Conclusions: The present study shows that aneurysm sac filling may have a role as an adjuvant procedure to the present EVAR technique. The strength of the proximal fixation of three different stent grafts increases significantly in this in vitro setting. Further in vivo research must be done to see if this could facilitate the treatment of aneurysms with short infrarenal necks. (J Vase Surg 2010;52:152-8.)”
“Objective: Abdominal aortic aneurysm (AAA) development is associated with increased angiogenesis and overexpression of vascular endothelial growth factor (VEGF). Inhibition
of angiogenesis Pifithrin-�� mw results in attenuation of experimental aneurysms. This study investigated the effects of recombinant human (rh)VEGF on experimental aneurysms.
Methods: Apolipoprotein E-deficient
(apoE(-/-)) mice were assigned to one of four groups: (1) normal saline infusion (sham), (2) angiotensin-II (AngII) infusion, (3) AngII infusion plus 100 mu g daily rhVEGF for 14 days (AngII + 14dVEGF), or (4) AngII infusion plus 100 mu g daily rhVEGF for 21 days (AngII + 21dVEGF). Aortic maximum diameter and cross-sectional area were determined by magnetic resonance imaging and microscopy. All mice were sacrificed at day 28.
Results: Aneurysms developed in all mice in the AngII+14dVEGF and AngII+21dVEGF groups by day 21 compared with 40% in the AngII group. Treatment with rhVEGF increased maximum aortic diameter (P <.002) and crosssectional area of aneurysms (P <.005) at day 21. This effect was maintained at day 28 (P <.0005). Decreasing GW3965 molecular weight rhVEGF treatment from 21 to 14 days did not attenuate aneurysm formation. Treatment with rhVEGF upregulated matrix metalloproteinase 2 gene MK 2206 expression within the aortic wall (P <.0009).
Conclusions: Treatment with
rhVEGF intensified the formation of Angll-induced aneurysms. Further studies are needed to investigate if antiangiogenic therapy may be a valid medical therapy against aneurysm expansion or rupture. (J Vase Surg 2010;52:159-66.)”
“Objective: Vascular smooth muscle cells (SMCs) are exposed to fluid shear stress (FSS) after interventional procedures such as balloon-angioplasty. Whereas the effects of hemodynamic forces on endothelial cells are explored in detail, the influence of FSS on smooth muscle cell function is poorly characterized. Here, we investigated the effect of FSS on SMC gene expression and function.
Methods: Laminar FSS of arterial level (14 dynes/cm(2)) was applied to SMC cultures for 24 hours in a parallel-plate flow chamber. The effect of FSS on gene expression was first screened with microarray technology, and results further verified by real time polymerase chain reaction (RT-PCR) and immunoblotting. Tissue factor pathway inhibitor-2 (TFPI-2) and caspase-3 protein expression was studied in the rat carotid artery after balloon-injury, and the effect of TFPI-2 on SMC DNA synthesis and apoptosis was examined in vitro.