BACKGROUNDAortic dissection during pregnancy is a rare but life-threatening event for mothers and fetuses. It often occurs in the third trimester of pregnancy and the postpartum period. Most patients have connective tissue diseases such as Marfan syndrome. Thus, the successful repair of a sporadic aortic dissection with maternal and fetal survival in the early second trimester is extremely rare.CASE SUMMARYA 28-year-old woman without Marfan syndrome presented with chest pain at the 16th gestational week. Aortic computed tomographic angiography confirmed an acute type A aortic dissection (TAAD) with aortic arch and descending aorta involvement. Preoperative fetal ultrasound confirmed that the fetus was stable in the uterus. The patient underwent total arch replacement with a frozen elephant trunk using moderate hypothermic circulatory arrest with the fetus in situ. The patient recovered uneventfully and continued to be pregnant after discharge. At the 38th gestational week, she delivered a healthy female infant by cesarean section. After 2.5 years of follow-up, the patient is uneventful and the child’s development is normal.CONCLUSIONA fetus in the second trimester may have a high possibility of survival and healthy growth after aortic arch surgery.

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Background: Aortic dissection (AD) represents a significant mortality; however, there is rare epidemiologic information about the demography of AD in Chinese, especially its incidence rate. Methods: A retrospective cohort study was established using the Urban Employee Basic Medical Insurance claims data covering 346.7 million residents from 23 provinces in China, 2015-2016. AD cases were then linked to database of the Urban Employee Basic Endowment Insurance for death information. Incidence rate was age-and sex-standardized to the 2010 China census population. The associations between AD and related factors were evaluated with Poisson regression models. Moreover, mortality and sex-and age-adjusted survival rate was estimated by Cox models. Findings: 6084 adult AD cases were included in incidence analysis. Totally 4692(77.1%) were men and 5641(92.7%) were Han Chinese. The overall age-and sex-adjusted incidence rate of AD was 2.78(95%CI:2.59-2.98) per 10 0,0 0 0 person-years. In terms of geographic disparities, the crude incidence rate was significantly higher in Northwest China than South vs. 2.04[95%CI:0.38-3.71] per 10 0,0 0 0 person-years; risk ratio: 2.67[95%CI: 2.34-3.04]). Moreover, survival analysis of 4518 AD patients with 683 recorded deaths during follow-up (median 2.2 years) showed that overall 3-year survival was 83.7%(95%CI:82.4-84.8). Interpretation: This contemporary population-based cohort study provides a first comprehensive assessment of incidence of AD in urban Chinese adults. The distinct signatures of different incidence with respect to geographic variations may have important implications for clinical management of AD.

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Acute aortic dissection (AAD) is an emergent vascular disease. Currently, its diagnosis depends on clinical and radiological investigations but lacking of serum biomarkers. In this study, we aimed to identify potential serum biomarkers for AAD using label-free proteomics approach. A total of 90 serum samples were collected from three groups: patients with acute aortic dissection (AAD, n=30), patients with acute myocardial infarction (AMI, n=30), and healthy controls (n=30), and the first four samples from each group were selected for label-free proteomics analysis. Using label-free approach, a total of 22 differentially expressed proteins were identified in the serum samples of the AAD group, of which 15 were upregulated and 7 were downregulated as compared to the AMI and healthy control groups. The most prominent increased protein was vinculin, which was selected to validate in total samples. The level of vinculin was significantly elevated in AAD patients (15.8 ng/ml, IQR: 9.3-19.9 ng/ml) than that in AMI patients (8.6 ng/ml, IQR:5.3-11.4 ng/ml) and healthy volunteers (5.3 ng/ml, IQR:2.8-7.6 ng/ml), P<0.0001. Furthermore, the concentration of vinculin both increased in type A and B dissection. At the early stage of AAD, vinculin maintained a high level to 48 hours compared with that of AMI. Our study demonstrated that vinculin may play a role in the early diagnosis of AAD.

Background: Several methods of arch vessel reconstruction, such as en bloc (island) and branched graft techniques, have been proposed to treat aortic arch pathologies during total arch replacement (TAR). We seek to review our experience with modified en bloc technique and left subclavian (LSCA)-left carotid artery (LCCA) transposition in TAR and frozen elephant trunk (FET) procedure for chronic type A aortic dissection (CTAAD). Methods: From September 2010 to September 2016, 35 consecutive patients with CTAAD underwent modified en bloc arch reconstruction with LSCA-LCCA transposition during TAR and FET procedure. Computed tomographic angiography (CTA) was performed during follow-up. Results: In-hospital mortality was 5.7% (2/35). No neurological deficit or spinal cord injury occurred. Reexploration for bleeding and continuous renal replacement therapy were required in 2 patients each (5.7%). Follow-up was complete in 100% for a mean duration of 4.1±1.8 years (range, 0.5-6.7 years). One patient experienced a transient stroke and thoracoabdominal aortic replacement was performed in 1. There were 2 late non-cardiac deaths. Survival was 87.9% (95% CI, 70.7-95.3%) at 6 years. At 6 years, the incidence was 3% for reoperation, 12% for late death, and 85% of patients were alive without reoperation. The anastomosis between the LSCA and LCCA was patent in 100%. Conclusions: Acceptable early and mid-term outcomes were achieved for patients with chronic type A dissection using en bloc technique with LSCA-LCCA transposition during TAR and FET procedure. This technique may be an alternative approach to chronic type A dissection in selected patients.

New Findings What is the central question of this study?Insulin‐like growth factor 1 and its major binding protein insulin‐like growth factor binding protein 3 (IGFBP3) are involved in collagen deregulation in several cardiovascular diseases: what is the role of IGFBP3 in thoracic aortic dissection and does it regulate aortic smooth muscle cells’ phenotypic switch? What is the main finding and its importance?IGFBP3 inhibits aortic smooth muscle cells’ phenotypic switch from a contractile to a synthetic phenotype, decreases matrix metalloproteinase 9 activation and suppresses elastin degradation. These findings provide a better understanding of the pathogenesis of thoracic aortic dissection. Abstract Thoracic aortic dissection (TAD) is characterized by aortic media degeneration and is a highly lethal disease. An aortic smooth muscle cell (AoSMC) phenotypic switch is considered a key pathophysiological change in TAD. Insulin‐like growth factor binding protein 3 (IGFBP3) was found to be downregulated in aortic tissues of TAD patients. The present work aimed to study the function of IGFBP3 in AoSMCs’ phenotypic switch and matrix metalloproteinase (MMP) expression. We established a mouse model of TAD by angiotensin (Ang) II infusion to β‐aminopropionitrile‐administrated mice, and found decreased IGFBP3 expression accompanied by aortic dilatation and elastin degradation in vivo. Further, mouse (m)AoSMCs were isolated from mouse thoracic aorta and treated with Ang II. Ang II induced downregulation of IGFBP3 in vitro. To further study the function of IGFBP3, primary mAoSMCs were infected with adenovirus expressing IGFBP3 followed by Ang II induction. Enforced upregulation of IGFBP3 decreased MMP9 expression and activation as well as increasing tissue inhibitor of metalloproteinase (TIMP) 1 expression in Ang II‐induced mAoSMCs. No difference was observed in MMP2 and TIMP3 expression. IGFBP3 suppressed subsequent Ang II‐induced elastin degradation in vitro. IGFBP3 inhibited Ang II‐induced mAoSMCs’ phenotypic switch as evidenced by increased smooth muscle actin α‐2 (ACTA2) and myosin heavy chain 11 (MYH11) expression and decreased secreted phosphoprotein 1 (SPP1) and vimentin expression. Taken together, the present study demonstrates the role of IGFBP3 in preserving AoSMCs’ contractile state and reducing MMP9 activation and thus promoting elastic fibre synthesis, which provides a better understanding of the pathogenesis of TAD.

Background: This study analyzes the outcomes of a one-stage hybrid procedure combining thoracic endovascular aortic repair (TEVAR) with extra-anatomic bypass in patients with distal aortic arch disease. Methods: This retrospective study collected 103 hybrid procedures combining TEVAR with extraanatomic bypass (mean age, 62.2±9.3 years; 90 males) performed from January 2009 to January 2019 at Beijing Anzhen Hospital. We analyzed 30-day and mid-term outcomes including survival rate and the incidence of stroke, spinal cord injury (SCI), and endoleak. Results: Five deaths (4.6%) occurred within 30 days, including type I endoleak in Zone 1 (n=1), hemorrhagic shock (n=1), stroke (n=2), and stent migration (n=1). Two patients developed SCI. The median follow-up time was 39.5 (interquartile range, 13.6-69.0) months. In all, 14 late deaths occurred; these were due to stroke (n=2), severe pneumonia (n=1), aortic rupture caused by type I endoleak (n=3), and sudden death (n=8). Six late endoleaks occurred including three type I and one type II in Zone 1 and two type I in Zone 2. In a competing risks analysis, the incidences of reintervention at 7 years, late death, and survival without reintervention were 8%, 22%, and 70%, respectively. In a Cox risk model, stroke (HR, 21.602; 95%