The percutaneous technique decreases the invasiveness of endovascular therapy of aortic aneurysm and reduces operative time and time to ambulation. Complications were roughly equivalent in severity. The additional cost for the device appears to justify its use for this form of aneurysm treatment.

We describe a case of abdominal aortic aneurysm (AAA) with rupture 16 months after treatment by an endograft. A 76-year-old patient on Coumadin after aortic valve replacement had initially successful exclusion by stentgraft. There was no evidence of an endoleak seven months after stentgraft repair, although a computed tomography scan detected an enlargement of the aneurysm sac. Sixteen months after initial endograft surgery, rupture of the aneurysm occurred and we performed open emergency surgery. We treated the aneurysm by conventional technique, and the patient survived the rupture. This case emphasized the fact that patients after endograft AAA repair require a close follow-up. An expansion of the aneurysm sac after the procedure should signal failed exclusion, even if a computed tomography scan does not demonstrate an endoleak. Anticoagulation can be an important factor in failure after endoluminal graft treatment. Supravisceral aortic cross clamping is helpful in dealing with a stented aorta.

Aldosterone triggers the stiff endothelial cell syndrome (SECS), characterized by an up-regulation of epithelial sodium channels (ENaCs) and mechanical stiffening of the endothelial cell cortex accompanied by endothelial dysfunction. In vivo, aldosterone antagonism exerts sustained protection on the cardiovascular system. To illuminate the molecular mechanisms of this time-dependent effect, a study on endothelial cells in vitro and ex vivo was designed to investigate SECS over time. Endothelia (from human umbilical veins, bovine aortae, and explants of human arteries) were cultured in aldosterone-supplemented medium with or without the mineralocorticoid receptor (MR) antagonist spironolactone. MR expression, ENaC expression, cortical stiffness, and shear-mediated nitric oxide (NO) release were determined after 3 d (short term) and up to 24 d (long term). Over time, MR expression increased by 129%. ENaC expression and surface abundance increased by 32% and 42% (13.8 to 19.6 molecules per cell surface), paralleled by a 49% rise in stiffness. Spironolactone prevented this development and, after 3 wk of treatment, increased NO release by 50%. Thus, spironolactone improves endothelial function long-lastingly by preventing a time-dependent manifestation of SECS. This emphasizes the key role of vascular endothelium as a therapeutical target in cardiovascular disorders and might explain blood pressure independent actions of MR antagonism.

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Here, we report differential responses of human ex-vivo vessels to amiloride. Although the mechanism of differential amiloride response is still unknown, the data indicate that drug action on endothelial function could differ strongly among patients, especially in those with a vascular end-organ damage determined by PWV.