Treatment of type II endoleak with a transcatheter transcaval approach: Results at 1-year follow-up

PurposeThis study assessed the feasibility and mid-term outcomes in the treatment of type II endoleak using transcatheter transcaval embolization (TTE).MethodsDuring an 8-month period, 12 patients underwent TTE. After direct transcaval puncture of the aneurysm sac, embolization was performed by injecting thrombin and placing coils. Systemic and intrasac pressures were recorded throughout the entire procedure. Computed tomography (CT) scans were performed at 24 hours, 30 days, 6 months, and 1 year after TTE to evaluate endoleaks and changes in sac diameter. Technical success was defined as the feasibility of the procedure; clinical success was defined as no evidence of leaks during the follow-up evaluation.ResultsTTE was feasible in 11 of 12 patients (technical success 92%). The mean systemic pressure was 117 mm Hg. The mean intrasac pressure before embolization was 75 mm Hg (range, 39 to 125 mm Hg), 16.5 mm Hg (range, 7 to 40 mm Hg) in 10 patients after embolization, and it increased in one patient. CT scans at 24 hours showed stable contrast medium inside the sac in 10 patients. Only minor complications were observed during follow-up. At the 1-year follow-up, no recurrence of leaks was noted, and sac diameter was reduced in 10 of 11 patients. As a result, TTE clinical success was obtained in 10 (83%) of 12 patients.ConclusionTTE appears to be a feasible technique for the complete exclusion of type II endoleaks. Technical and clinical successes are comparable with other treatment strategies, and TTE should be considered an alternative to direct translumbar puncture of the aneurysm sac

Three years experience with thermal and excimer lasers in the treatment peripheral artery disease

Laser angioplasty is an effective tool to revascularize peripheral artery disease, but the major limitation is a high restenosis rate. Our experience with the hot tip laser system has shown a high primary success, 59-73% of the arteries were patent at 18 months, although 21% resulted in severe restenosis. The excimer laser seems to have a better long-term patency. Histology of restenosis specimens removed by atherectomy, shows the key role of the smooth muscle cells in this process

Expression of circulating miR-17-92 cluster and HDAC9 gene in atherosclerotic patients with unstable and stable carotid plaques

Aims: The miR-17-92 cluster and HDAC9 gene are involved in inflammatory, apoptotic, and angiogenic processes that are activated in the vulnerable carotid plaque. The aim of this research was to determine whether expression of one or more of the miRs of the cluster and/or HDAC9 expression could represent biomarkers for patients with unstable atherosclerotic carotid plaques. Materials and Methods: Plasma levels of miRs and HDAC9 expression in peripheral blood were analyzed by real-time PCR in patients with histologically classified stable or unstable plaques. Results: No differences were observed between the two groups. Discussion and Conclusions: Levels of the miR-17-92 cluster in plasma and HDAC9 gene expression in peripheral blood cannot be considered appropriate biomarkers to identify patients with unstable plaques at risk of rupture

Correlations between gene expression highlight a different activation of ACE/TLR4/PTGS2 signaling in symptomatic and asymptomatic plaques in atherosclerotic patients

Inflammation has a key role and translates the effects of many known risk factors for the disease in atherosclerotic vulnerable plaques. Aiming to look into the elements that induce the development of either a vulnerable or stable atherosclerotic plaque, and considering that inflammation has a central role in the progression of lesions, we analyzed the expression of genes involved in the ACE/TLR4/PTGS2 signaling in carotid plaques of symptomatic and asymptomatic patients. Patients with internal carotid artery stenosis undergoing carotid endarterectomy at Verona University Hospital were included in this study. A total of 71 patients was considered for gene expression analysis (29 atherothrombotic stroke patients and 42 asymptomatic patients). Total RNA was extracted from the excised plaques and expression of PTGS2, ACE, TLR4, PTGER4, PTGER3, EPRAP and ACSL4 genes was analyzed by real-time PCR. The correlation between the pair of genes was studied by Spearman coefficient. From the analyzed genes, we did not observe any individual difference in gene expression but the network of co-expressed genes suggests a different activation of pathways in the two groups of plaques

High levels of COX-2 gene expression in peripheral blood of cardioembolic and atherothrombotic stroke patients

Aim: To determine if COX-2 and TLR4 gene expression in atherothrombotic strokes represents a marker of atherosclerotic plaque destabilization and rupture, or it rather is related to the inflammatory response caused by stroke itself. Secondly, to determine if COX-2 and TLR4 gene expression could be specific for stroke subtype. Methods: Total RNA was extracted from peripheral blood samples from atherosclerotic (N=30) and cardioembolic stroke (N=25) patients, and controls (N=27). Gene expression was analysed by real time RT-PCR. Results: Expression of COX-2 gene was increased in cardioembolic compared to atherothrombotic stroke patients or healthy controls (p<0.0001). TLR4 expression was higher cardioembolic stroke patients compared to controls (p=0.0001). Conclusions: Cardioembolic show higher levels of COX-2 expression compared to atherothrombotic stroke patients independent of clinical severity. Additional studies are warrant to establish if high level of COX-2 gene expression could be a marker of cardioembolic stroke