Percutaneous endovascular therapy for symptomatic chronic total occlusion of the left subclavian artery.

INTRODUCTION: Percutaneous endovascular therapy is an accepted and preferred procedure for symptomatic subclavian artery disease. However, the technical feasibility and effectiveness of treating chronic total occlusion of the subclavian artery with this approach is uncertain. We aimed to evaluate the initial and mid-term results of endovascular therapy for patients with symptomatic chronic total occlusion of the left subclavian artery. METHODS: Consecutive patients who underwent balloon angioplasty and stenting for chronic total occlusion of the left subclavian artery between January 2010 and February 2014 were included. RESULTS: Overall, 16 patients (10 male, 6 female; mean age 56 ± 13 years) underwent balloon angioplasty and stenting for chronic total occlusion of the left subclavian artery. 6 (37.5%) had arm claudication, 8 (50.0%) had vertebrobasilar insufficiency and 2 (12.5%) had coronary steal. 18 balloon-expandable stents were implanted in 15 patients. Central luminal passage was not achieved in one patient because of the subintimal position of the guidewire (procedural success rate 93.8%). There were no procedure-related complications. Mean preprocedural and postprocedural systolic blood pressure differences between the upper extremities were 37 ± 13 (range 25-60) mmHg and 11 ± 9 (range 5-38) mmHg, respectively; the improvement was statistically significant. Outpatient follow-up revealed one asymptomatic restenosis at two years. The patency rate at two years was 93.3%. CONCLUSION: Balloon angioplasty and stenting for chronic total occlusion of the left subclavian artery is safe and effective, with good acute success rate and mid-term patency. Prospective randomised studies on larger patient populations would provide more precise results.

Altered Plasma MicroRNA Expression in Patients with Mitral Chordae Tendineae Rupture.

BACKGROUND: Mitral chordae tendineae rupture (MCTR) is a progressive disorder which leads to severe mitral regurgitation. Despite its importance, the precise pathogenetic mechanism of MCTR remains unclear. The study aim was to investigate the expression profile of circulating microRNAs (miRNAs) as being potentially involved in the development of MCTR. METHODS: Twenty-one patients with 'primary' MCTR, and 30 age- and gender-matched controls, were enrolled in the study. Comparisons were made between the expression levels of circulating miRNAs in MCTR patients and controls. Four target gene databases were used to predict target genes and pathways of differentially expressed miRNAs. RESULTS: Compared to controls, the expression of 22 miRNAs (hsa-miR-106b-5p, hsa-miR-126-3p, hsa-miR-150-5p, hsa-miR-17-5p, hsa-miR-195-5p, hsa-miR-19a-3p, hsa-miR-19b-3p, hsa-miR-20a-5p, hsa-miR-21-5p, hsa-miR-222-3p, hsa-miR-223-3p, hsa-miR-23a-3p, hsa-miR-25-3p, hsa-miR-92a-3p, hsa-miR-93-5p, hsa-miR-26b-5p, hsa-miR-30e-5p, hsa-miR-373-3p, hsa-miR-15b-5p, hsa-miR-16-5p, hsa-miR-191-5p, hsa-miR-26a-5p) were significantly down-regulated in the MCTR group. Bioinformatic analysis indicated that the following potential miRNA targets and pathways are commonly related to the development of MCTR: MMPs, TIMP-2,TGFBR2, VEGFA, PIK3R2, NRAS, PPP3CA, PPP3R1, PTGS 2 were predicted as putative targets of 13 of these miRNAs. CONCLUSIONS: The present study is the first to describe altered miRNA expression in patients with MCTR. Bioinformatic analysis has revealed that target genes involved in MCTR development were regulated by miRNAs.