PURPOSE: This study aimed to identify the key genes involved in the development of AAA by various bioinformatics methods and explore their potential mechanisms. METHODS: Feature genes were screened by machine learning and other methods, and ROC curves were used to verify the model performance in the internal and external validation sets. Cluster analysis and immune infiltration analysis were then performed, and two key genes were finally determined and experimentally verified. GSEA, GO and KEGG analyses were performed. RESULTS: DEGs were identified by the “limma” package. DENETs were obtained by intersecting DEGs with NETs. GSEA, GO and KEGG analyses revealed that these genes were enriched in pathways such as cell response to lipopolysaccharide and chemokine signaling. Cluster analysis was performed to compare the expression differences of 25 DENETs between clusters, and immune infiltration analysis revealed immune dysregulation in AAA. Then, IL6 and PADI4 were finally identified as DENETs, and further GSEA analysis revealed that they were related to inflammation and immune response. In the wet experiment, IL6 and PADI4 finally showed expression trends consistent with the results of bioinformatics analysis. CONCLUSIONS: Our study identified IL6 and PADI4 as hub genes. They play an important role in promoting the development of AAA through inflammation, providing potential molecular targets for further treatment and intervention of AAA in the future.

Infected wounds pose a significant clinical challenge due to bacterial colonization, excessive inflammation, and impaired tissue regeneration. Inspired by the adhesive properties of mussel foot proteins, this study developed a novel multifunctional wound dressing by incorporating polydopamine (PDA)-modified copper-based metal-organic framework (CuMOF) into a polyethylene glycol (PEG) hydrogel network. The synthesized PEG/PDA@CuMOF (PPCM) hydrogel combines the extracellular matrix (ECM)-mimetic properties of PEG with the robust wet adhesion, antimicrobial, and pro-regenerative activities of CuMOF. Comprehensive characterization confirmed successful PDA coating on CuMOF and covalent integration into the hydrogel, which exhibited excellent porosity and swelling capacity. In vitro assessments demonstrated outstanding biocompatibility, significant promotion of cell proliferation and migration, and powerful antibacterial efficacy against both methicillin-resistant Staphylococcus aureus (MRSA) and Escherichia coli (E. coli). In a rat model of full-thickness MRSA-infected wounds, the PPCM significantly accelerated wound closure, enhanced collagen deposition, promoted neovascularization, and effectively reduced bacterial burden, all while maintaining excellent systemic biocompatibility. These findings highlight the PPCM hydrogel as a promising multifunctional platform for advanced infected wound management.

Multidrug-resistant (MDR) infections pose a formidable threat to global health, with hypoxia and infection representing two major interconnected challenges that impede wound healing. Current therapeutic approaches often fail to provide sustained oxygen supply or effectively combat MDR bacteria. Herein, we developed an innovative living hydrogel dressing to address these issues. Chlorella vulgaris (CV) was employed as a bioreactor for the green synthesis of zinc oxide nanoparticles (ZnO NPs). The resulting CV/Zn complex was encapsulated within an alginate hydrogel matrix to form CV/Zn@Gel. This composite system enables continuous and stable oxygen release through microalgal photosynthesis. Meanwhile, CV/Zn@Gel confers potent antibacterial activity against MDR pathogens by inducing oxidative macromolecular damage and eliciting broad transcriptional reprogramming. In vitro assessments confirmed that CV/Zn@Gel significantly promotes cell proliferation and migration while exhibiting robust antibacterial efficacy. In a murine model of MDR-infected wounds, CV/Zn@Gel dressing markedly accelerated wound healing by alleviating hypoxia, reducing bacterial load, and modulating the immune response. Collectively, this work presents a novel and potent strategy for managing multidrug-resistant infections.

OBJECTIVES:To investigate the synergistic mechanism of the traditional Chinese medicine Rosa laevigata Michx. (RLM) for treatment of pulmonary arterial hypertension (PAH). METHODS:Network pharmacological analysis was carried out to screen the active ingredients of RLM and PAH disease targets and construct the "component-target-disease" interaction network, followed by gene enrichment analysis and molecular docking studies. In the cell experiments, primary cultures of rat pulmonary arterial smooth muscle cells were exposed to hypoxia for 24 h and treated with solvent or 100, 200 and 300 mg/mL RLM, and the changes in cell proliferation were detected using Western blotting for PCNA and immunofluorescence staining. In the animal experiment, male SD rats were randomized into 5 control group, monocrotaline (MCT) solvent group, and MCT with RLM (100, 200 and 300 mg/mL) treatment groups. HE staining and immunofluorescence staining were used to observe histopathological changes in the pulmonary blood vessels of the rats. RESULTS:Seven core active ingredients (including β-sitosterol and kaempferol) in RLM and 39 key disease targets were identified, and molecular docking showed that SRC was a high-affinity target. KEGG enrichment analysis showed that the differential genes were significantly enriched in calcium signaling and PI3K-AKT pathways. In rat pulmonary arterial smooth muscle cells, hypoxic exposure significantly up-regulated cellular expression of PCNA and phosphorylation levels of Src and AKT1, which were obviously lowered by RLM treatment. In RLM-treated rat models, the mean pulmonary artery pressure and right ventricular hypertrophy index (Fulton index) were significantly reduced, the tricuspid annular plane systolic excursion (TAPSE) was improved, and pulmonary vascular wall thickening and fibrosis were obviously ameliorated. CONCLUSIONS:RLM inhibits pulmonary arterial smooth muscle cell proliferation in rat models of hypertension possibly by regulating the Src-AKT1 axis, suggesting the potential of RLM as a new natural drug for treatment of pulmonary hypertension.

Aortic dissection (AD) is a severe aortic disease characterized by high morbidity and mortality. However, the primary treatments for AD possess limited efficacy. The role and specific mechanisms of mitogen-activated protein kinase kinase 2 (MAP2K2) in AD are not elucidated. Human aortic vascular smooth muscle cells (HAVSMCs) induced by platelet-derived growth factor-BB (PDGF-BB) and C57BL/6 mice treated with β-aminopropionitrile were used as AD models in vitro and in vivo, respectively. RNA-sequencing analysis was conducted to explore the downstream pathway of MAP2K2. The expression of tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), IL-8, malondialdehyde (MDA), superoxide dismutase (SOD), and reactive oxygen species (ROS) was determined by enzyme-linked immunosorbent assay. The protein levels of MAP2K2, alpha-smooth muscle actin (α-SMA), smooth muscle protein 22-alpha (SM22α), Janus kinase 2 (JAK2), p-JAK2, signal transducer and activator of the transcription 3 (STAT3), and p-STAT3 were detected by western blot. We found that MAP2K2 was abnormally increased in AD. MAP2K2 knockdown repressed the expression levels of TNF-α, IL-1β, IL-8, MDA, ROS, α-SMA, and SM22α, and promoted SOD expression in vitro and in vivo. In addition, the JAK/STAT signaling pathway was identified as the downstream pathway of MAP2K2. MAP2K2 knockdown inhibited the expression of p-JAK2/JAK2 and p-STAT3/STAT3. Activating the JAK/STAT pathway by its activator RO8191 reversed the effect of MAP2K2 knockdown on inflammation, oxidative stress, and abnormal phenotypic transformation in HAVSMCs induced by PDGF-BB. In conclusion, MAP2K2 knockdown could alleviate AD by inhibiting the JAK/STAT signaling pathway to repress inflammation, oxidative stress, and abnormal phenotypic transformation of HAVSMCs.

Perfluorooctane sulfonate (PFOS), a pervasive environmental contaminant, is ubiquitously detected in water, air, soil, and food chains. Emerging evidence has implicated PFOS in the pathogenesis of cardiovascular diseases, particularly atherosclerosis - the fundamental pathological process underlying diverse cardiovascular and cerebrovascular disorders. A previous study demonstrated that PFOS exacerbates atherosclerosis in apolipoprotein E-deficient (ApoE-/-) mice through pro-inflammatory M1 macrophage polarization. However, the effects of PFOS on vascular smooth muscle cells (VSMCs) and their contribution to intimal hyperplasia and atherosclerosis remain unexplored. Our in vitro investigations revealed that PFOS potentiates proliferation, migration, and phenotypic switching in primary human aortic smooth muscle cells (HASMCs). Moreover, we also demonstrated that PFOS exposure aggravated neointimal formation in a femoral artery injury model and promoted atherosclerosis. To elucidate the role of VSMCs in these processes in vivo, we established a VSMCs lineage-tracing model utilizing Myh11-Cre/ERT2; R26-tdTomato; ApoE-/- mice. Following 16 weeks of PFOS exposure, atherosclerotic plaque progression exhibited a positive correlation with intraplaque VSMCs accumulation. RNA sequencing analysis and subsequent validation confirmed PFOS-induced tissue plasminogen activator (tPA) upregulation in VSMCs at both transcriptional and translational levels. Notably, tPA knockdown abrogated PFOS-driven proliferation, migration, and phenotypic switching in HASMCs. Mechanistic studies revealed ERK signaling pathway activation as the primary mediator of PFOS-induced tPA expression. Collectively, these findings provide novel mechanistic insights into how PFOS aggravates intimal hyperplasia and atherosclerosis, highlighting its role in exacerbating cardiovascular pathogenesis. They further suggest that ERK inhibitors may mitigate the detrimental effects of PFOS on the vasculature.

Myocardial infarction (MI) is one of the leading causes of cardiovascular death worldwide. Hypoxia and oxidative stress are key factors in myocardial injury and repair. In this study, we developed a novel self-oxygenating hydrogel designed to simultaneously produce oxygen and scavenge reactive oxygen species (ROS), thereby improving the microenvironment after myocardial infarction and promoting myocardial repair. This hydrogel is a composite of biocompatible polymer silk fibroin methacryloyl (SFMA), hyaluronic acid-modified RGD peptide (HA-RGD), calcium peroxide (CaO2), and copper-epigallocatechin gallate (Cu-EGCG). It integrates functions essential for oxygen generation, antioxidation, and cell adhesion and repair. SFMA provides structural support, HA-RGD enhances cell adhesion and growth, CaO2 releases oxygen to alleviate hypoxia, and Cu-EGCG offers potent antioxidant effects and effectively reduces oxidative stress. Additionally, the slow release of Cu2+ promotes angiogenesis synergistically. In vitro experiments demonstrated that the SFMA/HA-RGD/CPCE hydrogel exhibited good cell adhesion and proliferation, along with significant antioxidant activity, which notably improved cell survival. In vivo experiments indicated that the hydrogel effectively promoted myocardial tissue repair, attenuated myocardial fibrosis, spurred neoangiogenesis, and enhanced cardiac function. In summary, the SFMA/HA-RGD/CPCE hydrogel, as an innovative therapeutic material, shows great potential for myocardial infarction repair and offers new ideas and strategies for clinical treatment.

Pulmonary artery smooth muscle cell (PASMC) dysfunction is the central pathogenic mechanism in pulmonary hypertension (PH). This study explored the mechanism of action of RUNX1, a potential therapeutic target for PH, in PASMCs. A PH mouse model was used to investigate the impacts of RUNX1 knockdown on hemodynamics, right ventricular hypertrophy (RVH), and pulmonary artery remodeling (HE staining). Isolated PASMCs were transfected with RUNX1- or CBX5-related vectors and then subjected to cell function assays. Immunoprecipitation was used to detect molecular binding and ubiquitination. RUNX1 knockdown reduced right ventricular systolic pressure, RVH, and pulmonary artery remodeling in mice with PH. Knockdown of RUNX1 or CBX5 suppressed proliferation, invasion, and migration and stimulated apoptosis in PASMCs under hypoxia. RUNX1 enhanced USP15 promoter activity. USP15 bound to CBX5 and reduced CBX5 ubiquitination, thereby promoting CBX5 expression. CBX5 overexpression promoted the proliferation and movement of hypoxic PASMCs with reduced RUNX1 expression and decreased their apoptosis. In conclusion, RUNX1 knockdown alleviates PH in mice and reduces hypoxia-induced PASMC dysfunction by inhibiting USP15 transcription, thereby promoting the ubiquitination and degradation of CBX5.

Abdominal aortic aneurysm (AAA), a life-threatening pathological dilation of the abdominal aorta, is characterized by chronic inflammation and extracellular matrix degradation. While surgical interventions remain the standard treatment, they are associated with substantial risks and severe complications. This study presents an innovative injectable hydrogel medication, Rh-GFFY-CTT, which synergistically targets the key pathogenic mechanisms underlying AAA. Rh-GFFY-CTT incorporates the anti-inflammatory compound Rhein and the matrix metalloproteinase-9 (MMP-9) inhibitory peptide CTT. Rhein blocks the initiation of the NF-kappa B signaling cascade, suppressing inflammatory mediators such as MMP-9, IL-6, and IL-1 beta. Concurrently, CTT directly inhibits MMP-9 activity, thereby mitigating adverse vascular remodeling. This dual-action approach offers a novel therapeutic strategy for AAA. In vitro studies have confirmed that Rh-GFFY-CTT can effectively suppress macrophage activation, secretion of inflammatory cytokines, and MMP-9 activity. In a murine AAA model, Rh-GFFY-CTT effectively attenuated the dilation of the abdominal aorta and matrix degradation by reducing macrophage infiltration and MMP-9 secretion. Compared to conventional surgical resection, this minimally invasive hydrogel medication coats diseased arteries, reducing patient trauma and eliminating the risk of ischemic organ injury. The combined targeting of inflammation and matrix degradation pathways involved in AAA pathogenesis represents a significant innovation with considerable clinical potential for treating this life-threatening vascular disease.

Objectives:Epicardial adipose tissue (EpAT) is known for its role in supporting the cardiomyocytes. Lysine-specific demethylase 1 (LSD1), a typical lysine demethylase, is an essential regulator for the maintenance of beige adipocytes. However, the effect of LSD1 in the adipogenic differentiation of beige adipocytes in EpAT, and its function on oxygen and glucose deprivation (OGD)-injured cardiomyocytes remain unclear.Materials and Methods:Heart tissues from young mice and elder mice were collected for immunohistochemical staining. LSD1 in 3T3-L1 cells was knocked down by LSD1-shRNA lentivirus infection. The qRT-PCR, western blotting, and Oil Red O staining were employed to detect the adipogenic differentiation of 3T3-L1 cells and formation of beige adipocytes. The cardiomyocytes co-cultured with beige adipocytes were used for OGD treatment. Cell apoptosis was analyzed by flow cytometry. The lactate dehydrogenase (LDH) and superoxide dismutase (SOD) activity were analyzed using commercially available kits.Results:The decrease of LSD1 was related to the age-dependent loss of beige adipocytes in mice EpAT. LSD1 knockdown inhibited the adipogenic differentiation of 3T3-L1 cells and formation of beige adipocytes. The down-regulation of LSD1 in 3T3-L1 cells decreased the protective effect of mature adipocytes on OGD-injured cardiomyocytes.Conclusion:The decreased expression of LSD1 in mice EpAT was associated with age-dependent ablation of beige adipocytes. The protective effect of beige adipocytes on OGD-injured cardiomyocytes is reduced by knockdown of LSD1 in adipocytes. The present study provided exciting insights into establishing novel therapies against age-dependent cardiac diseases.

Background: Tetramethylpyrazine (TMP) is an effective treatment for pulmonary arterial hypertension (PAH), but it is unclear whether its mechanism is related to the regulation of endothelial progenitor cells (EPCs). In this study, we aimed to explore the effect and mechanism of TMP on EPCs.Methods: A rat model of PAH was established by intraperitoneally injecting monocrotaline in Sprague Dawley rats, followed by intraperitoneal injection with 100 mg/kg TMP. The effects of TMP on pulmonary pathological morphology were evaluated using hematoxylin-eosin staining. The hemodynamics and right ventricular hypertrophy index (RVHI) of PAH rats were evaluated. EPCs were isolated from healthy rats and identified by double positive staining with acetylated low-density lipoprotein (acLDL), Ulex europaeus agglutinin-1 (UEA-1), and flow cytometry assay. The expression of Nuclear factor erythroid 2-related factor 2 (NRF2) in lung tissue and EPCs was determined using quantitative reverse transcription polymerase chain reaction (qRTPCR). After NRF2-specific short hairpin RNA (shNRF2) transfection and/or TMP (50, 100, 200 & mu;M) treatment on EPCs, the viability, proliferation, senescence, and protein expression levels of NRF2, p53 and p21 in EPCs were determined by 3-(4,5dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), 5-ethynyl-2 & PRIME;-deoxyuridine (EdU), & beta;-Galactosidase staining andResults: TMP treatment improved the pathological condition of lung tissue, hemodynamic score and RVHI of PAH rats (p < 0.001). On the contrary, NRF2 silencing had negative effects on EPCs, including inhibition of viability and proliferation, promotion of senescence, and elevation of the protein levels of P53 and P21 in EPCs (p < 0.001). However, TMP treatment reversed the above effects of NRF2 silencing on EPCs (p < 0.01).Conclusions: TMP protects EPCs from senescence by activating the NRF2 pathway.

Background:Tetramethylpyrazine (TMP), a potent anti-free radical and anti-inflammations substance, has been demonstrated to possess a direct vessel relaxation property. This study aimed to evaluate the effect of TMP treatment in pulmonary hypertension (PH) and test the hypothesis that TMP prevents or reverses the process of PH.Methods:Rats (n = 36) injected with 50 mg/kg of monocrotaline (MCT) subcutaneously 4 weeks to develop PH were then randomized to TMP (5 mg/kg per day) for another 4 weeks. Hemodynamics was evaluated via the right ventricle. Pulmonary vessels structural remodeling and inflammation were examined by histologic and transmission electron microscopy observation. The expression of inducible nitric oxide synthase (iNOS) and cGMP-dependent protein kinases 1 (PKG-1) was detected by immunohistochemical staining and Western blot. Generation of reactive oxygen species (ROS) and antioxidation species was measured by biochemical analyses.Results:MCT increased PH and right ventricle hypertrophy. TMP alleviated pulmonary arterial pressure elevation, leukocyte infiltration, and structural remodeling of pulmonary arterials induced by MCT successfully. TMP treatment significantly increased the PKG-1 expression and suppressed the iNOS expression. The activity of superoxide dismutase (SOD), glutathione peroxidase (GSH), and catalase (CAT) was significantly higher than control group, while malondialdehyde (MDA) levels were lower compared with MCT group.Conclusion:TMP can suppress established MCT-induced PH through the ROS/iNOS/PKG axis. The underlying mechanisms may be associated with its anti-inflammatory, antioxidant, and antiproliferative properties in pulmonary arterial.

Cardiac reprogramming has emerged as a novel therapeutic approach to regenerating the damaged heart by directly converting endogenous cardiac fibroblasts (CFs) into induced cardiomyocytes (iCMs). Cardiac reprogramming requires the activation of the cardiogenic transcriptional program in concert with the repression of the fibroblastic transcriptional program. Lysine-specific demethylase 1 (LSD1) plays an instrumental role in many physiological processes such as cell growth, differentiation and metabolism. The epigenetic modifications of histones are essential for the accurate expression of genes in cardiomyocytes and the normal functioning of the heart. However, the effect of LSD1 in regulating the cardiogenic transcriptional program under myocardial ischemia/reperfusion (I/R) injury remains unclear. Thus, mice I/R injury was induced by 4 and 24 h reperfusion after 1-h occlusion of the left anterior descending coronary artery. The primary CFs and CMs were exposed under oxygen and glucose deprivation (OGD) to mimic I/R injury. The expression of LSD1 significantly decreased in I/R injured heart tissue and OGD-injured primary CFs and CM, and methylated histone presented a notable increase in OGD-injured primary CFs. Overexpression of LSD1 inhibited the injury of primary CFs induced by OGD, but showed limited inhibition on injured primary CMs. Under the OGD condition, LSD1 overexpression significantly increased cell viability, decreased cell apoptosis and reactive oxygen species (ROS) production of primary CFs. The expression of core cardiogenic transcription factors and cardiac genes were significantly decreased in OGD injured primary CFs, whereas LSD1 overexpression reversed the decrease of transcription factors and cardiac genes under the OGD condition. In conclusion, the overexpression of LSD1 has a protective role in I/R injury by inhibiting the histone methylation of primary CFs and regulates the expressions of core cardiogenic transcription factors and cardiac genes, which can prove to be a potential approach for direct cardiac reprogramming.

瓣膜性心脏病的发生率随着年龄的增长而增加,其主要治疗手段是瓣膜置换.而近年来微创介入治疗的出现,改变了传统的治疗模式,让外科手术的高危患者看到了曙光.3D打印技术自1990年开始应用于医学领域以来,发展迅速,凭借其精细化的还原技术,现已广泛应用于多个外科学专业.但目前3D打印技术在心血管外科的应用仍处于起步阶段,尤其在瓣膜性心脏病领域的应用更是少之又少.本文结合瓣膜性心脏病,就3D打印技术的基本原理、在瓣膜性心脏病诊疗中的优势及临床应用现状进行综述,并阐述目前存在的问题及展望未来发展方向.

Micro-/macroangiopathy, neuropathy and prolonged inflammation are common in diabetic wound, however, traditional wound dressing cannot treat these problems in the same time. Herein, we developed a multifunctional hydrogel with promoted angiogenesis, cell proliferation and anti-inflammation ability to treat diabetic wound. The hydrogel was composed of natural polymers, including gelatin and chitosan, which have excellent biocompatibility. Histatin-1 (His-1) was added into the hydrogel to improve the cell adhesion, proliferation and angiogenesis. Besides, polypyrrole based conductive nanoparticles (G-Ppy) were introduced in the hydrogel to enhance the electrical signal conduction between skin and promote the mechanical strength of the hydrogel. The polypyrrole nanoparticles were growth in the chain of methacryloyl grafted gelatin (Gel-MA), leading to a better biocompatibility and water dispersibility. In vivo wound healing experiment proved that the hydrogel accelerated the wound healing rate, down regulation the expression of pro-inflammation factor TNF-α and upregulation the expression of CD31 and α-SMA, indicating the prospects in the application of diabetic wound healing.

目的 探究急性Stanford A型主动脉夹层术后行连续肾脏替代疗法(CRRT)的独立危险因素及预防策略.方法 回顾性分析南方医科大学珠江医院2020年9月至2021年12月收治的急性Stanford A型主动脉夹层患者115例(男/女为93/22),年龄(53.16±11.43)岁;根据术后是否行CRRT将术后患者分为CRRT组(n=23),非CRRT组(n=92),采用单因素分析得出危险因素并纳入多因素logistic回归以明确独立危险因素.结果 围术期死亡19例(16.88％),其中CRRT组死亡9例,非CRRT组死亡10例,两组死亡率差异有统计学意义(χ2=10.655,P=0.001).CRRT组与非CRRT组单因素分析提示术前肌酐、术前夹层累及肾动脉、阻断时间、体外循环时间、手术时间、术中输红细胞量、术中输血浆量与急性Stanford A型主动脉夹层术后行CRRT有关,而经logistic回归分析进一步明确术前肌酐(OR=1.875,P=0.014)、阻断时间(OR=1.874,P=0.008)、手术时间(OR=1.014,P=0.012)、术中输红细胞量(OR=2.183,P=0.017)为急性Stanford A型主动脉夹层术后行CRRT的独立危险因素.ROC曲线分析得出,术前肌酐在预测急性Stan-ford A型主动脉夹层术后行CRRT的效能最高.结论 术前肌酐、阻断时间、体外循环时间和术中输红细胞量是急性Stanford A型主动脉夹层术后行CRRT的独立危险因素;围手术期对患者实施有效评估和对应措施,可降低急性Stanford A型主动脉夹层术后行CRRT的风险.

目的:回顾性总结295例急性Stanford A型主动脉夹层围术期治疗效果,分析术后感染发病率、种类及相关影响因素,探究急性Stanford A型主动脉夹层术后感染的主要危险因素及预防策略.方法:回顾性分析本中心2007年7月-2019年7月收治的急性Stanford A型主动脉夹层患者295例,根据围术期感染标准将术后患者分为感染组(111例)与非感染组(184例),总结围手术期的各项数据及资料,采用单因素分析筛选危险因素并纳入多因素logistic回归以明确独立危险因素.结果:围术期死亡60例(20.33％),其中感染组死亡36例(32.43％),非感染组死亡24例(13.04％),两组死亡率差异有统计学意义(P＜0.001).死亡原因包括多器官功能衰竭31例,低心排综合征15例,脑出血9例,呼吸衰竭5例.围术期感染111例(37.6％),包括肺部感染81例(73％),泌尿系感染8例(7.2％),切口感染7例(6.3％),感染性心内膜炎5例(4.5％),肠道感染5例(4.5％),脓毒血症3例(2.7％),纵隔感染2例(1.8％).感染组与非感染组年龄、吸烟、糖尿病、术前氧分压、术前肌酐水平、术前乳酸值、术后呼吸机辅助时间、纵隔及心包引流管留置时间、体外循环时间、ICU时间、围手术期RRT及人工主动脉瓣植入均差异有统计学意义(均P＜0.05).经logistic回归分析进一步明确糖尿病(OR:8.960;P=0.017)、术前乳酸值(OR:1.461;P=0.004)、围手术期RRT(OR:29.238;P＜0.001)、术后呼吸机辅助时间(OR:2.442;P＜0.001)、纵隔心包引流管留置时间(OR:2.054;P＜0.001)、ICU时间(OR:1.051;P=0.02)为术后感染的独立危险因素.ROC曲线分析显示,术后呼吸机辅助时间预测术后感染的效能最高.结论:围术期感染是急性Stanford A型主动脉夹层术后常见并发症;明确糖尿病、术前乳酸值、围手术期RRT、术后呼吸机辅助时间、纵隔心包引流管留置时间、ICU时间是急性Stanford A型主动脉夹层术后感染独立危险因素;围手术期对患者实施有效评估并采取对应措施,可降低术后感染风险、提高患者的预后及减轻患者家庭的经济负担.