No abstract

Coil embolization of the internal iliac artery (IIA) is used to extend the application of endovascular aneurysm repair (EVAR) in cases of challenging iliac anatomy. Pelvic ischemia is a complication of the technique, but reports vary as to the rate and severity. This study reports our experience with IIA embolization and compares the results to those of other published series. The vascular unit database of the Leicester Royal Infirmary was used to identify patients who had undergone IIA coil embolization prior to EVAR. Data were collected from hospital case notes and by telephone interviews. Thirty-eight patients were identified; 29 of these were contactable by telephone. A literature search was performed for other studies of IIA embolization and the results were pooled. In this series buttock claudication occurred in 55% (16 of 29 patients) overall: in 52% of unilateral embolizations (11 of 21) and 63% of bilateral embolizations (5 of 8). New erectile dysfunction occurred in 46% (6 of 13 patients) overall: in 38% of unilateral embolizations (3 of 8) and 60% of bilateral embolizations (3 of 5). The literature review identified 18 relevant studies. The results were pooled with our results, to give 634 patients in total. Buttock claudication occurred in 28% overall (178 of 634 patients): in 31% of unilateral embolizations (99 of 322) and 35% of bilateral embolizations (34 of 98) (p = 0.46, Fisher's exact test). New erectile dysfunction occurred in 17% overall (27 of 159 patients): in 17% of unilateral embolizations (16 of 97) and 24% of bilateral embolizations (9 of 38) (p = 0.33). We conclude that buttock claudication and erectile dysfunction are frequent complications of IIA embolization and patients should be counseled accordingly.

BACKGROUND: Symptomatic carotid disease due to thromboembolism has been associated with acute plaque instability and intraplaque haemorrhage. These features may be influenced by the fragility and position of plaque neovessels. The purpose of this study was, therefore, to determine whether any association existed between neovessel density, position, morphology and thromboembolic sequelae. METHODS: Carotid endarterectomy (CEA) samples were collected from 15 asymptomatic patients with greater than 80 per cent stenosis and from 13 patients with greater than 80 per cent stenosis and symptoms within 30 days of CEA. Groups were matched for sex, age, risk factors and plaque size. Samples were stained with haematoxylin and eosin, and Van Gieson stains. An endothelial-specific antibody to CD31 was used for immunohistochemistry. Plaques were assessed for histological characteristics while neovessels were counted and characterized by size, site and shape. RESULTS: There were more neovessels in plaques (P < 0.00001) and fibrous caps (P < 0.0001) from symptomatic than asymptomatic patients. Symptomatic plaque neovessels were larger in size (P< 0.004) and more irregular in shape. There was a significant increase in plaque necrosis and rupture in symptomatic plaques. Plaque haemorrhage and rupture were associated with more neovessels within the plaque (P < 0.02, P < 0. 001) and fibrous cap (P < 0.05, P < 0.004). Patients with preoperative or intraoperative embolization had more plaque and fibrous cap neovessels (P < 0.03, P < 0.001). CONCLUSION: Symptomatic carotid disease is associated with increased neovascularization within the atherosclerotic plaque and fibrous cap; these vessels appear larger in size, more irregular in shape and may contribute to plaque instability and onset of thromboembolic events.

Symptomatic carotid plaques contain abnormal, immature microvessels similar to those found in tumors and healing wounds. Such vessels could contribute to plaque instability by acting as sites of vascular leakage by inflammatory cell recruitment. The immature vessels within plaques may be therapeutic targets for promoting plaque stabilization.