OBJECTIVE:To investigate the clinical predictors of malperfusion in patients with acute type A aortic dissection (ATAAD) and to construct a diagnostic model to identify high-risk individuals. METHODS:A retrospective analysis of 553 ATAAD patients from Tongji Hospital divided into malperfusion and non-malperfusion groups was conducted. Logistic regression was used to identify independent predictors of the outcome. Model performance via the Hosmer-Lemeshow test, decision curve analysis (DCA), the area under the receiver operating characteristic curve (AUC), sensitivity, specificity, and predictive values. RESULTS:Malperfusion was observed in 28.4% of ATAAD patients. Significant predictors included elevated lactate dehydrogenase (LDH) (OR: 1.0019, 95% CI: 1.0002-1.0036, P = 0.027), alanine aminotransferase (ALT) (OR: 0.9936, 95% CI: 0.987-1.000, P = 0.046) and estimated glomerular filtration rate (eGFR) (OR: 0.9877, 95% CI: 0.977-0.998, P = 0.021), suggesting roles for tissue ischemia and impaired renal or hepatic function. Other variables, such as D-dimer, uric acid, creatinine, and NT-proBNP, showed trends toward significance but did not reach the 0.05 threshold. The model demonstrated good calibration (Hosmer-Lemeshow P = 0.318), moderate discriminatory power (AUC = 0.725), high specificity (93.62%), and low sensitivity (26.75%). CONCLUSION:The model based on routine biochemical markers provides a practical approach for the early identification of malperfusion in ATAAD patients. It shows strong specificity and clinical utility, although its limited sensitivity highlights the need for further refinement. Future improvements should focus on incorporating additional clinical or imaging data to increase diagnostic accuracy.

Objective:To assess outcomes of emergency central aortic repair (ECAR) in patients with acute type A aortic dissection (ATAAD) complicated by malperfusion, focusing on in-hospital mortality and long-term survival. Methods:This retrospective cohort study included 545 ATAAD patients treated surgically at a single center. Patients were stratified into malperfusion (n = 149) and non-malperfusion (n = 396) groups. Preoperative laboratory parameters, intraoperative strategies, and postoperative outcomes were compared. Kaplan-Meier analysis evaluated long-term survival. Results:Patients with malperfusion presented with significantly higher D-dimer and creatinine levels and more frequent emergency surgery (73.8% vs. 63.9%, P = 0.028). In-hospital mortality was similar between malperfusion and non-malperfusion groups (16.1% vs. 14.1%, P = 0.60), but increased with the number of affected organs: 13.3% (single), 18.4% (double), and 30.8% (triple or more). Cardiac and cerebral malperfusion had the highest mortality (40.0%). At 60 months, survival was significantly lower in malperfusion patients (60% vs. 70%, log-rank P = 0.00035). Conclusion:ECAR provides acceptable early survival in ATAAD patients with malperfusion. However, multi-organ involvement significantly worsens both in-hospital and long-term outcomes.

Objective: This study seeks to assess the predictive precision of the GERAADA score for 30-day mortality in patients with Type A aortic dissection. Methods: A retrospective study analyzed data from 382 survivors and 90 non-survivors, examining demographic, clinical, and surgical variables. GERAADA scores were calculated by a blinded cardiac surgeon using a web-based application. Results: The overall mortality is 19.06% and 18.18% for GERAADA prediction. The presence of malperfusion in more than two organs emerged as a significant risk factor for hospital mortality p=0.028. Longer surgery times were significantly associated with elevated mortality p=0.002. Moreover, postoperative ECMO, CPR, and IABP were significantly linked to increased mortality rates. Additionally, ICU stay duration, lung infection, MODS, and respiratory failure p<0.05 independently posed as risk factors for hospital mortality. Patients with Hemiparesis and peripheral malperfusion experienced no deaths, as predicted by GERAADA score. Additionally, patients with a dissection tear located at the root of the aorta exhibited a lower mortality rate of 7.14%, contrasting the higher 19.87% GERAADA prediction. Conclusion: GERAADA predictions were mostly accurate, but exceptions occurred with inotrope use, hemiparesis, peripheral malperfusion, and aortic dissection at the root. We suggest enhancing the GERAADA score by incorporating intraoperative and postoperative factors.

Background: Aortic dissection (AD) is frequently associated with abnormalities in electrocardiographic findings. Advancements in medical technology present an opportunity to leverage these observations to improve patient diagnosis and care. Objectives: This study aimed to develop a deep learning artificial intelligence (AI) model for AD detection using electrocardiograms (ECGs) and introduce the AI-Aortic-Dissection-ECG (AADE) score to provide clinicians with a measure to determine AD severity. Methods: From a cohort of 1878 patients, including 313 with AD, and 313 with chest pain (control group), we created training and validation subsets (7:3 ratio). A convolutional neural networks (CNN) model was trained for AD detection, with performance metrics like accuracy and F1 score (the harmonic mean of precision and recall) monitored. The AI-derived AADE score (0-1) was investigated against clinical parameters and ECG features over a median follow-up of 21.2 months. Results: The CNN model demonstrated robust performance with an accuracy of 0.93 and an F1 score of 0.93 for the AD group, and an accuracy of 0.871 with an F1 score of 0.867 for the chest pain group. The AADE score showed correlations with specific ECG patterns and demonstrated that higher scores aligned with increased mortality risk. Conclusions: Our CNN-based AI model offers a promising approach for AD detection using ECG. The AADE score, based on AI, can serve as a pivotal tool in refining clinical assessments and management strategies.

Acute kidney injury (AKI) is a clinical syndrome caused by various reasons that results in the rapid decline of renal function in a short period of time. Severe AKI can lead to multiple organ dysfunction syndrome. Circular RNA HIPK3 (circHIPK3) derived from the HIPK3 gene is involved in multiple inflammatory processes. The present research was performed to explore the function of circHIPK3 on AKI. The AKI model was established by ischemia/reperfusion (I/R) in C57BL/6 mice or hypoxia/reoxygenation (H/R) in HK-2 cells. The function and mechanism of circHIPK3 on AKI were explored via biochemical index measurement; hematoxylin and eosin (HE) staining; 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT); flow cytometry; enzyme-linked immunosorbent assay (ELISA); western blot; quantitative real-time polymerase chain reaction (RT-qPCR); detection of reactive oxygen species (ROS) and adenosine triphosphate (ATP); and luciferase reporter assays. circHIPK3 was upregulated in kidney tissues of I/R-induced mice and in H/R-treated HK-2 cells, while the microRNA- (miR-) 93-5p level was decreased in H/R-stimulated HK-2 cells. Furthermore, circHIPK3 silencing or miR-93-5p overexpression could reduce the level of proinflammatory factors and oxidative stress and recover the cell viability in H/R-stimulated HK-2 cells. Meanwhile, the luciferase assay showed that Krüppel-like transcription factor 9 (KLF9) was the downstream target of miR-93-5p. Forced expression of KLF9 blocked the function of miR-93-5p on H/R-treated HK-2 cells. Knockdown of circHIPK3 improved the renal function and reduced the apoptosis level in vivo. In conclusion, circHIPK3 knockdown alleviated oxidative stress and apoptosis and inhibited inflammation in AKI via miR-93-5p-mediated downregulation of the KLF9 signal pathway.

病人,女性,64岁.因胸痛伴呼吸困难加重20天入院.5 个月前因心悸2年余入心血管内科就诊.心电图检查:窦性心律,左前支传导阻滞,频发房性早搏;冠状动脉造影:未见异常;超声心动图检查:退行性主动脉瓣轻度功能不全,左心房扩大,二尖瓣和三尖瓣少量反流,左心室收缩舒张功能降低;胸部 CT平扫检查:左上叶纤维化、前纵隔肿块、畸胎瘤可疑.

A 66-year-old man was reported to have persistent chest pain for 4 hours after accidentally swallowing a fishbone. An isolated esophageal foreign body (EFB) was suspected in the community hospital. In our center, an emergency chest CT scan revealed an EFB in the upper part of the esophagus of the patient which penetrated the left esophageal wall as well as the distal aortic arch. However, the experience of the treatment strategy for this lesion is still not enough available. Considering the surgical trauma and the risk associated with advanced age of the patient, the option for open surgery was waived. In addition, there was also a risk of sudden death due to aortic rupture that could occur after direct removal of the fishbone. Therefore, emergency thoracic endovascular aortic repair was performed and the fishbone was removed under an endoscope. The patient successfully pulled through without any discomfort, with no complications.

Objective To explore the mediating effects of perceived stress and uncertainty tolerance on health literacy and decision satisfaction of decision makers in patient undergoing cardiac macrovascular surgery,and to provide references for improving the satisfaction of decision-making. Methods 260 surgical patient’s decisionmakers in the cardiac macrovascular surgery of a hospital in Wuhan were selected by convenience sampling. All Aspects of Health Literacy Scale,Perceived Stress Scale,Intolerance of Uncertainty Scale-12 and decision satisfaction scale were used to investigate. Results 251 valid questionnaires were recovered,with an effective recovery rate of96.54%. The health literacy score was（23.05±5.61）;the perceived stress score was（20.31±6.08）;the uncertainty tolerance score was（26.41±5.94）;the decision satisfaction score was（43.86±10.54）. The 4 variables were correlated（P＜0.001）. The mediating model found that health literacy had a significant direct effect on decision satisfaction.Meanwhile,health literacy also indirectly affected decision satisfaction through 3 paths,including the independent mediating effect of perceived stress（β=0.096,P＜0.001）,the independent mediating effect of uncertainty tolerance（β=0.093,P=0.001）,the chain mediating effect of perceived stress and uncertainty tolerance（β=0.076,P＜0.001）,accounting for 49.17% of the total effect. Conclusion Perceived stress and uncertainty tolerance play a mediating role in the relationship between health literacy and decision satisfaction of decision makers in cardiac macrovascular surgery,which can improve decision makers’ health literacy,reduce perceived stress,and help them perceive surgical risks rationally,thus improving decision satisfaction.

Background: Complex surgical plans and consideration of risks and benefits often cause decisional conflicts for decision-makers in aortic dissection (AD) surgery, resulting in decision delay. Shared decision-making (SDM) improves decision readiness and reduces decisional conflicts. The purpose of this study was to investigate the impact of SDM on decision quality in AD. Methods: One hundred and sixty AD decision-makers were divided into two groups: control (n = 80) and intervention (n = 80). The surgical plan for the intervention group was determined using patient decision aids. The primary outcome was decisional conflict. Secondary outcomes included decision preparation, decision satisfaction, surgical method, postoperative complications, actual participation role, and duration of consultation. The data were analyzed with SPSS 26.0 (IBM Corp., Chicago, IL, USA). p < 0.05 was considered statistically significant. Results: The decisional conflict score was significantly lower in the intervention group than in the control group (p < 0.001). The decision preparation and decision satisfaction scores in the intervention group were significantly higher than those in the control group (p < 0.001). There were more SDM decision-makers in the intervention group (16 [20%] vs. 42 [52.50%]). There was no statistical significance in the choice of surgical, postoperative complications, duration of consultation, and hospital and post-operative intensive care unit stay time (p = 0.267, p = 0.130, p = 0.070, p = 0.397, p = 0.421, respectively). Income, education level, and residence were the influencing factors of decision-making conflict. Conclusions: SDM can reduce decisional conflict, improve decision preparation and satisfaction, and help decision-makers actively participate in the medical management of patients with AD without affecting the medical outcome.

病人,男,23 岁,体重指数(BMI) 24.41 kg/㎡,因胸闷胸痛2 个月余入院. 2021 年5 月22 日23 时左右无明显诱因突发心前区疼痛,伴大汗,胸闷,持续不能缓解,濒死感.冠脉造影检查提示:前降支近端狭窄近90％,血栓负荷重,急诊经皮冠状动脉介入治疗(PCI)手术,行血栓抽吸及导管内溶栓,出院后未遵医嘱服用抗血小板药物及其他血管活性药物及调脂药物,2021 年 8 月 12 日因胸闷、胸痛再次入院.

Background: Thoracic aortic aneurysm (TAA) is a type of common and serious vascular disease, in which inflammation, apoptosis and oxidative stress are strongly involved in the progression. Cordycepin, a bioactive compound from Cordyceps militaris, exhibits anti-inflammatory and anti-oxidative activities. This study aimed to address the role and mechanism of cordycepin in TAA.Methods: The thoracic aortas were perivascularly administrated with calcium chloride (CaCl2), and human aortic smooth muscle cells (HASMCs) were incubated with angiotensin II (Ang II) to simulate the TAA model in vivo and in vitro, respectively. The effect and mechanism of cordycepin in TAA were explored by hematoxylin and eosin (HE) staining, immunohistochemistry (IHC), immunofluorescence (IF), western blot, biochemical test, cell counting kit-8 (CCK-8), and terminal deoxynucleotidyl transferase deoxyuridine triphosphate (dUTP) nick end labeling (TUNEL) assays. Results: Cordycepin improved the CaCl2-induced the aneurysmal alteration and disappearance of normal wavy elastic structures of the aorta tissues, TAA incidence and thoracic aortic diameter in rats, and Ang II-induced the cell viability of HASMCs. Cordycepin reversed the CaCl2-induced the relative protein expression of cleaved caspase 9, cleaved caspase 3, interleukin (IL)-6, tumor necrosis factor (TNF)-alpha and IL-1 beta, and the relative levels of glutathione (GSH), malonaldehyde (MDA) and reactive oxygen species (ROS) in vivo, or Ang II-induced these changes in vitro. Mechanically, cordycepin reduced the relative protein expressions of vascular endothelial growth factor (VEGF), VEGF receptor 2 (VEGFR2), cluster of differentiation 31 (CD31) and endothelial nitric oxide synthase (eNOS) in the Ang II-induced HASMCs. Correspondingly, overexpression of VEGF increased the levels of the indicators involved in apoptosis, inflammation and oxidative stress, which were antagonized with the cordycepin incubation in the Ang II-induced HASMCs.Conclusion: Cordycepin inhibited apoptosis, inflammation and oxidative stress of TAA through the inhibition of VEGF.

Background: Aortic dissection (AD) is a fatal vascular disease in absence of effective pharmaceutical therapy. Adenosine monophosphate-activated protein kinase alpha (AMPK alpha) plays a critical role in various cardiovascular diseases. Whether AMPK alpha is involved in the pathogenesis of aortic dissection remains unknown. We aimed to determine whether activation of AMPK alpha prevents the formation of AD. Methods and results: Reduced expression of phosphorylated AMPK alpha (Thr172) and exacerbated phenotypic switching were observed in human aortic tissues from aortic dissection patients compared with those in tissues from controls. In vivo, the formation of aortic dissection in ApoE(-/-)mice was successfully induced by continuous infusion of angiotensin II (AngII) for two weeks, characterized by the activation of vascular inflammation, infiltration of macrophages and phenotypic switching of vascular smooth muscle cells (VSMCs). rAAV2-mediated overexpression of constitutively active AMPK alpha (CA-AMPK alpha) enhanced the expression of phosphorylated AMPK alpha (Thr172) and attenuated AngII-induced occurrence of aortic dissection by suppressing the infiltration of macrophages, activation of vascular inflammation and phenotypic switching of VSMCs. The pathogenesis above was conversely exacerbated by rAAV2-mediated overexpression of dominant negative AMPK alpha 2 (DN-AMPK alpha). In vitro, we demonstrated that the administration of an AMPK agonist (AICAR) or transfection of CA-AMPK alpha induced the activation of AMPK alpha and then ameliorated AngII-induced phenotypic switching in the VSMCs and inflammation in the bone marrow-derived macrophages (BMDMs). This could be reversed by the addition of AMPK inhibitor compound C or transfection of DN-AMPK alpha. Conclusion: Impaired activation of AMPK alpha may increase the susceptibility to aortic dissection. Our findings verified the protective effects of AMPK alpha on the formation of aortic dissection and may provide evidence for clinical prevention or treatment.

目的:探讨无痛性主动脉夹层的临床诊治情况.方法:收集81例无痛性主动脉夹层病例进行统计分析.结果:按时间跨度分成两组:2009年至2014年为A组29例,2015年至2020年为B组52例,下列指标两组间差异有统计学意义(P＜0.05):以神经系统症状首诊的比例(27.6％vs.51.9％),从首诊到确诊的时间超过48h比例(72.4％vs.32.6％),保守治疗比例(62.1％vs.26.9％),在院病死率(41.4％vs.19.2％).以临床症状分为神经系统症状及非神经系统症状两组,神经系统症状组A型夹层比例(71.4％vs.36.9％)及病死率(40.0％vs.17.4％)均高于和非神经系统症状组(P＜0.05).以治疗方案分保守治疗组和非保守治疗组,保守治疗组病死率(46.8％)高于非保守治疗组(14.3％,P＜0.05).结论:无痛性主动脉夹层发病凶险,随着诊断和手术治疗水平的提高,得到及时诊治,病死率明显下降.

BACKGROUND:The choice of treatment is an unavoidable challenge faced in the day to day medical decision making pertaining to patients with organic heart disease. As a professional discipline, cardiac surgery focuses on creating and using the most advanced evidence-based patient decision aids (PtDAs) to achieve high-quality decision-making. OBJECTIVES:To describe the basic situation, influencing factors, and the outcome of indicators of PtDAs among cardiac surgery patients. METHODS:Seven electronic databases were systematically searched for relevant reviews on the application of PtDAs among cardiac surgery patients. The methodological framework proposed by Arskey and O'Malley was used to guide the scoping review. The extracted data was analyzed qualitatively and quantitatively. RESULTS:After dual, blinded screening of titles and abstracts, 12 articles were included in the review. 10 were quantitative studies, 1 was a mixed study, 1 was a qualitative study. CONCLUSIONS:Compared with the burden of heart disease and the huge evidence base, the application of PtDAs in cardiac surgery is obviously insufficient. The published literature mainly provide information about the factors to be solved from the perspective of researchers, and also summarize obstacle factors. This is the basis for the application and construction of PtDAs in cardiac surgery patients.

Objectives Spontaneous isolated celiac artery dissection (SICAD) is a rare condition that has not been fully investigated and reported, and very little is known regarding its prognosis and management. Here, we aimed to provide more evidence on the management strategy and outcome for symptomatic SICAD based on the experience of a single center. Methods From January 2018 to December 2021, a total of consecutive 51 patients with symptomatic SICAD were retrospectively included in this study. These patients had been selectively treated with conservative treatment (n = 31) or endovascular treatment (n = 20). Baseline data, imaging findings, treatment strategy, outcomes, and follow-up data have been described and analyzed. Results The mean age of the patients was 53.2 ± 9.6 years, 44 (86.3%) were male, and 36 (70.6%) had hypertension. The median length of stay was 10.0 days. The complete remission rate was 92.2% on discharge. The median follow-up time was 21.0 months. A secondary intervention was required for two patients during follow-up in the conservative group, wherein one underwent a stent placement three months after discharge because of progression of symptoms and extension of dissection, and the other required intervention one month after discharge because of symptomatic progression. No secondary intervention was required in the endovascular group. Occasional and mild relapse of symptoms occurred in two patients in both the conservative and endovascular groups, with no secondary intervention. The length of dissection (25.5 ± 11.8 mm vs. 19.1 ± 7.4 mm, P = 0.022) and complete remodeling rate (85.7% vs. 15.4%, P < 0.001) in the endovascular group were greater than that in the conservative group. Conclusion Patients with symptomatic SICAD who were selectively treated with conservative treatment or endovascular treatment had satisfactory early and medium-term outcomes. Endovascular treatment showed significant advantages in the complete remodeling of the celiac artery and presented with a lower rate of secondary intervention. Moreover, it was found to be a safe and effective remedy for failed conservative treatment.

"Pulmonary artery dissection secondary to pulmonary hypertension due to patent ductus arteriosus: echocardiography and computed tomography findings." Acta Cardiologica, ahead-of-print(ahead-of-print), pp. 1–2

Purpose To clarify the regulatory effect of Nuclear-enriched abundant transcript 1 (NEAT1) on abdominal aortic aneurysm (AAA) model rats and isolated endothelial progenitor cells (EPCs). Methods The AAA rat model was established by CaCl2 stimulation, and overexpressed NEAT1 was injected into rats through tail vein. Abdominal aorta lesions and numbers of EPCs in tissues and peripheral blood were examined by hematoxylin-eosin, immunofluorescence and flow cytometry. The extracted EPCs were identified by microscopy, DiI-ac-LDL staining and flow cytometry. Effect of overexpressed/silencing NEAT1 on the viability, migration, tube formation and VEGF content of EPCs was investigated by MTT-, wound-healing, tube formation assays and ELISA, respectively. The expressions of NEAT1, miR-204-5p, Angiopoietin-1 (Ang-1)/ERK pathway were determined by qRT-PCR and Western blot as needed. The targeting relationships between NEAT1 and miR-204-5p, and miR-204-5p and Ang-1 were predicted on starBase, TargetScan and confirmed by dual-luciferase experiments. The mutual regulation effect was studied through rescue experiments. Results Overexpressed NEAT1 not only reduced inflammatory infiltration and increased the number of EPCs in abdominal aorta and peripheral blood, but also promoted the viability, migration, tube formation of EPCs, increased VEGF content and upregulated the expression of the Ang-1/ERK pathway in EPCs. However, silencing NEAT1 produced opposite results. NEAT1 targeting miR-204-5p inhibited the functional effects of miR-204-5p on of EPCs. Overexpressed/silencing Ang-1 partially reversed the effects of NEAT1 or miR-204-5p on the characteristics of EPCs. Conclusion NEAT1 competitively binds with miR-204-5p and up-regulates Ang-1 expression in EPCs to effectively improve the proliferation, migration and angiogenesis of EPCs.

Background: Nuclear paraspeckle assembly transcript 1 (NEAT1) has been reported to be involved in the progression of many cancers; however, the role and mechanisms underlying NEAT1 in abdominal aortic aneurysm (AAA) remain unclear. Methods and Results: The expression of NEAT1, miR-30d-5p and A disintegrin and metalloprotease 10 (ADAM10) was measured by qRT-PCR and western blot. Functional experiments were conducted by using a CCK-8 assay, EDU assay, flow cytometry, western blot, ELISA, and commercial kits. The target relation was confirmed by dual-luciferase reporter assay and the RIP assay. It was then found that NEAT1 was upregulated in peripheral blood of AAA patients similar to 3.46-fold, smooth muscle cells (SMCs) isolated from AAA tissues similar to 2.6-fold and in a hydrogen peroxide (H2O2)-induced injury model of human vascular SMC (HVSMCs) similar to 2.0- and 3.9-fold at 50 mu mol/L and 200 mu mol/L H2O2 treatment, respectively. NEAT1 deletion attenuated H2O2-induced cell proliferation promotion (40.0% vs. 74.3%), apoptosis inhibition (25.0% vs. 13.5%), and reduction of inflammatory response and oxidative stress in HVSMCs. Mechanistically, NEAT1 targeted miR-30d-5p to prevent the degradation of its target, ADAM10, in HVSMCs. Further rescue experiments suggested miR-30d-5p inhibition mitigated the effects of NEAT1 deletion on H2O2-induced HVSMCs. Moreover, ADAM10 overexpression counteracted the inhibitory functions of miR-30d-5p on H2O2-evoked HVSMC injury. Conclusions: NEAT1 promoted H2O2-induced HVSMC injury by inducing cell apoptosis, inflammation and oxidative stress through miR-30d-5p/ADAM10 axis, indicating the possible involvement of NEAT1 in the pathogenesis of AAA.

目的 比较Stanford A型主动脉夹层术后发生急性肾功能损伤和未发生急性肾功能损伤两组病人的预后,分析发生急性肾功能损伤的高危因素.方法 2014年5月 ～2016年5月Stanford A型夹层术后发生急性肾功能损伤75例为病例组,按照年龄和体重1:1匹配75例肾功能正常病人作为对照组,分析发生急性肾功能损伤的高危因素,比较两组预后.结果 急性肾功能损伤组较未发生组早期并发症率增加1.9倍,肺部感染率增加1.7倍.随访3年,随访率97.0％,平均随访28个月.急性肾功能损伤组病人术后1个月、12个月、24个月及36个月免于远期并发症生存率明显低于未发生组(94.2％、91.2％、80.5％和26.4％比100％、98.6％、91.5％和77.8％,Log-rank P<0.01).围术期大剂量血管活性药(OR=3.455,95％CI:1.163～10.265)和静力型肾血管受损(OR=8.726,95％CI:2.149～35.426)是导致Stanford A型夹层术后发生急性肾功能损伤的高危因素.结论 Stanford A型主动脉夹层手术风险大,围术期大剂量血管活性药和静力型肾血管受损是术后并发急性肾功能损伤的独立高危因素,术后发生急性肾功能损伤病人预后相对较差,积极预防胜过治疗.

目的:回顾性分析青年主动脉夹层14年来发病的临床特点和治疗变迁的情况.方法:收集我院2006年至2019年,年龄＜45岁的青年主动脉夹层患者临床资料,按时间跨度平均分为两组:第一时间段2006年1月至2012年12月,第二时间段2013年1月至2019年12月.统计两时间段的临床资料并进行比较分析.结果:病例总数518例,其中第一时间段152例,第二时间段366例.下列指标的比例在第二时间段明显高于第一时间段:首诊时知晓高血压病史的比例(62.6％vs.45.4％,P＜0.01);BMI≥32 kg/m2重度肥胖的比例(12.9％vs.6.0％,P＜0.05);腹围男性＞110 cm,女性＞100 cm,重度腹型肥胖的比例(24.7％vs.13.4％,P＜0.01);血脂异常的比例(17.8％vs.10.1％,P＜0.05);痛风或高尿酸血症的比例(15.8％vs.9.2％,P＜0.05).临床治疗方案中,保守治疗比例第二时间段明显低于第一时间段(13.4％vs.25％,P＜0.05),第二时间段的在院病死率稍低于第一时间段(9.8％vs.13.2％),但差异无统计学意义(P＞0.05).结论:青年主动脉夹层发病的临床特点随时代变化,大众健康教育和治疗手段的进步是主动脉夹层防治中的关键.