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A 68-year-old man complained of urinary frequency and hypogastric discomfort. He was a smoker and had hypertension. Digital rectal examination showed a painful prostate but he had no fever. Urine analysis showed a pyuria and a bacteriuria of enterococcus species. The patient was treated with amoxicillin. 2 days after his admission, he suddenly developed acute right fl ank pain with hypotension. Blood tests showed a decrease in haemoglobin from 140 g/L on admission to 70 g/L. The CT showed that an abdominal aortic aneurysm was fi ssured in the retroperitoneum but with

Objective— Despite the fact that mechanical stresses are well recognized as key determinants for atherosclerotic plaque rupture, very little is known about stress amplitude and distribution in atherosclerotic lesions, even in the standard apolipoprotein E (apoE) −/− mouse model of atherosclerosis. Our objectives were to combine immunohistology, atomic force microscopy measurements, and finite element computational analysis for the accurate quantification of stress amplitude and distribution in apoE −/− mouse aortic atherosclerotic lesions. Methods and Results— Residual stresses and strains were released by radially cutting aortic arch segments from 7- to 30-week-old pathological apoE −/− (n=25) and healthy control mice (n=20). Immunohistology, atomic force microscopy, and biomechanical modeling taking into account regional residual stresses and strains were performed. Maximum stress values were observed in the normal arterial wall (276±71 kPa), whereas low values ( Conclusion— Low mechanical stress amplitude was observed in apoE −/− mouse aortic atherosclerotic lesions. This original study provides a basis for further investigations aimed at determining whether low stress levels are responsible for the apparently higher stability of murine aortic atherosclerotic lesions.

International audience; PURPOSE: To report our experience with endovascular stent-graft repair of descending thoracic aorta diseases in high risk patients. MATERIALS AND METHODS: Between 2000 and 2007, 49 high surgical risk patients (mean age: 64.6 years) underwent stent-graft placement, including 24 cases presenting acutely. Mean follow-up was 25.4 months. Etiologies included 15 aneurysms, 11 dissections, 10 penetrating ulcers, 9 false aneurysms, 2 ruptures of the aortic isthmus, 2 intramural hematomas. RESULTS: Access failure occurred in one patient. The overall mortality was 27.1% (n=13), nine related to the presenting pathology or treatment. Thirty-day mortality was 10.4% (n=5). Complications included vascular injury at the iliac or femoral artery access (10.2%), 1 case of flaccid paraplegia, 2 cases of transient paraparesis, 2 strokes, 2 stent migrations and 1 stent rupture. The rate of early endoleak was 39.6% while the rate of delayed endoleak was 14.6%. Seven patients (14.6%) required repeat endovascular interventions. Explantation was required in 2 cases. The latest available follow-up showed no lesion enlargement in 70.7% (n=29/41) of our patients. CONCLUSION: Descending thoracic aortic pathology can be treated using endografts in high risk patients, although significant morbidity and mortality remain. Because of the high rate of endoleaks, close follow-up is required.

International audience; Usual imaging after endovascular aneurysm repair (EVAR) of abdominal aortic aneurysm (AAA) consists of AAA diameter monitoring and endoleak detection. Among additional predictor parameters previously proposed to help clinicians in better identifying subgroups of AAA still at risk of rupture, AAA wall motion after EVAR has been studied, but its value was not clearly established. Tissue Doppler imaging (TDI) is an ultrasonographic modality which allows wall motion measurements along an arterial segment. The aim of the current study was to analyze AAA wall motion with TDI before and after EVAR and to describe its evolution in patients with more than 1 month of follow-up. Twenty-five consecutive patients undergoing EVAR between February 2005 and June 2007 gave informed consent to be prospectively investigated with the TDI system before EVAR and at each visit during follow-up. The mean (SD) follow-up was 13.7 (9.7) months. Maximum mean segmental dilation (MMSD), segmental compliance, dilation at maximum diameter, pressure strain elastic modulus (Ep), and stiffness were compared between three periods (before stenting, before discharge, and at last follow-up), and their relation with AAA diameter was analyzed. A significant decrease in AAA compliance was immediately observed after successful EVAR and remained stable during later follow-up. On the other hand, AAA diameter progressively decreased along time and was statistically lower at the last control compared to the initial value. MMSD, segmental compliance, and dilation at maximum diameter were positively related to AAA diameter. This means that the larger the AAA diameter after stenting, the higher the value for these parameters can be expected. On the contrary, percentage of AAA diameter decrease and percentage of MMSD decrease were not related after successful EVAR. There was no parallelism between loss in compliance and diameter decrease along time, and there is not a unique pattern of AAA diameter and compliance evolution after EVAR. Even if comparison between patients without and with endoleak was weak due to the small sample of the latter group (five patients with endoleak), compliance tended to be greater in case of endoleak. AAA wall motion after successful EVAR reflects complex interactions between all the components of the stented aneurysm which evolve over time, including true compliance of the aneurysm wall itself; intra-aneurysm sac pressure with possible different effects for peak, mean, and pulse pressures; remodeling of the thrombus; stiffness characteristics of the graft; and systemic pressure. Combining simultaneous MMSD records with actual intrasaccular pressure measurements in patients with and without endoleak would improve our understanding of the clinical pulsatility mechanism within AAA after EVAR.