diameter and length. AAA diameters were 57.1 +/- 9.0 mm for NE, 63.4 +/- 11.4 mm for TE, and 55.6 +/- 4.2 mm for PE. The inferior mesenteric artery (IMA) was patent in 5 (31%) NE patients, 6 (43%) TE patients, and 13 (81%) PE patients (p < 0.01). The number of patent lumbar arteries visualized preoperatively was 0.5 +/- 1.0 in NE, 1.3 +/- 0.8 in TE, and 2.4 +/- 0.6 in PE (p < 0.0001). Patent IMAs (RR 0.82, p < 0.01) and >2 lumbar arteries (RR 0.40, p < 0.0001) were identified as independent preoperative risk factors for persistent endoleaks. There were no changes in mean diameter or volume in aneurysms with persistent endoleaks.No adverse clinical events were related to the presence of type-II endoleaks, but there was no decrease in aneurysm size in patients with persistent type-II leaks. Patients with a large, patent IMA, or >2 lumbar arteries on preoperative CT angiography are at higher risk for persistent type-II endoleaks.
