The total aortic arch replacement with frozen elephant trunk is increasingly being used. However, deep hypothermic circulatory arrest is inevitable. We performed a novel surgical technique, the ‘aortic balloon occlusion’, in the surgical treatment of Stanford type A aortic dissection to reduce the adverse effects caused by deep hypothermic circulatory arrest.

Background: Stanford type A aortic dissection (AAD) is a catastrophic disease. An immune infiltrate has been found within the aortic wall of dissected aortic specimens. The recall and activation of macrophages are key events in the early phases of AAD. Herein, the immune filtration profile of AAD was uncovered.Methods: Gene expression data from the GSE52093, GSE98770 and GSE153434 datasets were downloaded from the Gene Expression Omnibus (GEO). The differentially expressed genes (DEGs) of each dataset were calculated and then integrated. A protein-protein interaction (PPI) network was established with the Search Tool for the Retrieval of Interacting Genes/Proteins (STRING), and the hub genes were identified in Cytoscape. Furthermore, gene ontology (GO) functional annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis of hub genes were performed. Finally, we set GSE52093 and GSE98770 as the training set and GSE153434 as the validation set to assess immune infiltration in AAD using CIBERSORTx and analyzed the correlations between immune cells and hub genes in both the training and validation sets.Results: Sixty-one integrated DEGs were identified. The top 10 hub genes were selected from the PPI network, and 140 biological process (BP) terms and 12 pathways were enriched among the top 10 hub genes. The proportions of monocytes and macrophages were significantly higher in AAD tissues than in normal tissues. Notably, this result was consistent in the training set and the validation set. In addition, we found that among the hub genes, CA9, CXCL5, GDF15, VEGFA, CCL20, HMOX1, and SPP1 were positively correlated with CD14, a cell marker of monocytes, while CA9, CXCL5, GDF15, and VEGFA were positively correlated with CD68, a cell marker of macrophages in the training set. Finally, according to the results of the GO and KEGG analysis of hub genes, we found that the monocyte/macrophage-related genes were involved in immune-inflammatory responses through degradation of the extracellular matrix, endothelial cell apoptosis, hypoxia and the interaction of cytokines and chemokines.Conclusion: The monocyte-macrophage system plays a major role in immune-inflammatory responses in the development of AAD. Several hub genes are involved in this process via diverse mechanisms.

Marfan syndrome (MFS) is an autosomal dominant connective tissue disorder caused by mutations in the FBN1 gene. Approximately 90% of classic MFS patients have a FBN1 mutation that can be identified by single-gene sequencing or gene-panel sequencing targeting FBN1. However, a small proportion of MFS patients carry a large genomic deletion in FBN1, which cannot be detected by routine sequencing. Here, we performed an MLPA (multiplex ligation-dependent probe amplification) test to detect large deletions and/or duplications in FBN1 and TGFBR2 in 115 unrelated Chinese patients with suspected MFS or early-onset aneurysm/dissection. Five novel large deletions encompassing a single exon or multiple exons in the FBN1 gene were characterized in five unrelated patients, of which four were proven by Sanger sequencing, and the breakpoints were identified. Three of them met the revised Ghent criteria when genetic results were not available, and the other two patients were highly suspected and diagnosed with MFS until the FBN1 deletions were identified. Our finding expands the mutation spectrum of large FBN1 deletions and emphasizes the importance of screening for large FBN1 deletions in clinical genetic testing, especially for those with classic Marfan phenotype.

To retrospectively analyze the role of intercostal artery reconstruction in the spinal cord protection for patients undergoing extensive thoracoabdominal aortic aneurysm repair. From August 2007 to 2014, thoracoabdominal aortas (Crawford II) of 81 consecutive patients with mean age 39.4 ± 10.32 years were repaired. Seventy-three of these patients (90.12%) were diagnosed with aortic dissection in our group, 25 (30.86%) with Stanford type A dissection and 48 (59.26%) with Stanford B aortic dissection. All 25 patients with type A dissection have previously undergone surgical procedures which include Bentall's procedures in 11 cases, ascending aortic replacement in 6 cases, and total aortic arch replacement in 8 cases. All procedures were performed under profound hypothermia with interval cardiac arrest after making a thoracoabdominal incision. Extracorporeal circulation was instituted with 2 arterial cannulae and a single venous cannula in the right atrium. T6-T12 intercostal arteries and L1 and L2 lumbar arteries were formed to a neo-intercostal artery in place and were connected to an 8 mm branch for maintaining spinal cord blood perfusion. Visceral arteries were joined into a patch and anastomosed to the end of the main graft. The left renal artery was anastomosed to an 8 mm branch or joined to the patch. The other 10 mm branches were anastomosed to iliac arteries. With 100% follow-up, early mortality was 7.4%. Six deaths were recorded; 1 patient died of cerebral hemorrhage, 3 of renal failure, 1 of heart failure because of myocardial infarction, and the last one died from the rupture of celiac artery dissection. The rate of postoperative spinal cord deficits was 3.7%, 2 patients with paraplegia and 1 patient with paraparesis. None had bladder or rectum dysfunction. Neo-intercostal arteries were clogged in 12 patients within follow-up period and formed pseudoaneurysm in 2 patients with Marfan syndrome. The mean survival time in this group was 54.22 ± 3.03 months (95% confidence interval 44.37-59.90 months) with survival rate of 92.37% after 1 year, 89.02% after 2 years, and 85.54% after 5 years. All patients were free from spinal cord deficits. Intercostal artery reconstruction is an effective technique for spinal cord protection in patients with the thoracoabdominal aortic repair. It can achieve favorable results and avoid spinal cord deficits with long-term follow-up.

Background: Obesity is dramatically increasing worldwide, and more obese patients may develop aortic dissection and present for surgical repair. The study aims to analyse the impact of body mass index (BMI) on surgical outcomes in patients with acute Stanford type A aortic dissection (ATAAD). Methods: From January 2017 to June 2019, the clinical data of 268 ATAAD patients in a single centre were retrospectively reviewed. They were divided into three groups based on the BMI: normal weight (BMI 18.5 to < 25 kg/m², n = 110), overweight (BMI 25 to < 30 kg/m², n = 114) and obese (BMI ≥30 kg/m², n = 44). Results: There was no statistical difference among the three groups in terms of the composite adverse events including 30-day mortality, stroke, paraplegia, renal failure, hepatic failure, reintubation or tracheotomy and low cardiac output syndrome (20.9% vs 21.9% vs 18.2% for normal, overweight and obese, respectively; P = 0.882). No significant difference was found in the mid-term survival among the three groups. The proportion of prolonged ventilation was highest in the obese group followed by the overweight and normal groups (59.1% vs 45.6% vs 34.5%, respectively; P = 0.017). Multivariable logistic regression analysis suggested that BMI was not associated with the composite adverse events, while BMI ≥30 kg/m² was an independent risk factor for prolonged ventilation (OR 2.261; 95% CI 1.056–4.838; P = 0.036). Conclusions: BMI had no effect on the early major adverse outcomes and mid-term survival after surgery for ATAAD. Satisfactory surgical outcomes can be obtained in patients with ATAAD at all weights.