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BACKGROUND: Distal entry tears have undesirable influence in type B aortic dissection (TBAD) after thoracic endovascular aortic repair (TEVAR), including inhibition of aortic remolding and increase of late aortic events. Therefore, distal entry tears should be managed. Nowadays, main strategies for managing distal entry tears included total and selective strategies. However, which strategy is better still remains controversial. The objective of the study is to investigate the outcomes of selective strategy for distal entry tears after TEVAR in TBAD. METHODS: A total of 43 consecutive patients with TBAD with distal entry tears after TEVAR were administered with selective strategy for distal entry tears, including occlusion of the tear in the thoracic aortic segment, thrombosis of the reverse blood flow channel in the false lumen, and selective occlusion of distal entry tears. Mortality, complications, and aortic remolding in early follow-up (12 months after operation) were analyzed. RESULTS: All 43 patients survived during the follow-up period. Operation was performed again for femoral artery reconstruction in 1 patient who had occlusion of the approach vessel during the follow-up period, and the remaining 42 patients had no uncomfortable symptoms and operation-related complications. The maximum diameter of the aorta was 32.03 ± 6.35 mm and 27.36 ± 4.92 mm, respectively, for before and after reintervention, and the difference was significant (t = 5.899, P < 0.001). The unthrombotic range of the false lumen after reintervention was significantly shrunken in all patients, compared with the range before reintervention. CONCLUSIONS: Selective strategy was safe and effective, at least in early follow-up. Its effectiveness should be further verified by more clinical observation results and long-term follow-up results.

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BACKGROUND: Thromboangiitis obliterans (TAO), also called Buerger's disease, is a chronic peripheral vascular occlusive disease. It is an obliterative vasculitis characterized by arterial thrombosis and strongly associated with tobacco exposure. The pathogenesis and etiology of TAO are not well understood, but genetic factors may be important in its development. A case-control study was undertaken to identify genetic factors potentially involved in the pathogenesis of TAO in a Xinjiang Uyghur population of China, where TAO is common. METHODS: We ascertained 177 TAO patients by clinical screening and 86 healthy individuals from the HAPMAP database. The genotypes of single-nucleotide polymorphisms (SNPs) of the participants were identified using the Affymetrix Genome-Wide Human SNP Array 6.0 to perform a genome wide association study (GWAS). The association between the SNPs and incidence of TAO was quantified using race stratification exposure. RESULTS: Through a case-control GWAS study 26 SNPs were significantly associated with incidence of TAO following a Bonferroni correction. However, after genomic control correction for population stratification only three of these SNPS were highly significantly associated with TAO: rs376511 in IL17RC (OR = 24.4, 95% CI:8.68 - 68.62, p < 0.0001), rs7632505 in SEMA5B (OR = 29.47, 95% CI:7.16 - 121.3, p < 0.0001), and rs10178082 (OR = 18.09, 95% CI: 6.56 - 49.92, p < 0.0001) showed a significant risk of TAO in the Uyghur population. CONCLUSIONS: This study shows an association between these 3 SNPs and susceptibility to TAO in the Uyghur population, suggesting that polymorphisms in the IL-17RC and Sema 5B genes may pre-dispose individuals in this population to development of TAO. These findings require replication.

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To assess the association between polymorphisms of prothrombin gene and hereditary thrombophilia in Xinjiang Kazakhs population. Through cross-sectional investigation, permanent Kazakh population of Ili Kazakh Autonomous Prefecture was selected as the study object to measure their antithrombin III (AT-III), protein C, protein S activity and activated C protein resistance value, thus defining the situation of the crowd's hereditary thrombophilia. Sequenom Massarray detection technology was used to conduct a genotype test of the six sites selected by the case and control groups. Haploview software was used to perform linkage disequilibrium analysis of the six sites, and the impact of the interaction between genetic variations and environment on hereditary thrombophilia was researched by the use of sum model. A total of 1005 Kazakh volunteers participated in the test (332 men and 673 women), average age (41.13 ±â€Š11.50) years; the prevalence of hereditary thrombophilia in Xinjiang Kazakh population was 31.0%, and the prevalence of AT-III deficiency, protein C deficiency, protein S deficiency and activated protein C resistance was 16.4, 14.9, 20.6 and 7.8%, respectively. The difference in allele frequency of the hereditary thrombophilia patient group at rs3136447 and rs5896 sites was statistically significant (P = 0.0483 and P = 0.0302, respectively). rs5896 and rs2070852 had high linkage disequilibrium (r = 0.99), and constituted a single-domain block 1. The rs3136447 and the rs5896 polymorphisms located in the region of the prothrombin gene may be associated with hereditary thrombophilia in the Xinjiang Kazakhs population. There is additive interactive effect of rs5896 polymorphism (CT + TT) and smoke on hereditary thrombophilia.

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