Coronary artery disease (CAD) as a major cardiovascular disease is the leading global cause of mortality, Klotho/FGF23 axis involved in development of cardiovascular disease, while the function and underlying mechanism of Klotho/FGF23 axis in CAD is unclear. Blood samples from 67 CAD patients with coronary artery bypass graft (CABG) surgery were collected, and the level of Klotho and FGF23 of those patients was measured by using an ELISA kit. Cardiomyocyte was isolated from 0 to 3 days Sprague Dawley (SD) rats. Expression of Klotho, FGF23 and the cardiomyocyte marker α-sarcomeric actin (α-SA), myosin heavy chain (MHC) and cardiac troponin I (cTnI) was assessed by immunofluorescence staining. Expression of Klotho and FGF23 mRNA was detected by qRT-PCR. Apoptosis and cell cycle were measured by flow cytometry. Cell viability was detected by using CCK-8. The protein expression of ERK/MAPK pathway related protein and cytokines production was measured by western blotting. The levels of Klotho in CAD patients increased after CABG surgery, while FGF23 decreased. Isolated cardiomyocyte morphology and structure were completed, and with stabilized beating within culture for 15 days, besides, α-SA, MHC, and cTnI proved positive. After transfected Lenti-Klotho and Lenti-FGF23 into isolated cardiomyocyte, fluorescence staining showed that the transfection was successful, and qRT-PCR results showed that the expression levels of Klotho and FGF23 mRNA significant increased compared with NEG (empty vector) group. Immunofluorescence staining results showed that compared with NEG group, there was a higher Klotho positive rate and lower FGF23 positive rate in Klotho overexpression (Klotho) group, while, there was a higher FGF23 positive rate and lower Klotho positive rate in FGF23 overexpression (FGF23) group. In addition, the expression of p-ERK1/2 and p-P38 increased in Klotho group but decreased in FGF23 group. Furthermore, overexpression of Klotho inhibited cardiomyocyte apoptosis, increased S phase fraction, promoted proliferation and elevated expression of transforming growth factor β1 (TGF-β1), nuclear factor-kappa B (NF-κB), angiotensin-II (AT-II), and activator protein-1 (AP-1), overexpression of FGF23 showed the opposite effect, however, ERK agonist (TPA) and inhibitor (U0126) reversed the effect caused by overexpression of Klotho and FGF23 separately. Klotho/FGF23 axis play a critical role in CAD progression through regulating ERK/MAPK pathway in Cardiomyocyte.

Background Levosimendan preconditioning has been shown to attenuate myocardial apoptosis in animal models. However, protective effects of levosimendan postconditioning against myocardial apoptosis following myocardial infarction (MI) have not been evaluated. Therefore, we investigated the effects of levosimendan postconditioning on myocardial apoptosis in MI rat models. Methods In an anoxia/reoxygenation (A/R) model, H9c2 cells were pretreated with or without levosimendan postconditioning after which their apoptosis rates were assessed by flow cytometry, RT-qPCR, and western blot analyses. Then, postconditioning was performed with or without levosimendan in MI rat models. Myocardiocyte apoptosis was evaluated by echocardiography, TTC staining, TUNEL staining, immunohistochemical staining, RT-qPCR, and western blot analysis. Results Levosimendan postconditioning inhibited H9c2 cell apoptosis in A/R models by elevating Bcl-2 while suppressing Caspase-3 and Bax at both mRNA and protein levels. Moreover, it improved cardiac functions and reduced the left ventricle infarction area in MI rat models. Compared to the MI control group, cardiomyocyte apoptosis rates in the levosimendan postconditioning group were low. The reduced cardiomyocyte apoptosis rates were associated with downregulation of Bax and Caspase-3 as well as with upregulation of Bcl-2 at mRNA and protein levels. Conclusions Levosimendan postconditioning of MI rat models protected against cardiomyocyte apoptosis, implying that it is a potential strategy for preventing cardiomyocyte apoptosis in the treatment of cardiac dysfunction following MI.

代谢组学可检测出小分子代谢产物,跳过复杂的调控过程直接反映出最终的代谢变化,代谢产物在多种疾病的发生、发展中起着重要的作用.主动脉夹层是一种进展迅速、病死率高的破坏性疾病,没有有效的药物根治手段,手术为唯一的根治方法,而它的确切病因尚不清楚.近年来,我国人群主动脉夹层的发病率呈明显上升趋势,发病年龄也有年轻化趋势,主动脉夹层是一种病死率极高的高风险疾病,严重消耗医疗和社会资源,给家庭和国家造成沉重负担.主动脉夹层的发生与发展必定伴随着复杂的代谢调控过程,而代谢组学及相关代谢产物则直接反映出主动脉夹层最终的代谢变化.本文就代谢组学应用于主动脉夹层的研究进展作一综述.

目的 探讨体外循环辅助(cardiopulmonarybypass,CPB)心脏术后发生急性肾损伤(acute kidney injury,AKI)患者使用局部枸橼酸抗凝对NLRP3及下游炎性通路表达的影响.方法 选取2019年4月至2021年4月在昆明医科大学附属延安医院心脏大血管外科收治并接受体外循环辅助的开放性心脏手术的急性肾损伤患者共37例,其中心脏术后需行CRRT的AKI组患者31例;并随机选取心脏术后无AKI对照组32例.分别测定各组心脏超声、体外循环辅助时间、肝肾功能、心肌酶学等基线资料,采用qRT-PCR法测定NLRP-3及凋亡通路Caspase-1 mRNA相对表达量,采用ELISA法测定下游细胞因子(IL-1β、IL-6、IL-18)的表达水平,并将NLRP-3与上述各项指标进行相关性分析.结果 与对照组相比,AKI组的体外循环辅助时间(转流时间、阻断时间、停跳时间、并行循环时间)显著延长(P＜0.05).qRT-PCR结果显示:在AKI组中,CVVH治疗24 h、48 h后较治疗前NLRP-3和Caspase-1的mRNA表达下降(P＜0.05),且随治疗时间延长其表达进一步下降(P＜0.05).在对照组中,术后各时间点NLRP-3和Caspase-1的mRNA表达均较术前升高(P＜0.05),在术后48 h表达开始下降(P＜0.05).ELISA结果显示:在AKI组中,CVVH治疗24 h、48 h后较治疗前下游细胞因子IL-1β、IL-6与IL-18表达下降(P＜0.05).在对照组中,术后各时间点下游细胞因子IL-1β、IL-6与IL-18表达均较术前升高(P＜0.05),在术后48 h表达开始下降(P＜0.05).根据Spearman相关性分析结果提示:经局部枸橼酸抗凝CVVH治疗后的NLRP-3表达与阻断时间、停跳时间呈正相关(r=0.514,P=0.003;r=0.401,P=0.025).结论 体外循环心脏术后AKI患者NLRP-3及下游炎性因子表达升高;局部枸橼酸抗凝方式可有效降低NLRP-3及下游炎性因子的表达;CVVH治疗后的NLRP-3表达与阻断时间、停跳时间呈正相关.

目的 探讨体外循环辅助行冠状动脉旁路移植术(CABG)对Klotho-FGF23轴的影响,以及对血管生长因子的表达变化产生的意义.方法 选取2018年8月至2020年6月在我院心脏大血管外科接受CABG患者67例作为研究组,分别于术前、术后12h、术后48h测定抗衰老相关基因(Klotho)、成纤维细胞生长因子23(FGF23)、核转录因子-κB(NF-κB)、血管生成素-2(Ang-2)、内皮素-1(ET-1)、弹性蛋白微原纤维界面因子-1(EMILIN-1)、纤维粘连蛋白(FN)、血管内皮细胞生长因子(VEGF)的表达水平,随后将Klotho-FGF23轴分别在术前、术后12 h及术后48 h与上述各因子进行相关性分析.结果 本研究共纳入67例接受CABG患者,接受单纯CABG患者46例(68.66％),同时接受单机械瓣置换者13例(19.40％),双机械瓣置换者6例(8.95％),改良Cabrol术者2例(2.99％).与CABG术前相比,Klotho、NF-κB、Ang-2、EMILIN-1、FN的表达升高(P值分别为0.002、0.048、0.025、0.032、0.031),FGF23表达降低(P=0.034).随时间延长,在术后48 h,Klotho、ET-1、EMILIN-1、VEGF水平仍表达升高(P值分别为0.048、0.029、0.006、0.004);FGF23仍表达降低(P=0.042).在CABG术前,Klotho及FGF23均与Ang-2、EMILIN-1、ET-1、NF-κB、FN呈显著正相关(r值分别为0.731、0.484;0.718、0.422;0.765、0.245;0.857、0.260;0.757、0.397;P值均<0.05),FGF23还与VEGF呈显著正相关(r=0.549;P<0.05);在CABG术后12 h,Klotho及FGF23均与Ang-2、EMILIN-1、NF-κB呈显著正相关(r值分别为0.798、0.314;0.842、0.258;0.943、0.276;P值均<0.05),Klotho还与ET-1、FN呈显著正相关(r值分别为0.861、0.886;P值均<0.05);在CABG术后48 h,Klotho与Ang-2、EMILIN-1、ET-1、NF-κB、FN、VEGF呈显著正相关(r值分别为0.721、0.748、0.723、0.819、0.771、0.431;P值均<0.05).结论 体外循环CABG后Klotho表达上调、FGF23表达下调,符合Klotho-FGF23轴调控特征;Klotho-FGF23轴能够调控促血管生长因子及促血管纤维化因子的表达.

目的 总结单中心小样本左西孟旦治疗体外循环心内直视下心脏术后低心排血量综合征(low cardiac output syndrome,LCOS)的临床疗效及生存分析.方法 随机选择2016年12月至2017年12月昆明医科大学附属延安医院心脏大血管外科体外循环心内直视下心脏术后LCOS患者36例,左室射血分数≤35％,在常规治疗疗效不佳情况下给予左西孟旦辅助治疗,剂量为0.1 μg/(kg· min),持续24 h,观察用药前后射血分数、心输出量、心肌酶学、肝肾功、Pro-BNP、累积生存率等指标的变化.结果 加用左西孟旦治疗后在提高心输出量及射血分数、降低Pro-BNP水平、提高累积生存率等指标方面差异有统计学意义(P＜0.05);左西孟旦对术后肝肾功能及心肌酶学的损伤差异无统计学意义(P＞0.05).结论 对于体外循环心内直视下心脏术后并发LCOS的患者,在常规治疗效果不佳的基础上加用左西孟旦可有效改善患者的心功能.

目的本研究旨在构建并制备增强型荧光蛋白（EGFP）基因和Klotho基因重组腺病毒载体AdEGFP-Klotho,并将其感染HEK293细胞,为基因治疗提供研究基础。方法设计含有NheⅠ与NotⅠ双酶切位点的引物,应用PCR方法扩增Klotho基因,将其连接到EGFP标记的pDC316-mCMV穿梭质粒上,构建重组穿梭质粒pDC316-mCMV-EGFP-Klotho,利用Polyfectin脂质体将骨架质粒和重组穿梭质粒共转染HEK293细胞进行同源重组,得到重组腺病毒Ad-EGFP-Klotho,并包装扩增,测定病毒颗粒数及滴度。采用PCR方法对重组腺病毒载体Ad-EGFP-Klotho进行鉴定,并进行Klotho基因测序。结果经PCR和NheⅠ、NotⅠ双酶切鉴定,重组腺病毒载体Ad-EGFP-Klotho中证实含有Klotho基因,测序结果和设计序列比对一致,重组腺病毒载体Ad-EGFP-Klotho构建成功。滴度为2.0×1010 Tu/mL,成功感染HEK293细胞,感染复数（MOI）=100,感染效率达91.75%,从Ad-EGFP-Klotho重组腺病毒载体中可以检测到3 045bp的条带,表明目的基因已成功整合在重组腺病毒载体Ad-EGFP-Klotho基因组中。结论应用细胞内同源重组方法成功构建了含有EGFP和Klotho基因的重组腺病毒载体Ad-EGFP-Klotho,制备获得高滴度的病毒,可高效感染HEK293细胞并表达目的蛋白。

To study the role of heart rate management for cardiac functional repair of 56 cases that received coronary artery bypass grafting (CABG) surgery attacking electrical storm. A total of 56 cases with post-CABG operative electrical storm in our hospital from 2011-01 to 2015-06 were retrospectively

目的 总结昆明市延安医院云南省心脏移植中心11例同种异体原位心脏移植术后的监测治疗.方法 选择2003年3月-2008年9月进行同种异体原位心脏移植术患者11例,手术均按标准法行同种异体原位心脏移植,术后抗排斥反应治疗采用环孢素(CsA)+霉酚酸酯(MMF)+ 泼尼松(Pred)三联方案,并给予严密的监测治疗.结果 11例患者均一期恢复良好出院,出院后6例患者存活至今,心理状态良好,血流动力学稳定,无明显免疫排斥迹象;3例患者死亡,其中1例因患者自己暗地里不规律服用免疫抑制药物引起急性排斥反应,经我科救治好转后出院,仍然不规律服用免疫抑制药物而猝死家中,1例肺部严重感染,1例急性右心衰竭经再次入院抢救,无效死亡.结论 心脏移植是目前终末期心脏病最有效的治疗手段,术后的监测治疗十分关键.

As an invasive operation,percutaneous coronary intervention(PCI)can cause a variety of clinical complications during intraoperative and postoperative period,such as acute coronary stenosis or occlusion,perforation and cardiac tamponade,no reflow of coronary artery,thrombus,hematoma,pseudoaneurysm and arteriovenous fistula;and non-vascular complications(such as hypotension,acute coronary artery spasm,ventricular fibrillation,vasovagal reflex and radiographic contrast nephropathy).The occurrence of these complications would seriously affect the surgical results,even induce a treatment failure.Although measures of preventing and treating these complications have been improved remarkably,efficacy of PCI is mainly impacted by these complications.

经皮冠状动脉介入治疗(PCI)是广泛用于恢复病变冠状动脉前向血流的主要方法,已成为治疗缺血性心脏病的基石。但目前有许多问题尚未解决,限制了PCI的进一步临床应用。随着新装置、新技术和新辅助治疗的创立及验证,冠心病的PCI治疗已经取得了巨大的进展。本文对经皮冠脉介入治疗中应用的最新成果作一综述和展望,重点讨论冠状动脉内支架、直接心肌血运重建术、心肌梗死、抗血小板治疗及并发症的重要新进展。