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Objective Arterial aneurysms are life-threatening but usually asymptomatic before requiring hospitalization. Oculomics of retinal vascular features (RVFs) extracted from retinal fundus images can reflect systemic vascular properties and therefore were hypothesized to provide valuable information on detecting the risk of aneurysms. By integrating oculomics with genomics, this study aimed to (i) identify predictive RVFs as imaging biomarkers for aneurysms and (ii) evaluate the value of these RVFs in supporting early detection of aneurysms in the context of predictive, preventive and personalized medicine (PPPM). Methods This study involved 51,597 UK Biobank participants who had retinal images available to extract oculomics of RVFs. Phenome-wide association analyses (PheWASs) were conducted to identify RVFs associated with the genetic risks of the main types of aneurysms, including abdominal aortic aneurysm (AAA), thoracic aneurysm (TAA), intracranial aneurysm (ICA) and Marfan syndrome (MFS). An aneurysm-RVF model was then developed to predict future aneurysms. The performance of the model was assessed in both derivation and validation cohorts and was compared with other models employing clinical risk factors. An RVF risk score was derived from our aneurysm-RVF model to identify patients with an increased risk of aneurysms. Results PheWAS identified a total of 32 RVFs that were significantly associated with the genetic risks of aneurysms. Of these, the number of vessels in the optic disc (‘ntreeA’) was associated with both AAA (β = −0.36, P = 6.75e−10) and ICA (β = −0.11, P = 5.51e−06). In addition, the mean angles between each artery branch (‘curveangle_mean_a’) were commonly associated with 4 MFS genes (FBN1: β = −0.10, P = 1.63e−12; COL16A1: β = −0.07, P = 3.14e−09; LOC105373592: β = −0.06, P = 1.89e−05; C8orf81/LOC441376: β = 0.07, P = 1.02e−05). The developed aneurysm-RVF model showed good discrimination ability in predicting the risks of aneurysms. In the derivation cohort, the C-index of the aneurysm-RVF model was 0.809 [95% CI: 0.780–0.838], which was similar to the clinical risk model (0.806 [0.778–0.834]) but higher than the baseline model (0.739 [0.733–0.746]). Similar performance was observed in the validation cohort, with a C-index of 0.798 (0.727–0.869) for the aneurysm-RVF model, 0.795 (0.718–0.871) for the clinical risk model and 0.719 (0.620–0.816) for the baseline model. An aneurysm risk score was derived from the aneurysm-RVF model for each study participant. The individuals in the upper tertile of the aneurysm risk score had a significantly higher risk of aneurysm compared to those in the lower tertile (hazard ratio = 17.8 [6.5–48.8], P = 1.02e−05). Conclusion We identified a significant association between certain RVFs and the risk of aneurysms and revealed the impressive capability of using RVFs to predict the future risk of aneurysms by a PPPM approach. Our finds have great potential to support not only the predictive diagnosis of aneurysms but also a preventive and more personalized screening plan which may benefit both patients and the healthcare system. Graphical abstract

Aims Group 2 innate lymphoid cells (ILC2s) regulate adaptive and innate immunities. In mouse heart, production of myocardial infarction (MI) increased ILC2 accumulation, suggesting a role for ILC2 in cardiac dysfunction post-MI. Methods and results We produced MI in ILC2-deficeint Rorafl/flIl7rCre/+ mice and in Icosfl-DTR-fl/+Cd4Cre/+ mice that allowed diphtheria toxin-induced ILC2 depletion. Genetic or induced deficiency of ILC2 in mice exacerbated cardiac dysfunction post-MI injury along with increased myocardial accumulation of neutrophils, CD11b+Ly6Chi monocytes, and CD4+ T cells but deficiency of eosinophils (EOS) and dendritic cells (DC). Post-MI hearts from genetic and induced ILC2-deficient mice contained many more apoptotic cells than those of control mice, and Rorafl/flIl7rCre/+ mice showed thinner and larger infarcts and more collagen-I depositions than the Il7rCre/+ mice only at early time points post-MI. Mechanistic studies revealed elevated blood IL5 in Il7rCre/+ mice at 1, 7, and 28 days post-MI. Such increase was blunted in Rorafl/flIl7rCre/+ mice. Administration of recombinant IL5 reversed EOS losses in Rorafl/flIl7rCre/+ mice, but IL5 did not correct the DC loss in these mice. Adoptive transfer of ILC2, EOS, or DC from wild-type mice, but not ILC2 from Il5−/− mice improved post-MI cardiac functions in Rorafl/flIl7rCre/+ recipient mice. EOS are known to protect cardiomyocytes from apoptosis. Here we showed that DC acted like EOS in blocking cardiomyocyte apoptosis. Yet, ILC2 or IL5 alone did not directly affect cardiomyocyte apoptosis or TGF-β (transforming growth factor-β)-induced cardiac fibroblast Smad signalling. Conclusion This study revealed an indirect cardiac reparative role of ILC2 in post-MI hearts via the IL5, EOS, and DC mechanism.

Aims Blood eosinophil (EOS) counts and EOS cationic protein (ECP) levels associate positively with major cardiovascular disease (CVD) risk factors and prevalence. This study investigates the role of EOS in cardiac hypertrophy. Methods and results A retrospective cross-section study of 644 consecutive inpatients with hypertension examined the association between blood EOS counts and cardiac hypertrophy. Pressure overload- and β-adrenoreceptor agonist isoproterenol-induced cardiac hypertrophy was produced in EOS-deficient ΔdblGATA mice. This study revealed positive correlations between blood EOS counts and left ventricular (LV) mass and mass index in humans. ΔdblGATA mice showed exacerbated cardiac hypertrophy and dysfunction, with increased LV wall thickness, reduced LV internal diameter, and increased myocardial cell size, death, and fibrosis. Repopulation of EOS from wild-type (WT) mice, but not those from IL4-deficient mice ameliorated cardiac hypertrophy and cardiac dysfunctions. In ΔdblGATA and WT mice, administration of ECP mEar1 improved cardiac hypertrophy and function. Mechanistic studies demonstrated that EOS expression of IL4, IL13, and mEar1 was essential to control mouse cardiomyocyte hypertrophy and death and cardiac fibroblast TGF-β signalling and fibrotic protein synthesis. The use of human cardiac cells yielded the same results. Human ECP, EOS-derived neurotoxin, human EOS, or murine recombinant mEar1 reduced human cardiomyocyte death and hypertrophy and human cardiac fibroblast TGF-β signalling. Conclusion Although blood EOS counts correlated positively with LV mass or LV mass index in humans, this study established a cardioprotective role for EOS IL4 and cationic proteins in cardiac hypertrophy and tested a therapeutic possibility of ECPs in this human CVD.

To report the results of optimal medical treatment (OMT) and endovascular aortic repair (EVAR) in patients with uncomplicated isolated abdominal aortic dissection (IAAD).A retrospective review of 96 consecutive patients with uncomplicated IAAD (uIAAD) managed at a single tertiary vascular unit between January 2011 and July 2021 was conducted. Standard methods for univariate and survival analyses were used. The primary outcomes were all-cause mortality. Secondary end points included uIAAD progression, interventional complications, and follow-up aortic intervention.Initially, 53.1% of patients (51/96) were managed with OMT. No in-hospital deaths occurred. During follow-up, three patients died, and three and two patients who were initially managed with OMT subsequently required endovascular treatment and surgical management, respectively. Initially, 46.9% of patients (45/96) underwent EVAR. One patient died during hospital admission; nine patients had an endoleak after operation and one needed reintervention. Furthermore, during follow-up, five patients died; four patients needed reoperation, one surgery and three endovascular treatments. The overall long-term mortality was 8.4%, and follow-up aortic intervention rate was 9.5% (median follow-up, 54 months; interquartile range, 33-81 months) with no significant difference between groups. Of note, 12 patients (12.6%) suffered uIAAD progression, which was higher in the OMT group than EVAR group (10 [19.6%] vs 2 [4.5%]; P = .03).uIAAD may be managed safely by OMT with regular surveillance, despite the risk of disease progression. Compared with OMT, EVAR could significantly prevent uIAAD progression. For anatomically suitable patients with uIAAD progression and who are unresponsive to OMT, pre-emptive EVAR is a safe and feasible option.

Jitao Liu,1,&ast; Fan Yang,2,&ast; Songyuan Luo,1,&ast; Chenxi Li,3 Weijie Liu,4 Yuan Liu,1 Wenhui Huang,1 Enmin Xie,5 Lyufan Chen,6 Sheng Su,5 Xinyue Yang,6 Qingshan Geng,1 Jianfang Luo1,5 1Department of Cardiology, Guangdong Cardiovascular Institute, Guangdong Provincial Key Laboratory of Coronary Heart Disease Prevention, Guangdong Provincial People’s Hospital, Guangdong Academy of Medical Sciences, Guangzhou, People’s Republic of China; 2Department of Emergency and Critical Care Medicine, Guangdong Provincial People’s Hospital, Guangdong Academy of Medical Sciences, Guangzhou, People’s Republic of China; 3Department of Cardiac Surgery Intensive Care Unit, Guangdong Cardiovascular Institute, Guangdong Provincial People’s Hospital, Guangdong Academy of Medical Sciences, Guangzhou, People’s Republic of China; 4Center for Information Technology and Statistics, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, People’s Republic of China; 5The Second School of Clinical Medicine, Southern Medical University, Guangzhou, People’s Republic of China; 6School of Medicine, South China University of Technology, Guangzhou, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Jianfang Luo; Qingshan GengDepartment of Cardiology, Guangdong Cardiovascular Institute, Guangdong Provincial Key Laboratory of Coronary Heart Disease Prevention, Guangdong Provincial People’s Hospital, Guangdong Academy of Medical Sciences, #106 Zhongshan Second Road, Yuexiu District, Guangzhou, Guangdong, 510080, People’s Republic of ChinaTel +86-20-83827812Fax + 86-20-83875453Email jianfangluo@sina.com; gengqingshan@gdph.org.cnPurpose: The present study aimed to investigate the incidence and predictors of post-operative delirium (POD) in patients with complicated type B aortic dissection (TBAD) undergoing TEVAR with/without concomitant procedures and to assess the association of POD with early and follow-up outcomes.Methods: A retrospective single-center cross-sectional analysis was conducted using a prospectively maintained database from 2010 to 2017. Outcomes were postoperative clinical outcomes, early and follow-up survival.Results: A total of 517 complicated TBAD patients were enrolled. POD was observed in 13.3% (69/517) patients and was associated with increased hospital length of stay (LOS) and hospital costs (P< 0.001 for both). Besides, POD was found to be an independent risk factor for prolonged ICU stay (odds ratio [OR] 4.39, 95% confidence interval [CI] 2.40– 8.01, P< 0.001) and early death (OR 4.42, 95% CI 1.26– 15.54, P= 0.020). Predictors of POD were hybrid procedure (OR 2.17, 95% CI 1.20– 3.92, P= 0.010), the use of benzodiazepine (OR 1.86, 95% CI 1.07– 3.23, P= 0.027) or quinolone (OR 2.35, 95% CI 1.26– 4.38, P= 0.007), creatinine > 2 mg/dL (OR 3.25, 95% CI 1.57– 6.72, P= 0.001) and preoperative blood transfusion (OR 3.31, 95% CI 1.76– 6.21, P< 0.001). After a median follow-up of 73.6 months, POD remained as an independent indicator for follow-up mortality (hazard ratio [HR] 2.40, 95% CI 1.31– 4.38, P= 0.005) after adjusting potential confounders.Conclusion: POD after TEVAR has an incidence of around 13% and could profoundly increase the in-hospital LOS, hospital costs, as well as the early and follow-up mortality. A series of risk factors, including hybrid procedure, the use of benzodiazepine or quinolone, creatinine > 2 mg/dL and preoperative blood transfusion, were identified as independent risk factors for POD. Effective risk-stratification and patient-tailored management strategy should be developed to reduce the incidence of POD.Keywords: type B aortic dissection, thoracic endovascular aortic repair, hybrid procedure, postoperative delirium, predictors, outcomes

OBJECTIVES This study aimed to investigate the morphological evolution and risk stratification of ulcer-like projection (ULP) in patients with uncomplicated acute type B aortic intramural haematoma. METHODS A retrospective study was conducted on patients with uncomplicated acute type B intramural haematoma admitted in our institution from January 2015 to June 2020. The primary end points were adverse aortic events (AAE), including aortic rupture, aortic dissection, aortic aneurysm and ULP enlargement. RESULTS The study cohort comprised 140 patients, including 62 (44%) and 78 (56%) patients with and without initial ULP, respectively. AAE occurred in 13 patients (9%) in the early term and 42 patients (33%) in the mid-term. Compared with patients without ULP, patients with initial ULP had no significant difference in early outcomes but a higher mid-term AAE rate [8% vs 11%, odds ratio (OR) 1.5, P = 0.47; 17% vs 55%, OR 6.0, P CONCLUSIONS High-risk ULP is a rapidly evolving entity and a marker of AAE despite optimal medical therapy. Therefore, close follow-up and prompt intervention are recommended for patients with high-risk ULP.

OBJECTIVES The aim of this work was to investigate the impact of machine-learning-derived baseline lean psoas muscle area (LPMA) for patients undergoing thoracic endovascular aortic repair. METHODS A retrospective study was undertaken of acute and subacute complicated type B aortic dissection patients who underwent endovascular treatment from 2010 to 2017. LPMA (a marker of frailty) was calculated by multiplying psoas muscle area and density measured at L3 level from the computed tomography. The optimal cut-off value of LPMA was determined by the Cox hazard model with restricted cubic spline. RESULTS A total of 428 patients who met the inclusion criteria were included in this study. Patients were classified into low LPMA group (n = 218) and high LPMA group (n = 210) using the cut-off value of 395 cm2 Hounsfield unit. An automatic muscle segmentation algorithm was developed based on U-Net architecture. There was high correlation between machine-learning method and manual measurement for psoas muscle area (r = 0.91, P CONCLUSIONS Baseline LPMA could profoundly affect the prognosis of patients undergoing thoracic endovascular aortic repair. It was feasible to integrate the automatic muscle measurements into clinical routine.

Diabetic patients show elevated plasma IL18 concentrations. IL18 has two receptors: the IL18 receptor (IL18r) and the Na-Cl co-transporter (NCC). Here, we report that IL18 is expressed on islet α cells, NCC on β cells, and IL18r on acinar cells in human and mouse pancreases. The deficiency of these receptors reduces islet size, β cell proliferation, and insulin secretion but increases β cell apoptosis and exocrine macrophage accumulation after diet-induced glucose intolerance or streptozotocin-induced hyperglycemia. Together with the glucagon-like peptide-1 (GLP1), IL18 uses the NCC and GLP1 receptors on β cells to trigger β cell development and insulin secretion. IL18 also uses the IL18r on acinar cells to block hyperglycemic pancreas macrophage expansion. The β cell-selective depletion of the NCC or acinar-cell-selective IL18r depletion reduces glucose tolerance and insulin sensitivity with impaired β cell proliferation, enhanced β cell apoptosis and macrophage expansion, and inflammation in mouse hyperglycemic pancreas. IL18 uses NCC, GLP1r, and IL18r to maintain islet β cell function and homeostasis.

OBJECTIVES Our goal was to investigate the accuracy of the two-dimensional and three-dimensional computed tomography imaging features in predicting the progression of acute uncomplicated type B aortic intramural haematoma (IMH). METHODS This study retrospectively screened 140 patients diagnosed with acute uncomplicated type B IMH in our institution from January 2015 to December 2020. Patients were classified as exhibiting progression (aortic dissection, aortic rupture, aneurysm formation, ulcer-like projection depth >10 mm or >10% increase in the initial thickness of the aortic wall) and regression (completely or partially reabsorbed haematoma) based on follow-up computed tomography. RESULTS During the 11.4-month follow-up [interquartile range (IQR), 2.6–17.8], 55 patients had haematoma progression. The progression group had higher haematoma volume (HV) and total lesion volume [94.8 (IQR, 80.0–108.2) cm3 vs 40.3 (IQR, 30.8–57.9) cm3; 278.0 (IQR, 238.6–369.3) cm3 vs 197.3 (IQR, 152.8–235.9) cm3, both P < 0.001) and longer lesion length [43.2 (IQR, 37.5–46.7) cm vs 30.4 (IQR, 28.1–37.6) cm, P < 0.001)] than the regression group. According to the area under the curve, HV > 66 cm3 is the greatest risk factor for haematoma progression. In multivariable analysis, HV was a powerful independent predictive factor for type B IMH progression, with a hazard ratio of 17.9 (95% confidence interval, 5.5–58.7; P < 0.001). CONCLUSIONS Volumetric parameters may help to predict disease progression more precisely for patients with acute uncomplicated type B IMH compared to standard axial measurements, which might optimize the initial treatment and follow-up protocol.

Natural products were extracted from traditional Chinese herbal emerging as potential therapeutic drugs for treating cardiovascular diseases. This study examines the role and underlying mechanism of dihydromyricetin (DMY), a natural compound extracted from Ampelopsis grossedentata, in atherosclerosis. DMY treatment significantly inhibits atherosclerotic lesion formation, proinflammatory gene expression and the influx of lesional macrophages and CD4‐positive T cells in the vessel wall and hepatic inflammation, whereas increases nitric oxide (NO) production and improves lipid metabolism in apolipoprotein E‐deficient (Apoe− / −) mice. Yet, those protective effects are abrogated by using NOS inhibitor L‐NAME in Apoe− / − mice received DMY. Mechanistically, DMY decreases microRNA‐21 (miR‐21) and increases its target gene dimethylarginine dimethylaminohydrolase‐1 (DDAH1) expression, an effect that reduces asymmetric aimethlarginine (ADMA) levels, and increases endothelial NO synthase (eNOS) phosphorylation and NO production in cultured HUVECs, vascular endothelium of atherosclerotic lesions and liver. In contrast, systemic delivery of miR‐21 in Apoe− / − mice or miR‐21 overexpression in cultured HUVECs abrogates those DMY‐mediated protective effects. These data demonstrate that endothelial miR‐21‐inhibited DDAH1‐ADMA‐eNOS‐NO pathway promotes the pathogenesis of atherosclerosis which can be rescued by DMY. Thus, DMY may represent a potential therapeutic adjuvant in atherosclerosis management.

Objectives: This study aimed to evaluate the effect of dihydropyridine calcium-channel blocker (CCB) on adverse aortic events (AAE) in patients undergoing thoracic endovascular aortic repair (TEVAR) for type B aortic dissection (TBAD). Methods: A retrospective study was conducted on patients undergoing TEVAR of TBAD from January 2010 to December 2017 in our center. Patients were divided into CCB group and non-CCB group according to the postoperative dihydropyridine CCB use. AAE including aorta-relative mortality and reintervention, were compared between these two groups. Propensity score matching analysis was performed to avoid the potential effect of known confounders.Results: Before matching, the study cohort comprised 548 patients, including 435 (79.4%) and 113 (20.6%) patients in the CCB and non-CCB groups, respectively. After matching, 101 patients in each group were eligible for the analysis. In the unmatched cohort, AAE occurred in 52 (12.0%) and 29 (25.7%) patients in the CCB and non-CCB groups, respectively (P < 0.001). In the matched cohort, AAE occurred in 8 (7.9%) and 22 (21.8%) patients in the CCB and non-CCB groups, respectively (P = 0.013). Log-rank test analysis revealed that the levels of freedom from AAE were significantly different between the 2 groups in both the unmatched and matched cohorts (P < 0.001 and P = 0.007, respectively). Multivariable analysis showed that CCB use (hazard ratio 0.50, 95% confidence interval 0.32–0.80; P = 0.003) was associated with a lower AAE rate after adjustment for other variables, and was minimally changed after the propensity score matching (HR 0.34, 95% CI 0.15–0.75; P = 0.008).Conclusions: Postoperative dihydropyridine CCB use is protective in patients undergoing TEVAR for acute and sub-acute TBAD.

Aims: The monocyte to high-density lipoprotein ratio (MHR), a novel marker of inflammation and cardiovascular events, has recently been found to facilitate the diagnosis of acute aortic dissection. This study aimed to assess the association of preoperative MHR with in-hospital and long-term mortality after thoracic endovascular aortic repair (TEVAR) for acute type B aortic dissection (TBAD).Methods: We retrospectively evaluated 637 patients with acute TBAD who underwent TEVAR from a prospectively maintained database. Multivariable logistic and cox regression analyses were conducted to assess the relationship between preoperative MHR and in-hospital as well as long-term mortality. For clinical use, MHR was modeled as a continuous variable and a categorical variable with the optimal cutoff evaluated by receiver operator characteristic curve for long-term mortality. Propensity score matching was used to diminish baseline differences and subgroups analyses were conducted to assess the robustness of the results.Results: Twenty-one (3.3%) patients died during hospitalization and 52 deaths (8.4%) were documented after a median follow-up of 48.1 months. The optimal cutoff value was 1.13 selected according to the receiver operator characteristic curve (sensitivity 78.8%; specificity 58.9%). Multivariate analyses showed that MHR was independently associated with either in-hospital death [odds ratio (OR) 2.11, 95% confidence interval (CI) 1.16-3.85, P = 0.015] or long-term mortality [hazard ratio (HR) 1.78, 95% CI 1.31-2.41, P < 0.001). As a categorical variable, MHR > 1.13 remained an independent predictor of in-hospital death (OR 4.53, 95% CI 1.44-14.30, P = 0.010) and long-term mortality (HR 4.16, 95% CI 2.13-8.10, P < 0.001). Propensity score analyses demonstrated similar results for both in-hospital death and long-term mortality. The association was further confirmed by subgroup analyses.Conclusions: MHR might be useful for identifying patients at high risk of in-hospital and long-term mortality, which could be integrated into risk stratification strategies for acute TBAD patients undergoing TEVAR.

Purpose This study aimed to quantitatively evaluate whether the severity of menton deviation (MD) influenced facial perceptions of laypeople. We also aimed to determine the effectiveness of surgery in normalizing the distribution of the facial visual attention of laypeople. Methods The scanning paths of 177 laypeople were recorded using an eye tracking device while observing images of individuals without MD and pre- and post-treatment subjects with different degrees of MD. The fixation durations on the areas of interest (AOIs) in each group were compared and analysed. Results When observing the images of non-MD subjects, the eyes were the focus of the most significant fixation (higher than the fixations on the nose and lower face). When the MD increased to 3°, attention on the lower face increased (p = 0.001) with decreased attention to the eyes (p = 0.0126). At an MD of 9°, attention to the lower face sharply increased, even more so than that to the eyes, with decreased attention to the nose (p = 0.0104). Compared with the findings for the post-treatment images, the laypeople who observed the pretreatment images focused longer on the lower face and less on the eyes and nose (p = 0.001, p = 0.0322 and p = 0.0023, respectively). The distribution of the fixation duration when observing the post-treatment images was similar to that when observing the images of the non-MD subjects. Conclusions Laypeople can perceive an MD of 3°, which causes changes in the distribution of visual attention, with attention focusing on the MD. When the deviation reaches 9°, it is very noticeable. Surgery can normalize the distribution of the facial visual attention of laypeople, as shown by the responses to the post-treatment images.

Background: Spinal cord ischemia (SCI) is a recognized grave complication after thoracic endovascular aortic repair (TEVAR). The present study aimed to evaluate the incidence and investigate risk of SCI after TEVAR based on current prophylactic strategies designed against established risk factors. Methods: The study retrospectively reviewed a prospectively maintained database to investigate patients who underwent TEVAR successfully between January 2009 and December 2012 in a single cardiovascular center. Detailed assessment of SCI risk was routinely performed for all patients before TEVAR was carried out. Prophylactic measures, including left subclavian artery (LSA) revascularization, blood pressure augmentation and cerebrospinal fluid (CSF) pressure control after TEVAR, were employed in high-risk patients and physical neurological examinations were regularly done to evaluate SCI after TEVAR. Patients were further divided into SCI group and non-SCI group. Results: A total of 650 patients were enrolled in the study. Eleven patients (1.69%) developed SCI after TEVAR. Baseline level of hemoglobin was significantly lower in the SCI group (113.00 vs. 128.50, P=0.023). More patients in the SCI patients in the SCI group underwent TEVAR under general anesthesia (45.5% vs. 17.7%, P=0.033). A significantly higher incidence of post TEVAR hypotension was found in the SCI group (2.7% vs. 27.3%, P=0.004). Logistic regression analysis revealed that post-TEVAR hypotension (OR, 8.379; 95% CI, 1.833–38.304; P=0.006) was strongly associated with development of SCI and high normal baseline hemoglobin was a protective factor (OR, 0.969; CI, 0.942–0.998; P=0.037). The mortality in hospital and mortality at 1 year were not significant different between the SCI and the non-SCI group (0% vs. 1.6% P=1.000; 9.1% vs. 3.0%, P=0.294, respectively). While length of post-TEVAR stay (13.00 vs. 7.00 days, P=0.000) and length of hospital stay (20.00 vs. 13.00 days, P=0.001) were significantly greater in the SCI group. Conclusions: Our study revealed that, based on current prophylactic measures to curtail SCI, including LSA revascularization, blood pressure augmentation and CSF pressure control after TEVAR, post-TEVAR hypotension remains a major and independent risk factor for SCI and high normal baseline hemoglobin level is protective. SCI results in longer post-TEVAR stay and hospital stay, but not associated with increased mortality. Robust precautions should be taken against underlying causes for post-TEVAR hypotension and low level of hemoglobin should be avoided.

We aimed to investigate whether sex differences influence the clinical outcomes of patients who undergo thoracic endovascular aortic repair (TEVAR) for type B aortic dissection (TBAD). We retrospectively analyzed a prospectively maintained single-center cohort of patients with TBAD who underwent TEVAR between January 2010 and June 2017. We evaluated the in-hospital and long-term mortality and composite end point. Of the 913 patients, 793 (86.8%) were male and 120 (13.1%) were female. Compared to male patients, the female patients were older, more likely to have diabetes mellitus, but less likely to smoke or have hypertension. The proximal landing zone in 0 and 1 was higher in male patients ( P = .023), who were more likely to require an aortic arch bypass. Endoleak, delirium, and ICU stay after stent-graft implantation were also more frequent in men. Sex factor was not associated with in-hospital or long-term mortality or the composite end point in the multivariable regression analyses and Cox regression model. The mean estimated survival time was similar between males and females (2462.9 ± 141.2 vs 2804.1 ± 117.4 days, P = .167) in the propensity score–matched cohort. Despite distinct characteristics between sex, there was no sex-related difference in long-term clinical outcomes after TEVAR for TBAD.

Supplemental Material, sj-pdf-1-ang-10.1177_0003319720987956 for Influence of Sex on Outcomes After Thoracic Endovascular Repair for Type B Aortic Dissection by Songyuan Luo, Yi Zhu, Enmin Xie, Huanyu Ding, Fan Yang, Lyufan Chen, Jitao Liu, Yuan Liu, Ling Xue, Ruixin Fan, JianFang Luo and Jiyan Chen in Angiology

Introduction: The regeneration of pancreatic β cells to restore insulin production is a promising therapeutic strategy for insulin-dependent type-1 (T1D) and type-2 diabetes (T2D). Plasma IL18 levels are increased in these patients. Prior studies suggest a role for IL18 in inducing islet insulin production. IL18 administration suppressed autoimmune diabetes in non-obese diabetic mice. We recently discovered that IL18 uses two receptors IL18r and NCC (Na-Cl co-transporter) with equal binding kinetics. Hypothesis: IL18r and NCC use different mechanisms to mediate IL18 activity in islet β cell insulin production. Methods and Results: Immunoblot and immunofluorescent staining localized IL18 on islet α cells, NCC on islet β cells, and IL18r on pancreas acinar cells. Development of T1D or T2D increased the α cell IL18 expression. From high fat diet (HFD)-induced T2D, deficiency of IL18r ( Il18r -/- ) or NCC ( Ncc -/- ), or combined deficiency of both receptors ( Il18r -/- Ncc -/- ) reduced insulin secretion, exacerbated β cell failure, decreased α cell content, reduced islet size, reduced β cell proliferation, and decreased the expression of islet proliferation markers. Deficiency of IL18r in Il18r -/- and Il18r -/- Ncc -/- mice aggravated β cell content and size reductions and glucose metabolism and increased β cell apoptosis after streptozotocin (STZ)-induced T1D. Il18r -/- Ncc -/- mice also showed increased macrophage accumulation in the islets from both T1D and T2D mice. Using α cell-selective IL18-deficient Gcg CreERT2 IL18 fl/fl mice, acinar cell-selective IL18r-deficient Mist1 CreERT2 Il18r fl/fl mice, and β cell NCC-deficient Ins1 Cre Ncc fl/fl mice, we demonstrated that these mice showed impaired insulin secretion and glucose metabolism, exacerbated β cell failure, and aggravated HFD-induced T2D. Mechanistic studies suggested that IL18 uses NCC on β cells to promote insulin secretion and uses IL18r on acinar cells to assist β cell development. Conclusions: Islet α cell IL18 uses NCC on β cells to promote β cell proliferation and uses IL18r on acinar cells to produce inflammatory molecules to assist β cell generation and insulin secretion. Both the IL18r and NCC signaling pathways are essential to β cell function in diabetic patients.

Rationale: Blood eosinophil count and ECP (eosinophil cationic protein) associate with human cardiovascular diseases. Yet, whether eosinophils play a role in cardiovascular disease remains untested. The current study detected eosinophil accumulation in human and murine abdominal aortic aneurysm (AAA) lesions, suggesting eosinophil participation in this aortic disease. Objective: To test whether and how eosinophils affect AAA growth. Methods and Results: Population-based randomized clinically controlled screening trials revealed higher blood eosinophil count in 579 male patients with AAA than in 5063 non-AAA control (0.236±0.182 versus 0.211±0.154, 10 9 /L, P P P =0.031) logistic regression analyses indicated that increased blood eosinophil count in patients with AAA served as an independent risk factor of human AAA. Immunostaining and immunoblot analyses detected eosinophil accumulation and eosinophil cationic protein expression in human and murine AAA lesions. Results showed that eosinophil deficiency exacerbated AAA growth with increased lesion inflammatory cell contents, matrix-degrading protease activity, angiogenesis, cell proliferation and apoptosis, and smooth muscle cell loss using angiotensin-II perfusion–induced AAA in Apoe −/− and eosinophil-deficient Apoe −/− ΔdblGATA mice. Eosinophil deficiency increased lesion chemokine expression, muted lesion expression of IL (interleukin) 4 and eosinophil-associated-ribonuclease-1 (mEar1 [mouse EOS-associated-ribonuclease-1], human ECP homolog), and slanted M1 macrophage polarization. In cultured macrophages and monocytes, eosinophil-derived IL4 and mEar1 polarized M2 macrophages, suppressed CD11b + Ly6C hi monocytes, and increased CD11b + Ly6C lo monocytes. mEar1 treatment or adoptive transfer of eosinophil from wild-type and Il13 −/− mice, but not eosinophil from Il4 −/− mice, blocked AAA growth in Apoe −/− ΔdblGATA mice. Immunofluorescent staining and immunoblot analyses demonstrated a role for eosinophil IL4 and mEar1 in blocking NF-κB (nuclear factor-κB) activation in macrophages, smooth muscle cells, and endothelial cells. Conclusions: Eosinophils play a protective role in AAA by releasing IL4 and cationic proteins such as mEar1 to regulate macrophage and monocyte polarization and to block NF-κB activation in aortic inflammatory and vascular cells.

Background Acute type B aortic intramural hematoma (IMH) with ulcer-like projections (ULP) is associated with various adverse aortic-related events (AAE) and recommended for preventive endovascular repair as alternative. However, we have no therapeutic criterion on which to decide preventive treatment. Objectives The purpose of this study was to determine the prognostic value and risk stratification of ULP in patients with acute type B IMH for proper treatment. Methods A retrospective study was conducted on 61 consecutive patients with acute type B IMH and with present of ULP from January 2015 to December 2018 in our center. All patients were treated medically initially and CT scans were performed on admission and during follow-up period. Results During a median follow-up of 4.5 months (range, 0.3 to 49.8 months) from onset, 36 patients (59.0%) had composites of adverse aortic events, including 1 patient died for aortic rupture, 6 patients converted to endovascular repair, 6 progressed into aortic dissection, and 28 developed to aortic enlargement. A cutoff value to estimate risk is 6.0 mm for maximal ULP width (72.2% sensitivity and 84.0% specificity) and 4.0 mm for maximal ULP depth (94.4% sensitivity and 52.0% specificity). Patients with widest (P=0.005) or deepest ULP (P=0.019) in aortic arch and proximal descending thoracic aorta had significant poorer aorta-related event-free survival rates. On multivariate analysis, maximal ULP width ≥6.0 mm [hazard ratio (HR) = 2.569, 95% confidence interval (CI):1.157 to 5.705, P=0.020], maximal ULP depth ≥4.0 mm (HR=5.198, 95% CI: 1.154 to 23.420, P=0.032) and widest ULP in aortic arch and proximal descending thoracic aorta (HR=2.363, 95% CI: 1.012 to 5.517, P=0.047) were independently associated with AAE. ULP with both risk location (widest ULP in aortic arch and proximal descending thoracic aorta) and size (maximal ULP width ≥6.0 mm) were significantly associated with a poorer aortic-related event-free survival rate than others (both P Conclusions Maximal ULP width ≥6.0 mm, maximal ULP depth ≥4.0 mm and widest ULP in aortic arch and proximal descending thoracic aorta are predictive for progression of acute type B aortic intramural hematoma. For patients with ULP in both risk location and size, preventive endovascular treatment should be considered. Figure 1 Funding Acknowledgement Type of funding source: Public hospital(s). Main funding source(s): This research was supported by grant DFJH201807 from High-level Hospital Construction Project of Guangdong Provincial People's Hospital.

Objective: By binding to its high-affinity receptor FcεR1, IgE activates mast cells, macrophages, and other inflammatory and vascular cells. Recent studies support an essential role of IgE in cardiometabolic diseases. Plasma IgE level is an independent predictor of human coronary heart disease. Yet, a direct role of IgE and its mechanisms in cardiometabolic diseases remain incompletely understood. Approach and Results: Using atherosclerosis prone Apoe −/− mice and IgE-deficient Ige −/− mice, we demonstrated that IgE deficiency reduced atherosclerosis lesion burden, lesion lipid deposition, smooth muscle cell and endothelial cell contents, chemokine MCP (monocyte chemoattractant protein)-1 expression and macrophage accumulation. IgE deficiency also reduced bodyweight gain and increased glucose and insulin sensitivities with significantly reduced plasma cholesterol, triglyceride, insulin, and inflammatory cytokines and chemokines, including IL (interleukin)-6, IFN (interferon)-γ, and MCP-1. From atherosclerotic lesions and peritoneal macrophages from Apoe −/− Ige −/− mice that consumed an atherogenic diet, we detected reduced expression of M1 macrophage markers (CD68, MCP-1, TNF [tumor necrosis factor]-α, IL-6, and iNOS [inducible nitric oxide synthase]) but increased expression of M2 macrophage markers (Arg [arginase]-1 and IL-10) and macrophage-sterol-responsive-network molecules (complement C3, lipoprotein lipase, LDLR [low-density lipoprotein receptor]-related protein 1, and TFR [transferrin]) that suppress macrophage foam cell formation. These IgE activities can be reproduced in bone marrow-derived macrophages from wild-type mice, but muted in cells from FcεR1-deficient mice, or blocked by anti-IgE antibody or complement C3 deficiency. Conclusions: IgE deficiency protects mice from diet-induced atherosclerosis, obesity, glucose tolerance, and insulin resistance by regulating macrophage polarization, macrophage-sterol-responsive-network gene expression, and foam cell formation.

Songyuan Luo,* Huanyu Ding,* Jianfang Luo, Wei Li, Bing Ning, Yuan Liu, Wenhui Huang, Ling Xue, Ruixin Fan, Jiyan Chen Cardiology Department, Guangdong Cardiovascular Institute, Guangdong Provincial Key Laboratory of Coronary Heart Disease Prevention, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong, China *These authors contributed equally to this work Background: Thoracic endovascular aortic repair (TEVAR) has become an emerging treatment modality for acute type B aortic dissection (TBAD) patients in recent years. The risk factors and impacts of acute kidney injury (AKI) after percutaneous TEVAR, however, have not been widely established.Methods: We retrospectively studied the clinical records of 305 consecutive patients who admitted to our institution and had TEVAR for TBAD between December 2009 and June 2013. The patients were routinely monitored for their renal functions preoperatively until 7 days after TEVAR. The Kidney Disease Improving Global Guidelines (KDIGO) criteria were used for AKI.Results: Of the total 305 consecutive patients, 84 (27.5%) developed AKI after TEVAR, comprising 66 (21.6%) patients in KDIGO stage 1, 6 (2.0%) patients in stage 2 and 12 (3.9%) patients in stage 3. From the logistic regression analysis, systolic blood pressure (SBP) on admission >140 mmHg (odds ratio [OR], 2.288; 95% CI, 1.319–3.969) and supra-aortic branches graft bypass hybrid surgery (OR, 3.228; 95% CI, 1.526–6.831) were independent risk factors for AKI after TEVAR. Local anesthesia tended to be a protective factor (OR, 0.563; 95% CI, 0.316–1.001). The preoperative renal function, angiotensin-converting enzyme inhibitor/angiotensin receptor blocker or statin administration, volume of contrast agent, range of TBAD and false lumen involving renal artery were not associated with post-operation AKI. The in-hospital mortality and major adverse events were markedly increased with the occurrence of AKI (7.1% vs 0.9%, P=0.006; 14.3% vs 3.2%, P

Objective/Background Epidemiological screening studies have demonstrated that the prevalence of abdominal aortic aneurysm (AAA) of Asian origin appears to be low and so increases uncertainty about the cost effectiveness of screening for AAAs in Chinese people. Some studies have demonstrated a higher prevalence of AAA in patients with atherosclerotic risk factors. The purpose of the study was to determine the prevalence of AAA and to explore the high risk group of AAA in Chinese patients with atherosclerotic risk factors. Methods From November 2014 to July 2015, a prospective observational study was conducted in Guangdong General Hospital. In total, 1582 consecutive patients with atherosclerotic risk factors and undergoing coronary angiography for suspected or known coronary artery disease were enrolled to be screened for AAA by abdominal aortic ultrasound. Because of inadequate ultrasound image quality, the analysis was based on the 1541 (97.4%) patients whose abdominal aortic ultrasound images were adequate. Results The prevalence of AAA was 1.6% in the whole study population and 2.9% in male patients aged over 65 years. In multivariate analysis, age ≥ 65 years ( p = .029), smoking ( p = .037), hypertension ( p = .026), and aortic root diameter > 30 mm ( p = .003) were independent predictors of AAA. The prevalence of AAA was 0% (0/153) in patients without any independent predictor, 0.6% (3/502) in patients with one predictor, 1.0% (6/597) in patients with two predictors, 4.8% (12/249) in patients with three predictors, and up to 10% (4/40) in patients with four predictors ( p .001; p value for trend Conclusion Age ≥ 65 years, smoking, hypertension, and aortic root diameter > 30 mm emerged as independent predictors of AAA in Chinese patients. Stepwise increases in the prevalence of AAA were found to depend on the number of independent predictors. Ultrasound screening for AAA could be considered in these high risk patients, especially those with three or four predictors.

Objective The aim of the present study is to report our single-center experience with chimney technique for aortic arch diseases and the early- and mid-term outcomes in these patients. Methods From August 2012 to October 2017, 226 patients (mean age 54±12 years; 197 men) with aortic arch diseases underwent thoracic endovascular aortic repair combined with chimney stents. Pathologies included type B aortic dissection (n=185), aortic arch aneurysm/descending thoracic aortic aneurysm (n=13), aortic arch pseudoaneurysm (n=10), penetrating aortic ulcer (n=7), intramural hematoma (n=7), and aortic rupture (n=4). Results The aortic stent-grafts were deployed in zone 0 (n=22), zone 1 (n=13), and zone 2 (n=191). A total of 230 chimney stents were deployed (innominate artery, n=21; right common carotid artery, n=1; left common carotid artery, n=13; left subclavian artery, n=195). The technical success rate was 84% (189/226) and immediate type Ia endoleak occurred in 37 (16%) patients. In the early-term, four patients died, of which from aortic rupture (n=1), ventricular fibrillation (n=1) or major stroke (n=2). Four major strokes occurred (two patients died and two recovered), but no reintervention was recorded. Spinal cord ischemia developed in three patients. The mean duration of follow-up was 22±16 months. Late type Ia endoleaks were recorded in two patients. Chimney stent occlusions were recorded in six patients. During follow-up, five patients died, of which from aortic rupture (n=3), cerebral hemorrhage (n=1) or rectal cancer (n=1). Two major strokes occurred (one patient died and one recovered) and reintervention performed in one case. Conclusion The chimney technique for aortic arch diseases is safe and feasible. And long-term follow-up observation is needed.

Cysteinyl cathepsins are lysosomal/endosomal proteases that mediate bulk protein degradation in these intracellular acidic compartments. Yet, studies indicate that these proteases also appear in the nucleus, nuclear membrane, cytosol, plasma membrane, and extracellular space. Patients with cardiovascular diseases (CVD) show increased levels of cathepsins in the heart, aorta, and plasma. Plasma cathepsins often serve as biomarkers or risk factors of CVD. In aortic diseases, such as atherosclerosis and abdominal aneurysms, cathepsins play pathogenic roles, but many of the same cathepsins are cardioprotective in hypertensive, hypertrophic, and infarcted hearts. During the development of CVD, cathepsins are regulated by inflammatory cytokines, growth factors, hypertensive stimuli, oxidative stress, and many others. Cathepsin activities in inflammatory molecule activation, immunity, cell migration, cholesterol metabolism, neovascularization, cell death, cell signaling, and tissue fibrosis all contribute to CVD and are reviewed in this article in memory of Dr. Nobuhiko Katunuma for his contribution to the field.

Aims Obesity is a risk factor of abdominal aortic aneurysm (AAA). Inflammatory cytokine interleukin-18 (IL18) has two receptors: IL18 receptor (IL18r) and Na-Cl co-transporter (NCC). In human and mouse AAA lesions, IL18 colocalizes to its receptors at regions rich in adipocytes, suggesting a role of adipocytes in promoting IL18 actions in AAA development. Methods and results We localized both IL18r and NCC in human and mouse AAA lesions. Murine AAA development required both receptors. In mouse AAA lesions, IL18 binding to these receptors increased at regions enriched in adipocytes or adjacent to perivascular adipose tissue. 3T3-L1 adipocytes enhanced IL18 binding to macrophages, aortic smooth muscle cells (SMCs), and endothelial cells by inducing the expression of both IL18 receptors on these cells. Adipocytes also enhanced IL18r and IL18 expression from T cells and macrophages, AAA-pertinent protease expression from macrophages, and SMC apoptosis. Perivascular implantation of adipose tissue from either diet-induced obese mice or lean mice but not that from leptin-deficient ob/ob mice exacerbated AAA development in recipient mice. Further experiments established an essential role of adipocyte leptin and fatty acid-binding protein 4 (FABP4) in promoting IL18 binding to macrophages and possibly other inflammatory and vascular cells by inducing their expression of IL18, IL18r, and NCC. Conclusion Interleukin-18 uses both IL18r and NCC to promote AAA formation. Lesion adipocyte and perivascular adipose tissue contribute to AAA pathogenesis by releasing leptin and FABP4 that induce IL18, IL18r, and NCC expression and promote IL18 actions.

BACKGROUND This study aimed to investigate whether miR-146a-5p was involved in the pathogenesis of thoracic aortic dissection (AD) via regulating the biological function of vascular smooth muscle cells (VSMCs). METHODS Circulating miR-146a-5p level was measured by quantitative polymerase chain reaction (qPCR) in AD patients and healthy controls. Human dissected aortic samples were obtained from patients with thoracic AD Stanford type A undergoing surgical repair, and normal control samples were from organ donors who died from nonvascular diseases. The expression level of miR-146a-5p was detected using qPCR in each sample. The expression of SMAD4, which is involved in the TGF-β pathway and indicated as the target gene of miR-146a-5p, was measured by qPCR and Western blot analysis at the mRNA level and protein level, respectively. Subsequently, VSMCs were transfected with miR-146a-5p mimics or inhibitors in vitro. VSMC proliferation and migration were detected using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and Transwell assay, respectively. Flow cytometry was used to identify apoptosis. The expression of SMAD4 in VSMCs was determined using qPCR and Western blot analysis. RESULTS Plasma level of miR-146a-5p is significantly higher in the AD group as compared with the control group. The expression of miR-146a-5p was significantly upregulated in dissected aorta compared with controls (P

The widespread coronavirus SARS-CoV-2 has already infected over 4 million people worldwide, with a death toll over 280,000. Current treatment of COVID-19 patients relies mainly on antiviral drugs lopinavir/ritonavir, arbidol, and remdesivir, the anti-malarial drugs hydroxychloroquine and chloroquine, and traditional Chinese medicine. There are over 2,118 on-going clinical trials underway, but to date none of these drugs have consistently proven effective. Cathepsin L (CatL) is an endosomal cysteine protease. It mediates the cleavage of the S1 subunit of the coronavirus surface spike glycoprotein. This cleavage is necessary for coronavirus entry into human host cells, virus and host cell endosome membrane fusion, and viral RNA release for next round of replication. Here we summarize data regarding seven CatL-selective inhibitors that block coronavirus entry into cultured host cells and provide a mechanism to block SARS-CoV-2 infection in humans. Given the rapid growth of the SARS-CoV-2-positive population worldwide, ready-to-use CatL inhibitors should be explored as a treatment option. We identify ten US FDA-approved drugs that have CatL inhibitory activity. We provide evidence that supports the combined use of serine protease and CatL inhibitors as a possibly safer and more effective therapy than other available therapeutics to block coronavirus host cell entry and intracellular replication, without compromising the immune system., Key messages • There are over 2118 on-going clinical trials for COVID-19 patients, but current results are limited. • Host cell membrane CatL and TMPRSS2 promote coronavirus cell entry by removing the virus surface spike protein S1 subunit. • In host cell endosomes, CatL removes the S1 subunit and promotes viral membrane fusion, viral RNA release, and replication. • At least 7 CatL-selective inhibitors effectively block coronavirus infection of human cells. • At least 10 US FDA-approved drugs exert CatL inhibitory activity. • Combined use of TMPRSS2 inhibitor camostat and CatL inhibitors or FDA-approved CatL inhibitory drugs merits consideration for urgent testing in COVID-19 patients. • Chloroquine-induced endosomal pH increase and protease inactivation inhibit coronavirus infection, but impair human adaptive immunity. • The protease inhibitor cocktail therapy proposed here could block coronavirus infection while sparing human adaptive immunity.

Background Superiority of the new-generation, self-expanding Evolut R compared with the first-generation CoreValve on outcomes after transcatheter aortic valve implantation (TAVI) is unclear. This meta-analysis sought to investigate the outcomes of Evolut R vs CoreValve after TAVI. Methods A systematic review of studies comparing outcomes of Evolut R and CoreValve after TAVI was performed through PubMed, EMBASE and Cochrane Library. Crude risk ratios (RRs) were calculated with 95% confidence intervals using a random effects model. Outcomes of interest were mortality, myocardial infarction (MI), stroke or transient ischaemic attack (TIA), severe bleeding, acute kidney injury (AKI), major vascular complications (MVC), permanent pacemaker implantation (PPI), moderate or severe paravalvular regurgitation (PVR), and device failure. Results Six studies involving 11,530 patients (4,597 receiving Evolut R and 6,933 receiving CoreValve) were included. There was no significant difference in 30-day all-cause mortality between Evolut R and CoreValve (3.4% vs 5.0%, p = 0.10). The incidence of MI (0.2% vs 0.5%, p = 0.02), AKI (6.0% vs 9.2%, p = 0.001), moderate or severe PVR (6.4% vs 8.0%, p = 0.04), and device failure (3.5% vs 5.2%, p = 0.04) were significantly lower in Evolut R than CoreValve. There were trends toward less severe bleeding (7.2% vs 8.8%, p = 0.05) and PPI (18.6% vs 20.8%, p = 0.05) in Evolut R. The rates of stroke or TIA and MVC were similar between the two prostheses. Conclusions Compared with CoreValve, Evolut R did not reduce 30-day all-cause mortality, but significantly improved periprocedural complications after TAVI.

Objective The objective of this study was to report our single-center experience of thoracic endovascular aortic repair (TEVAR) and concomitant procedures in patients with type B aortic dissection (TBAD) with an isolated left vertebral artery (ILVA) and the early to midterm outcomes in these patients. Methods Between March 2011 and June 2018, there were 31 patients (27 men; median age, 55 years; range, 31-66 years) with TBAD and an ILVA who received TEVAR and concomitant procedures in our center. Demographics, coexisting medical conditions, imaging features, operation details, and follow-up outcomes in these patients were retrospectively collected and analyzed. Results All patients received aortic stent grafts; nine patients also received chimney stents, and 10 patients received aortic arch bypasses. The technical success rate was 96.8% (30/31), with only one patient (3.2%) showing immediate type IA endoleak. One patient experienced transient neurologic deficit, and a puncture-related femoral artery pseudoaneurysm was observed in one patient; both recovered completely before their hospital discharge. There was no death in the early term. The median duration of follow-up was 33 months (range, 2-90 months). Reintervention for a type II endoleak by using coils to seal the origin of the left subclavian artery was performed in one (3.1%) case 72 months postoperatively. One (3.2%) death occurred 42 months after operation as a result of rectal cancer. No neurologic deficits, chimney stent occlusions, or bypass occlusions were observed during the follow-up period. Conclusions Our limited experience reveals that TEVAR and concomitant procedures are relatively safe and viable for treatment of TBAD with an ILVA. Further studies with larger samples of patients and longer follow-ups are needed to confirm these findings.

The aim of this study was to identify patients who are at high risk of developing postimplantation syndrome (PIS) after thoracic endovascular aortic repair (TEVAR) for type B aortic dissection.This retrospective study included 646 patients who underwent TEVAR for type B aortic dissection between January 2010 and December 2015 at the Guangdong General Hospital. PIS was defined as fever (38°C) and leucocytosis (12 000 μl-1) without evidence of infection. The PIS rate was calculated, and a multivariable logistic regression model was used to investigate the factors related to PIS.A total of 646 patients (58.8 ± 11.0 years, 87.9% men) were included in the analysis. PIS was diagnosed in 204 (31.6%) patients. Age60 years [odds ratio (OR) 1.828, 95% confidence interval (CI) 1.277-2.619; P 0.001), hypertension (OR 12.125, 95% CI 4.310-34.111; P 0.001),1 stent graft placed (OR 1.862, 95% CI 1.109-3.124; P = 0.011), arch vessel bypass (OR 2.107, 95% CI 1.397-3.176; P = 0.001) and Ankura stent graft placement (OR 1.951, 95% CI 1.298-2.933; P = 0.001) were positively associated with PIS, whereas statin use (OR 0.659, 95% CI 0.460-0.944; P = 0.023) was negatively associated with PIS in the multivariable logistic regression analysis based on a stepwise regression model.Age60 years, comorbid hypertension,1 stent graft placed, arch vessel bypass and Ankura stent graft placement emerged as independent predictors of PIS. Stepwise increases in the prevalence of PIS were found to depend on the number of independent predictors.