[Role of endovascular therapy for redo surgery in patients after aortoiliac aneurysm exclusion]. / Stellenwert der endovaskulären Therapie bei Reeingriffen nach Ausschaltung aortoiliakaler Aneurysmata.

INTRODUCTION: Redo surgery or reintervention following conventional or endovascular aortoiliac reconstruction often requires exclusion of new aneurysms. In the present study the potentials of endovascular management of such lesions are investigated. METHODS: All patients with endovascular reoperation for of newly developed aortoiliac aneurysms were identified from a prospectively run data-base. The indications and results of endovascular therapy were analysed retrospectively. In detail, data were analysed for the type of original operation, interval until and kind of reoperation, and results concerning survival, technical success and complications. RESULTS: From 12 / 2003 through 3 / 2007 195 patients with aortoiliac aneurysms were operated. Endovascular repair was performed in 15 cases of previously excluded aneurysms. Mean age of these 15 patients (12 men) was 73 (64-85) years. Ten patients had a primary conventional (group A) and 5 patients had a primary endovascular (group B) aneurysm repair. The mean time interval between the first and second operation was 8.9 (1-26) years. The secondary endovascular therapy in group A was successful in all cases. In group B endoleaks type I a (n = 1), I a / b (n = 1), II (n = 2) and III (n = 1) were treated. One type II endoleak could only be treated successfully by conversion to open repair, the other one was successfully treated by reintervention. All but one patient are alive and -remained free of pathological findings during a median follow-up of 13 (2-39) months. DISCUSSION: Because of the clearly elevated operation risk of redo surgery after conventional or endovascular aneurysm repair, endovascular aneurysm exclusion represents the method of first choice. The reasonable selection and combination of procedures allows for an optimal adaptation of therapy to the individual case.

Concentration changes of malondialdehyde across the cerebral vascular bed and shedding of L-selectin during carotid endarterectomy.

BACKGROUND AND PURPOSE: Oxidative stress has been postulated to account for delayed neuronal death due to ischemia/reperfusion. We investigated cerebral formation of malondialdehyde as an index of lipid peroxidation in relation to different sources of reactive oxygen species in patients undergoing carotid endarterectomy. METHODS: In 25 patients undergoing carotid endarterectomy, jugular venous-arterial concentration differences of brain metabolites, malondialdehyde, plasma total antioxidant status, and soluble P-selectin and L-selectin were measured. A carotid artery shunt (n=5) was placed only after complete loss of somatosensory evoked potentials, indicating a focal cerebral blood flow <15 mL/min per 100 g. RESULTS: As an indication of cerebral lipid peroxidation, jugular venous-arterial malondialdehyde concentration differences were significantly enhanced before reperfusion, and an additional rise was observed 15 minutes after reperfusion. Plasma total antioxidant status significantly decreased during carotid artery occlusion only in patients with carotid artery shunt. This decrease was matched by cerebral formation of adenosine, hypoxanthine, and nitrite/nitrate. While jugular venous-arterial concentration differences of soluble P-selectin showed changes similar to those of malondialdehyde, the concentration difference for soluble L-selectin was enhanced exclusively at 15 minutes after reperfusion. CONCLUSIONS: Short-term incomplete cerebral ischemia/reperfusion significantly enhanced cerebral lipid peroxidation, as indicated by malondialdehyde formation. The generation of reactive oxygen species by xanthine oxidase or nitric oxide metabolism might be involved in the induction of lipid peroxidation. The additional rise in cerebral release of malondialdehyde was found to coincide with a significant activation of polymorphonuclear leukocytes across the cerebral circulation.