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A spiral CT scan was performed at 6 months to detect presence of endoleaks. MMP-3 and MMP-9 levels were measured before EVG (nϭ30) and OSR (nϭ15) treatments and at 1, 3, and 6 months of follow-up by a sandwich ELISA technique. Healthy volunteers (nϭ10) were used as control subjects. Immunohistochemical staining for MMP-9 and MMP-3 was performed on tissue samples from surgical cases. Both MMP-9 and MMP-3 mean basal levels were significantly higher in patients affected by AAA than in control subjects (32.3Ϯ20.7 ng/mL for EVG and 28Ϯ9.9 ng/mL for OSR versus 8.9Ϯ2.5 ng/mL, 2PϽ0.05; 18.3Ϯ9.7 ng/mL and 26.7Ϯ10.8 ng/mL versus 8.2Ϯ5.3 ng/mL, 2PϽ0.001).In the OSR group, both MMP-9 and MMP-3 mean levels decreased after surgery (28Ϯ9.9 ng/mL at basal versus 14.7Ϯ6.6 ng/mL at 6 months, 2PϽ0.001; 26.7Ϯ10.8 versus 12Ϯ5.3 ng/mL; 2PϽ0.001). In the EVG group, a statistically significant difference at 6-month follow-up in MMP-9 and MMP-3 mean plasma values was detected in patients who had endoleakage in comparison with patients without endoleakage (44.3Ϯ20.7 versus 14.6Ϯ7.0 ng/mL, 2PϽ0.005; 25Ϯ11.5 versus 10.3Ϯ5.4 ng/mL, 2PϽ0.005). Conclusions-After EVG exclusion, MMP-9 and MMP-3 levels decreased to a level similar to that of patients undergoing OSR. In addition, a lack of decrease in MMP levels after EVG exclusion may help in identifying patients who will have endoleakage and consequent aneurysm expansion caused by continuous sac pressurization during follow-up.

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Aortic neck dilatation following endovascular AAA repair appears to be correlated with self-expanding endografts, which may contribute to a higher incidence of graft migration compared to that occurring with balloon-expandable endografts.

Oxidative stress plays a fundamental role in many conditions. Specifically, redox imbalance inhibits endothelial cell (EC) growth, inducing cell death and senescence. We used global transcriptome profiling to investigate the involvement of noncoding-RNAs in these phenotypes. By RNA-sequencing, transcriptome changes were analyzed in human ECs exposed to H2O2, highlighting a pivotal role of p53-signaling. Bioinformatic analysis and validation in p53-silenced ECs, identified several p53-targets among both mRNAs and long noncoding-RNAs (lncRNAs), including MALAT1 and NEAT1. Among microRNAs (miRNAs), miR-192-5p was the most induced by H2O2 treatment, in a p53-dependent manner. Down-modulated mRNA-targets of miR-192-5p were involved in cell cycle, DNA repair and stress response. Accordingly, miR-192-5p overexpression significantly decreased EC proliferation, inducing cell death. A central role of the p53-pathway was also confirmed by the analysis of differential exon usage: Upon H2O2 treatment, the expression of p53-dependent 5′-isoforms of MDM2 and PVT1 increased selectively. The transcriptomic alterations identified in H2O2-treated ECs were also observed in other physiological and pathological conditions where redox control plays a fundamental role, such as ECs undergoing replicative senescence, skeletal muscles of critical limb-ischemia patients and the peripheral-blood mononuclear cells of long-living individuals. Collectively, these findings indicate a prominent role of noncoding-RNAs in oxidative stress response.

Carotid artery stenting has been proposed as an option treatment of carotid artery stenosis. The aim of this single-institution study is to compare the dual-antiplatelet treatment and heparin combined with acetyl-acetic acid, in patients who underwent carotid artery stenting. We compared 2 groups of 50 patents each who underwent carotid artery stenting for primary atherosclerotic disease. Group A received heparin for 24 h combined with 325 mg acetyl-acetic acid and group B received 250 mg ticlopidine twice a day combined with 325 mg acetyl-acetic acid. Outcome measurements included 30-day bleeding and neurological complications and 30-day thrombosis/occlusion rates. The neurological complications were 16% in group A and 2% in group B (p < 0.05). Bleeding complications occurred in 4% in group A and 2% in group B (p > 0.05). The 30-day thrombosis/occlusion rate was 2% in group A and 0% in group B (p > 0.05). Dual antiplatelet treatment is recommended in all patients undergoing carotid artery stenting.

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