There is no approved special endovascular device for use in preventing entry tears in the distal part of ascending aorta or in the aortic arch and preserving the arch branch arteries. Thus, we have designed a novel branched stent-graft, and herein report the initial clinical outcomes. Between August 2009 and January 2014, 51 patients with aortic dissections involving the aortic arch were treated by endovascular branched stent-grafts. There were 7 Stanford type A aortic dissections, 22 retrograde type A aortic dissections, and 22 Stanford type B aortic dissections (including 4 localized aortic arch dissections). All patients were treated while in the chronic phase (>2 weeks). All of the proximal entry tears in the arch were successfully excluded, and all of the treated branch arteries remained patent. No new cerebral infarction occurred. There was 1 death from a retrograde type A dissection, occurring 6 days after the endovascular procedure. The median follow-up period was 44 months (range, 14-66 months). No additional complications or mortality occurred. Complete thrombosis in the false lumen of the aortic arch was formed in all patients, and significant true lumen recovery and false lumen shrinkage were demonstrated in different levels of the thoracic aorta according to computed tomography angiography at 1 year postsurgery (P < .001). In patients with aortic dissection involving the arch branches, the customized branched stent-graft may provide a feasible endovascular treatment option. A larger series of cases with longer follow-up is needed to substantiate these results.

Acute aortic dissection (AAD) is a catastrophic emergency with high mortality and misdiagnosis rate. We aimed to determine whether circulating microRNAs allow to distinguish AAD from healthy controls and chest pain patients without AAD (CP). Plasma microRNAs expression were determined in 103 participants, including 37 AAD patients, 26 chronic aortic dissection patients, 17 healthy volunteers, 23 patients without AAD. We selected 16 microRNAs from microarray screening as candidates for further testing via qRT-PCR. The results showed that plasma miR-15a in patients with AAD (n = 37) had significantly higher expression levels than it from control group (n = 40; P = 0.008). By receiver operating characteristic curve analysis, the sensitivity was 75.7%; the specificity was 82.5%; and the AUC was 0.761 for detection of AAD. Furthermore, 37 patients with AAD had significantly higher plasma expression levels of let-7b, miR-15a, miR-23a and hcmv-miR-US33-5p compared with 14 CP patients of 40 controls (P = 0.000, 0.000, 0.026 and 0.011, respectively). The corresponding sensitivity were 79.4%, 75.7%, 91.9% and 73.5%, respectively; the specificity were 92.9%, 100%, 85.7% and 85.7%, respectively; and the AUCs of these microRNAs were 0.887, 0.855, 0.925 and 0.815, respectively. These data indicate that plasma miR-15a and miR-23a have promising clinical value in diagnosing AAD.

This study aimed to assessed whether Talin-1 is involved in the pathogenesis of aortic dissection via regulating vascular smooth muscle cell (VSMC) biological function. Human aortic samples were obtained from organ donors who died from nonvascular diseases as normal controls and from patients undergoing surgical repair of thoracic aortic dissection. The expression level and distribution of Talin-1 were detected using westernblot analysis and immunohistochemistry in each sample. We inhibited the expression of Talin-1 via RNA interference in VSMCs. VSMC proliferation was detected by Cell-counting Kit-8 analyses. Scratch test and flow cytometry were used to identify the migration and apoptosis ability. Antibody microarray analysis and qRT-PCR were used to detect some protein and mRNA changes which were induced by Talin-1 downregulation. Talin-1 was significantly downregulated in the media of aortic dissection samples compared with controls (P < 0.05). Talin-1 knockdown significantly induced VSMC proliferation and migration in vitro. Proteins which involved in cell cycle can be regulated by downregulating Talin-1. Down regulation of Talin-1 can significanly increased the expression of anaphase-promoting complex subunit 2 (APC2) and decreased p19 alternative reading frame (p19ARF), Cullin-3, and beta actin’s expression. Talin-1 induces VSMCs proliferation and migration. It downregulated in aortic dissection, which might play a potential role in the development of aortic dissection.

Fibrin degradation products (FDP) and D-dimer have been considered to be involved in many vascular diseases. In this study we aimed to explore the diagnostic implication of FDP and D-dimer in aortic dissection patients. 202 aortic dissection patients were collected as the case group, 150 patients with other cardiovascular diseases, including myocardial infarction (MI, n = 45), pulmonary infarction (n = 51) and abdominal aortic aneurysm (n = 54) were collected as non-dissection group, and 27 healthy people were in the blank control group. The FDP and D-dimer levels were detected with immune nephelometry. Logist regression analysis was performed to evaluate the influence of FDP and D-dimer for the aortic dissection patients. ROC curve was used to determine the diagnostic value of FDP and D-dimer. The FDP and D-dimer levels were significantly higher in aortic dissection patients than in non-dissection patients and the healthy controls. FDP and D-dimer were both the risk factors for patients with aortic dissection. From the ROC analysis, diagnostic value of FDP and D-dimer were not high to distinguish aortic dissection patients from the non-dissection patients. However FDP and D-dimer could be valuable diagnostic marker to differentiate aortic dissection patients and healthy controls with both AUC 0.863.