Abdominal aortic aneurysm (AAA) is a late-age onset disorder that affects a high percentage of the population in industrialized countries, and rupture of AAA is associated with high mortality rates ( 1 ). The etiology of AAA is complex with a relevant contribution of genetic factors ( 2 ). Although much effort has been made to clarify the mechanism of AAA development, currently the only effective approach to prevent aneurysm rupture is surgical repair by conventional or endovascular techniques.Evidence has been established for a relationship between atherosclerosis and AAA, both disorders being characterized by an underlying chronic infl ammation . However, there are marked differences between atherosclerotic lesions and AAA. Whereas atherosclerotic plaque is characterized by leukocyte infi ltration at the lumen site and hyperproliferation of vascular smooth muscle cells (VSMCs) causing neointimal hyperplasia, AAA is characterized by leukocyte infi ltration into adventitia and depletion of VSMCs in the media. Other relevant features of AAA are the wall tension strength breakdown caused by proteolytic enzymes progressively destructing elastic fi bers ( 3 ) and hypervascularization of aortic tissue. It has been proposed that this vascularization might contribute to the development and rupture of aneurysms ( 4, 5 ). Abstract We investigated the prostaglandin (PG)E

CHIVA method for the treatment of chronic venous insu iciency.

Clinical management of abdominal aortic aneurysm (AAA) is currently limited to elective surgical repair because an effective pharmacotherapy is still awaited. Inhibition of histone deacetylase (HDAC) activity could be a promising therapeutic option in cardiovascular diseases. We aimed to characterise HDAC expression in human AAA and to evaluate the therapeutic potential of class I and IIa HDAC inhibitors in the AAA model of angiotensin II (Ang II)-infused apolipoprotein-E-deficient (ApoE−/−) mice. Real-time PCR, western blot and immunohistochemistry evidenced an increased expression of HDACs 1, 2 (both class I), 4 and 7 (both class IIa) in abdominal aorta samples from patients undergoing AAA open repair (n=22) compared with those from donors (n=14). Aortic aneurysms from Ang-II-infused ApoE−/− mice exhibited a similar HDAC expression profile. In these animals, treatment with a class I HDAC inhibitor (MS-275) or a class IIa inhibitor (MC-1568) improved survival, reduced the incidence and severity of AAA and limited aneurysmal expansion evaluated by Doppler ultrasonography. These beneficial effects were more potent in MC-1568-treated mice. The disorganisation of elastin and collagen fibres and lymphocyte and macrophage infiltration were effectively reduced by both inhibitors. Additionally, HDAC inhibition attenuated the exacerbated expression of pro-inflammatory markers and the increase in metalloproteinase-2 and -9 activity induced by Ang II in this model. Therefore, our data evidence that HDAC expression is deregulated in human AAA and that class-selective HDAC inhibitors limit aneurysm expansion in an AAA mouse model. New-generation HDAC inhibitors represent a promising therapeutic approach to overcome human aneurysm progression.

Based on the present data, endovascular treatment is feasible and safe with low postprocedural complications and mortality rate. Considering the increase in surgery and radiotherapy performed, UAF should be always debated in patients with massive hematuria.