Stent-graft limb deployment in the external iliac artery increases the risk of limb occlusion following endovascular AAA repair.

PURPOSE: To assess whether deployment of an endograft limb in the external iliac artery (EIA) increases the rate of limb occlusion following endovascular aneurysm repair (EVAR). METHODS: Interrogation of a prospectively maintained database identified 661 patients (596 men; median age 73 years, range 37-93) with infrarenal abdominal aortic aneurysm who underwent EVAR between 1996 and 2010 using Zenith stent-grafts predominately. Of these, 567 patients [56 (9.9%) women] had both endograft limbs deployed in the CIA (1203 limbs at risk), while 94 patients [9 (9.6%) women] had at least 1 limb in the EIA (22 bilateral; 116 limbs at risk). An adjunctive bare metal stent was used in 8 (9%) limbs deployed in the EIA. RESULTS: There were 31 limb occlusions, all unilateral: 17 (3%) patients in the CIA group had an occluded limb (1% of limbs at risk) vs. 14 (15%) patients in the EIA group (12% of limbs at risk; p<0.0001). The median time to occlusion was 3 months (0-60) in the CIA group and 1 month (0-36) in the EIA group. The majority of occlusions were treated by extra-anatomical revascularization, most often a femorofemoral crossover bypass. No legs were amputated following occlusion of a limb placed in the CIA, but there were 3 amputations in the EIA group (p=0.003). CONCLUSION: Deployment of endograft limbs into the EIA led to a higher rate of occlusion and leg amputation. Increased tortuosity of the EIA and a smaller caliber vessel are likely to account for the increased risk.

Feasibility and limitations of an automated 2D-3D rigid image registration system for complex endovascular aortic procedures.

PURPOSE: To examine the feasibility of an automated 2-dimensional (2D) to 3- dimensional (3D) image registration system to simplify the navigational challenges faced in complex endovascular aortic procedures. METHODS: An automated 2D-3D image registration system was used to overlay pre-acquired 3D computed tomography images onto fluoroscopy images taken during endovascular aneurysm repair. Errors between the 3D overlay and digital subtraction angiograms were measured and correlated with aortic neck angulation. A mean discrepancy < or =3 mm was considered clinically acceptable. RESULTS: There was a strong correlation between maximum neck angulation and maximum registration error (Pearson's r = 0.75). Aortas with a maximum neck angulation < or =30 degrees had a mean error of 2.5+/-1.2 mm, whereas aortas with neck angulation >30 degrees had a mean error of 6.2+/-2.5 mm (p<0.0001). CONCLUSION: The major source of registration errors is aortic deformation caused by the presence of the introducer and endovascular graft. Further work is required if this technology is to be routinely applied to severely angulated aortic anatomy.

Intraluminal thrombus enhances proteolysis in abdominal aortic aneurysms.

This study examined whether intraluminal thrombus in abdominal aortic aneurysms (AAAs) is a source of fibrinolytic activity and proteolysis that could weaken the aneurysm wall. Plasmin, tissue plasminogen activator (tPA), and urokinase plasminogen activator (uPA) activity, plasminogen activator inhibitor 1 (PAI-1), and alpha2-antiplasmin (alpha2AP) antigen were measured in the AAA wall and juxtamural and luminal aspects of intraluminal thrombus in 18 patients. The aneurysm wall contained 100-fold higher tPA activity (1.06 +/- 0.34 [standard error of measurement] U/mg soluble protein) compared with juxtamural thrombus (JMT) (0.011 +/- 0.001 ) and luminal thrombus (LT) (0.01 +/- 0.001) (p < .00001) and over 6-fold higher uPA activity (29.3 +/- 3.4 IU/mg compared with the JMT (4.3 +/- 2.4, p = .00024) and LT (7.9 +/- 1.76, p = .0005). The LT had significantly lower levels of PAI-1 (1.26 +/- 0.34 ng/mg) than the AAA wall (2.08 +/- 0.51, p = .04) and the JMT (3.94 +/- 0.85, p = .007). The levels of alpha2AP in the wall (19.4 +/- 3.1 ng/mg) were lower than in the JMT or LT (43.0 +/- 7.9 ng/mg, p = .013, and 47.6 +/- 6.0 ng/mg, p = .002, respectively). There was no significant difference, however, in plasmin activity among the AAA wall, JMT, and LT. There were significant amounts of latent gelatinase B (matrix metalloproteinase [MMP]-9) in the AAA, JMT, and LT. Mean levels of activated MMP-9 activity were similar in the AAA, JMT, and LT. Plasmin activation of MMPs at the interface between intraluminal thrombus and the aneurysm wall may enhance proteolysis and accelerate aneurysm expansion.

Stromelysin-1 (matrix metalloproteinase-3) and tissue inhibitor of metalloproteinase-3 are overexpressed in the wall of abdominal aortic aneurysms.

BACKGROUND: Atherosclerosis is implicated in the pathogenesis of abdominal aortic aneurysm (AAA) but more often causes aortic occlusive disease (AOD). The matrix metalloproteinases (MMPs) degrade extracellular matrix and may play a central role in the pathogenesis of AAA. The aim of this study was to examine differences in the patterns of MMP and MMP inhibitor expression between AAA and AOD. METHODS AND RESULTS: The expression of mRNA for 14 MMPs and 4 tissue inhibitors of metalloproteinases (TIMPs) was estimated in samples of aortic wall from 8 patients with AAA and 8 with AOD using the reverse-transcriptase polymerase chain reaction with a synthetic multicompetitor standard. AAA wall expressed significantly more stromelysin-1 (MMP-3) (mean log(10) ratio [copy enzyme cDNA/copy GAPDH cDNA], -1.9; range, -3.3 to -0.7) than the AOD wall (mean, 4; range, -5.7 to -2.4), P<0.005. TIMP-3 expression was significantly higher in AAA (mean, -1.7; range, -2.9 to -1.0) than AOD (mean, -3.6; range, -5.7 to -1.8), P<0.01. Expression of 8 other MMPs (1, 2, 7, 9, 11, 12, 14, and 17) was detected and was similar in AAA and AOD. Expression of the remaining 5 MMPs (-8, -10, -13, -15, and -16) was not detected in any of the samples. CONCLUSIONS: Both AAA and AOD walls express similar levels of a wide range of MMPs, including cell membrane-bound MT-MMPs. Stromelysin-1 (MMP-3) and TIMP-3 were, however, over expressed in the AAA samples and may be involved aneurysm pathogenesis. Stromelysin-1 could provide a target for pharmacological inhibition.