OBJECTIVE:To evaluate the clinical measurement accuracy of the BP2 oscillometric upper arm blood pressure monitor in the general population according to the ISO 81060-2:2018+Amd 1:2020 standard. METHODS:Participants were recruited and the same arm sequential method was used for blood pressure measurement according to the ISO 81060-2:2018+Amd 1:2020. The validation results were assessed following the protocol and the Bland-Altman scatterplot was used to show the difference between the test device and reference results. RESULTS:A total of 85 participants were included in the final analysis. For the validation criterion 1, the mean ± SD of the differences between the test device and reference readings was -2.93 ± 7.65 and -2.40 ± 6.82 mmHg for systolic and diastolic blood pressure, respectively. For criterion 2, the ±SD of the averaged differences between the test device and reference readings per participant was ±6.16 and ±5.74 mmHg for systolic and diastolic blood pressure, respectively. CONCLUSION:The BP2 upper arm blood pressure monitor passed all the requirements of the ISO 81060-2:2018+Amd 1:2020 standard and can be recommended for clinical use and self-measurement in the general population.

Objective: Validation of blood pressure (BP) monitors in pregnant women are needed to ensure the accurate measurement of BP in pregnancy. Therefore the study aimed to evaluate the measurement accuracy of the G.LAB MD41A0 oscillometric automatic upper-arm blood pressure monitor in pregnancy and pre-eclampsia women according to the AAMI/ESH/ISO Universal Standard (ISO 81060-2:2018). Methods: A total of 45 pregnant women were included in the cross-sectional validation study. The same left-arm sequential method was used for blood pressure measurement, and the blood pressure differences between the test device and the mercury standard reference were assessed according to the AAMI/ESH/ISO Universal Standard. Results: The participants included 15 normotensives, 15 gestational hypertension and 15 pre-eclampsia. The average (mean +/- SD) differences between the device and mercury standard was -0.84 +/- 3.88 mmHg and -0.58 +/- 3.35 mmHg for systolic and diastolic blood pressure, respectively, for the validation Criterion 1. The SD of the averaged differences between the device and reference readings per participant was 2.92 mmHg and 2.28 mmHg for systolic and diastolic blood pressure, respectively, for the Criterion 2 of the universal standard. Conclusion: The G.LAB MD41A0 automatic upper-arm blood pressure monitor fulfills the criteria of the AAMI/ESH/ISO Universal Standard and can be recommended for clinical use and self-measurement in pregnancy and pre-eclampsia.

目的:探讨葛根素(Pue)抑制内质网应激(ERS)对压力负荷下小鼠心肌肥厚的作用.方法:采用腹主动脉缩窄术(AAC)模拟压力负荷引起的心肌肥厚,将C57/bl小鼠随机分为四组(n=15):假手术组(Sham组)、葛根素对照组(Pue组)、腹主动脉缩窄术组(AAC组)和葛根素治疗AAC组(AAC+Pue组).Pue组和AAC+Pue组术后腹腔注射50 mg/(kg·d)Pue,Sham组和AAC组腹腔注射等量的0.9％氯化钠溶液,持续4周后,超声检测左室后壁厚度(LVPWd)、左室内径(LVId)和室间隔厚度(IVSd);测量心脏重量与体重比(HW/BW),WGA染色观察心肌细胞横截面积,Masson染色观察纤维化程度;RT-PCR检测ANP和Myh7的mRNA水平;Western blot检测PERK、CHOP和GRP78蛋白的表达.结果:Sham组和Pue组各指标间比较无统计学差异(均P>0.05);和Sham组相比,AAC组LVPWd、LVId和IVSd值增加(均P<0.01),HW/BW比增大,心肌横截面积和纤维化程度增加,ANP和Myh7的mRNA水平增加(均P<0.01),PERK和CHOP蛋白的表达增多,而GRP78表达降低(均P<0.01);和AAC组相比,AAC+Pue组LVPWd、LVId和IVSd值降低(均P<0.01),HW/BW比减小,心肌横截面积和纤维化程度降低,ANP和Myh7的mRNA水平减少(均P<0.01),PERK和CHOP蛋白的表达降低,而GRP78表达增加(均P<0.01).结论:Pue可通过抑制内质网应激减轻压力负荷引起的心肌肥厚.

目的 观察紫檀芪(PTE)灌胃对大鼠心肌肥厚的改善作用并探讨其分子机制.方法 将40只SD大鼠随机分为假手术组、模型组、PTE组、PTE+3-TYP组各10只,除假手术组外均采用腹主动脉缩窄术建立大鼠心肌肥厚模型.PTE组及PTE+3-TYP组大鼠术后均给予PTE灌胃处理,PTE+3-TYP组大鼠在给予PTE的同时经腹腔注射SIRT3特异性阻断剂3-TYP,假手术组及模型组大鼠给予相同体积生理盐水灌胃.8周后对大鼠进行心功能检查,包括左心室舒张末期压力(LVEDP)、左心室收缩末期压力(LVESP)、等容收缩期左心室内压力上升的最大速率(+dp/dt)和等容舒张期左心室压力下降的最大速率(-dp/dt)及血清B型利钠肽(BNP)水平.检测大鼠心肌肥厚指标,包括心体比(HM/BM)、心胫比(HM/TL)及心肌细胞横截面积.超氧化物阴离子荧光探针染色法检测心肌组活性氧(ROS)生成量,Western blotting法检测心肌组织中去乙酰化修饰酶SIRT3、FOXO3a去乙酰化后产物Ac-FOXO3a、抗氧化蛋白NOX2及氧化应激标志蛋白gp91phox的蛋白表达情况.结果 各组大鼠心功能指标LV-EDP、LVESP、血清BNP水平比较,模型组、PTE+3-TYP组>PTE组>假手术组;+dp/dt、-dp/dt比较,模型组、PTE+3-TYP组<PTE组<假手术组(P均<0.05);模型组与PTE+3-TYP组各心功能指标比较差异均无统计学意义.各组大鼠心肌肥厚指标(HM/TL、HM/BM、心肌细胞横截面积)及心肌ROS生成量比较,模型组、PTE+3-TYP组>PTE组>假手术组(P均<0.05),模型组与PTE+3-TYP组各指标比较差异均无统计学意义.各组大鼠心肌组织SIRT3、NOX2蛋白表达比较,模型组、PTE+3-TYP组<PTE组<假手术组;Ac-FOXO3a、gp91phox蛋白表达比较,模型组、PTE+3-TYP组>PTE组>假手术组(P均<0.05),模型组与PTE+3-TYP组各蛋白表达比较差异均无统计学意义.结论 PET可以通过减轻心肌组织氧化应激损伤改善大鼠腹主动脉缩窄所致的心肌肥厚,这种作用可能是通过激活SIRT3/FOXO3a信号通路实现的.

目的 探讨褪黑素在高糖诱导的原代心肌细胞损伤中的作用,并明确SIRT1在其中的作用及其机制.方法 将原代心肌细胞分为对照组(Con组)、褪黑素对照组(Con+Mel组)、高糖组(HG组)、高糖+褪黑素组(HG+Mel组)和SIRT1抑制剂理组(HG+Mel+EX527组).采用Cell Counting Kit-8(CCK-8)试剂盒检测细胞活性,丙二醛(MDA)和超氧化物歧化酶(SOD)试剂盒检测细胞氧化应激水平,TUNEL染色检测细胞凋亡,免疫印迹检测SIRT1、Beclin1、Atg5、cleaved Caspase-3、Bax和Bcl-2蛋白表达水平.结果 与Con组相比,HG组原代心肌细胞活力减低,氧化应激水平升高,细胞凋亡水平增加,SIRT1表达下调(P<0.05).给予褪黑素干预后,与Con组相比,Con+Mel组SIRT1表达量增加(P<0.05),而两组间细胞活力、氧化应激水平和细胞凋亡水平无显著差异(P>0.05).与HG组相比,HG+Mel组原代心肌细胞SIRT1表达量提高(P<0.05),细胞活力增加(P<0.05),氧化应激水平和细胞凋亡水平下降(P<0.05).免疫印迹结果显示,与Con组相比,HG组原代心肌细胞自噬相关蛋白Beclin1和Atg5表达减低(P<0.05),Con+Mel组Beclin1和Atg5表达明显上升(P<0.05);与HG组相比,HG+Mel组Beclin1和Atg5表达上升(P<0.05).此外,给予SIRT1特异性抑制剂EX527干预后,相比于HG+Mel组,HG+Mel+EX527组细胞凋亡比率增加(P<0.05),凋亡蛋白cleaved Caspase-3和Bax上调(P<0.05),抗凋亡蛋白Bcl-2下调(P<0.05),细胞自噬蛋白Beclin1和Atg5表达减低(P<0.05).结论 褪黑素可能通过上调SIRT1信号增强细胞自噬,改善高糖诱导的原代心肌细胞损伤.

目的 观察小檗胺(BBM)对糖尿病心肌病心肌损伤的保护作用并初步探讨其保护机制.方法 将60只雄性C57BL/6小鼠(8周龄)随机分为4组:正常对照组(control组),单纯药物处理组(Con+BBM组),糖尿病心肌病组(DCM组)和糖尿病心肌病+药物处理组(DCM+BBM组),每组15只.DCM组和DCM+BBM组小鼠采用腹腔注射链脲佐菌素(STZ)联合高热量饮食法建立糖尿病心肌病模型,control组和DCM组灌胃生理盐水12周,Con+BBM组灌胃BBM(100 mg/kg)12周,DCM+BBM组小鼠在STZ注射2周后,每天通过灌胃补充小檗胺处理(100 mg/kg)共12周.待实验结束后,用小动物超声仪检测小鼠心脏收缩功能;HE染色法观察小鼠左心室心肌细胞横截面积;计算各组小鼠全心质量指数(HMI)和左心室质量指数(LVMI);Masson染色法观察心肌组织纤维化程度;免疫组化染色法检测心肌组织Collagen-1表达程度;分光光度法检测心肌组织中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)和丙二醛(MDA)的含量;RT-PCR法检测心肌肥厚相关基因α-MHC和β-MHC的表达水平;Western blot法检测SIRT3、Ac-FOXO3a和gp91phox的蛋白表达水平.结果 与control组相比,DCM组小鼠心脏收缩功能显著降低,HMI和LVMI值明显升高,心肌肥厚相关基因的表达水平显著上升,心肌组织纤维化程度和氧化应激水平显著升高,且心肌SIRT3/FOXO3a信号通路被显著抑制(均P<0.05).与DCM组比较,DCM+BBM组小鼠心脏收缩功能障碍及心肌肥厚情况得到显著改善,心肌组织纤维化程度明显缓解,氧化应激损伤显著减轻,并且心肌SIRT3/FOXO3a信号通路也显著上调(均P<0.05).而Con+BBM组小鼠与control组相比,在心功能、心肌肥厚情况、心肌纤维化程度、氧化应激损伤和心肌SIRT3通路表达上的差异均无统计学意义(均P>0.05).结论 小檗胺通过减轻心肌组织氧化应激损伤发挥抗糖尿病心肌病心肌损伤的作用,其分子机制可能与激活心肌SIRT3/FOXO3a信号有关.

目的 评价经导管介入封堵瓦氏窦瘤破裂的安全性和有效性.方法 收集空军军医大学第二附属医院心血管内科2013年4月～2020年7月诊断为瓦氏窦瘤破裂并进行介入封堵治疗的27例患者.术后观察患者封堵器位置、有无残余漏、并发症等指标,比较术前术后患者的心功能、心脏杂音、心率、血压、心腔大小等指标的变化.结果 封堵术后心脏超声证实所有患者心功能明显改善:术后24 h心率较术前明显降低(P＜0.05);术后舒张压较术前明显升高(P＜0.05).术后72 h复查心脏超声确定右房内径较术前减小(P＜0.05).术后1年心脏超声发现右房内径、右室内径、左房内径、左室收缩期及舒张期内径较术前减小(P＜ 0.05).术后无封堵器脱落、感染性心内膜炎、血栓栓塞、溶血、残余漏、主动脉瓣反流等情况发生,随访期间也无上述状况出现.结论 对于符合适应症的患者,经导管介入封堵瓦氏窦瘤破裂是一种安全有效的方法.

Background: Heart failure (HF) is an epidemic disease with increased incidence annually. It has been reported that taurine can improve cardiac function. This study investigated the cardioprotective effects of taurine in pressure-loaded HF mice and elucidated the possible mechanism. Methods: HF models were established by transverse aortic constriction (TAC). Animals were treated with either taurine for 9 weeks and/or the SIRT1 inhibitor EX527 (5 mg/kg/day, every 2days) after TAC operation. Cardiac function and geometry were revealed by echocardiography. Myocardial hypertrophy and fibrosis were assessed using Fluorescent wheat germ agglutinin (WGA) staining and Masson's trichrome staining. Western blot and RTPCR were performed to elucidate the expression of target proteins and genes respectively. Apoptosis in cardiomyocytes was detected by TUNEL staining. Myocardial oxidative stress was assessed by detecting the concentration of myocardial super oxidative dismutase (SOD) and malonyldialdehyde (MDA) and reactive oxygen species (ROS). Taurine concentrations and NAD+/NADH ratio were determined by taurine and NAD+/NADH assay kit. Results: Taurine notably relieved cardiac dysfunction after TAC. The mechanisms were attributed to reduced myocyte hypertrophy and fibrosis, and alleviated apoptosis and oxidative stress. Meanwhile, taurine increased NAD+/NADH ratio,promoted the expression of SIRT1 and suppressed p53 acetylation. However, EX-527(in-hibitor of SIRT1) decreased NAD+/NADH ratio and increased acetyl-p53 levels, and abolished the cardioprotective effects of taurine on mice subjected to TAC and increased apoptosis and oxidative stress. Conclusion: The mechanism responsible for cardiac-protective effects of taurine in HF induced by pressure overload is associated with the activation of the SIRT1-p53 pathway.

Bakuchiol (BAK), a monoterpene phenol reported to have exerted a variety of pharmacological effects, has been related to multiple diseases, including myocardial ischemia reperfusion injury, pressure overload-induced cardiac hypertrophy, diabetes, liver fibrosis, and cancer. However, the effects of BAK on hyperglycemia-caused diabetic cardiomyopathy and its underlying mechanisms remain unclear. In this study, streptozotocin-induced mouse model and high-glucose-treated cell model were conducted to investigate the protective roles of BAK on diabetic cardiomyopathy, in either the presence or absence of SIRT1-specific inhibitor EX527, SIRT1 siRNA, or Nrf2 siRNA. Our data demonstrated for the first time that BAK could significantly abate diabetic cardiomyopathy by alleviating the cardiac dysfunction, ameliorating the myocardial fibrosis, mitigating the cardiac hypertrophy, and reducing the cardiomyocyte apoptosis. Furthermore, BAK achieved its antifibrotic and antihypertrophic actions by inhibiting the TGF-β1/Smad3 pathway, as well as decreasing the expressions of fibrosis- and hypertrophy-related markers. Intriguingly, these above effects of BAK were largely attributed to the remarkable activation of SIRT1/Nrf2 signaling, which eventually strengthened cardiac antioxidative capacity by elevating the antioxidant production and reducing the reactive oxygen species generation. However, all the beneficial results were markedly abolished with the administration of EX527, SIRT1 siRNA, or Nrf2 siRNA. In summary, these novel findings indicate that BAK exhibits its therapeutic properties against hyperglycemia-caused diabetic cardiomyopathy by attenuating myocardial oxidative damage via activating the SIRT1/Nrf2 signaling.

目的 探讨金丝桃苷对H9C2细胞缺血再灌注损伤的作用及可能机制.方法 采用H9C2细胞模拟缺血再灌注模型,缺血液培养45 ain,再恢复正常迭尔伯克改良伊格尔培养液培养4h.将H9C2细胞随机分为对照组,金丝桃苷组,缺血再灌注组,金丝桃苷处理+缺血再灌注组(联合组).光镜观察细胞形态变化,CCK-8法检测细胞活力,Western blot检测磷酸化腺苷酸活化蛋白激酶(AMPK)和磷酸化哺乳动物雷帕霉素靶蛋白(mTOR)蛋白水平,自噬相关蛋白LC3Ⅱ、Beclin1和P62以及凋亡相关蛋白裂解的半胱氨酸天冬氨酸蛋白酶(caspase-3)活性水平,TUNEL染色观察凋亡变化.结果 金丝桃苷组与对照组各项指标比较,差异无统计学意义(P＞0.05).与对照组比较,缺血再灌注组凋亡指数、caspase-3活性、LC3Ⅱ和Beclin1明显增高,细胞活力、磷酸化AMPK、磷酸化mTOR和P62蛋白明显降低,差异有统计学意义(P＜0.05).与缺血再灌注组比较,联合组细胞活力、磷酸化AMPK、磷酸化mTOR和P62蛋白明显增高,凋亡指数、caspase-3活性、LC3Ⅱ和Beclin1明显降低[(11.7±2.8)％ vs (27.6±4.5)％,1.4±0.1 vs 2.1±0.3,1.35±0.04 vs 2.17±0.07,1.30±0.18 vs 2.20±0.20,P＜0.05].结论 金丝桃苷通过激活AMPK/mTOR信号降低自噬减轻H9C2细胞缺血再灌注损伤.

Hyperhomocysteinemia induces stress response in endoplasmic reticulum (ERS). Here, we tested whether blockage of homocysteine (Hcy) induced ERS and subsequent apoptosis in vascular smooth muscle cells can be inhibited by  blockage of PERK/eIF2α/ATF4/CHOP signaling. Short-term exposure of vascular smooth muscle cells to Hcy led to the phosphorylation of PERK (pPERK), which in turn, phosphorylated eIF2 alpha (peIF2a) and inhibited the unfolded protein response. Long-term Hcy exposure, however, increased the expression of ATF-4 and CHOP and led to apoptosis. Treatment of cells with salubrinal, a specific inhibitor for eIF2a decreased the expression of ATF-4 and CHOP, and prevented apoptosis. Together, the results show that PERK pathway is involved in Hcy-induced vascular smooth muscle cell apoptosis and that blocking the PERK pathway protects against this injury.

目的:研究内质网应激(endoplasmic reticulum stress,ERS)在二十碳五烯酸(eicosapentaenoic acid,EPA)抵抗棕榈酸(palimitate,PAL)诱导的心肌细胞凋亡中的作用.方法:将培养的心肌细胞随机分为对照组、PAL处理组、EPA+PAL组、毒胡萝卜素(thapsigargin) +EPA+PAL组、thapsigargin组及thapsigargin+EPA组.采用CCK-8检测细胞活力、Tunel染色检测细胞凋亡率、Western印迹检测葡萄糖调节蛋白78(glucose-regulated protein 78,GRP78)和钙网蛋白(calreticulin,CRT),以及ERS促凋亡蛋白C/EBP同源蛋白(C/EBP homologous protein,CHOP)、JNK和半胱氨酸天冬氨酸蛋白酶12(caspase-12)的表达.结果:与对照组比较,PAL处理可显著降低心肌细胞活力,促进细胞凋亡,激活ERS应激相关GRP78和CRT,以及ERS促凋亡蛋白CHOP,p-JNK及活化的caspase-12(cleaved caspase-12)的表达(P＜0.05).相比于PAL组,EPA+PAL预处理可使PAL诱导的心肌细胞活力显著升高,GRP78,CRT,CHOP,cleaved caspase-12及p-JNK蛋白表达明显降低(P＜0.05),且使细胞凋亡率由43.9％降低至24.07％(P＜0.05).添加ERS特异性激活剂thapsigargin激活ERS后,与EPA+PAL组相比,thapsigargin+EPA+PAL组ERS应激相关蛋白GRP78和CRT蛋白表达比率显著升高,ERS促凋亡蛋白CHOP,JNK及caspase-12上调,心肌细胞活力下降,凋亡率增加.此外,与对照组比较,单独添加thapsigargin激活ERS,显著降低细胞活性,促进细胞凋亡,而EPA+thapsigargin组却明显逆转了thapsigargin对心肌细胞的促凋亡效应.结论:EPA可有效抑制PAL诱导的大鼠心肌细胞凋亡,其保护机制可能与抑制PAL诱导的心肌细胞ERS激活,进而抑制caspase依赖的级联凋亡反应有关.

ObjectiveAdropin, a newly identified regulatory protein encoded by Enho gene, suppressed tumor necrosis factor α‐induced THP1 monocyte adhesion to human umbilical vein endothelial cells. In addition, inflammation is demonstrated to be involved in the mechanism of atrial fibrillation (AF). Atrial remodeling is correlated with the persistence and progression of AF. Adropin is hypothesized to correlated with AF and atrial remodeling. This study aims to determine the correlation of serum adropin and the presence of AF and remodeling.MethodsThis study consisted of 344 AF patients and 210 healthy controls. AF patients were then divided into three subgroups of paroxysmal AF, persistent AF, and permanent AF. Serum adropin concentrations were examined using enzyme‐linked immunosorbent assay method. Left atrial diameter (LAD) was measured to evaluate atrial remodeling.ResultsDecreased serum adropin concentrations were found in AF patients compared with healthy controls. Logistic regression analysis confirmed that serum adropin was inversely associated with the presence of AF (OR 0.218, 95% CI 0.15‐0.316; P < 0.001). Permanent AF patients had significantly reduced serum adropin concentrations compared with persistent and paroxysmal AF patients. There were decreased serum adropin concentrations in persistent AF group than those in paroxysmal AF group. Simple linear regression analyses showed that serum adropin in AF patients were negatively correlated with BMI, SBP, and LAD. Multiple stepwise regression analysis showed that LAD remained to be inversely associated with serum adropin (β = 0.2, P = 0.010).ConclusionSerum adropin concentrations are inversely correlated with the presence of AF and atrial remodeling.

目的 初步探讨内质网应激PERK-ATF4-CHOP通路在褪黑素抵抗血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)诱导的心肌细胞肥厚中的作用.方法 将培养的心肌细胞随机分为对照组、AngⅡ处理组、褪黑素组.采用乳酸脱氢酶(lactate dehydrogenase,LDH)法检测细胞活性,原位切口末端标记法(TUNEL)检测细胞凋亡率,Western blot检测蛋白激酶R样内质网激酶(protein kinase r-like endoplasmic reticulum kinase,PERK)、活性转录因子(Activating Transcription Factor,ATF)4、C/EBP同源蛋白(C/EBP homologous protein,CHOP)的表达水平,实时荧光定量聚合酶链反应(quantitative real-time polymerase chain reaction,qRT-PCR)检测心肌肥厚相关标识物心房钠尿肽(atrial natriuretic peptide,ANP)、脑钠尿肽(brain natriuretic peptide,BNP)和心肌β-肌球蛋白重链(β-myosin heavy chain,β-MHC) mRNA 表达量的变化;免疫荧光检测心肌细胞横截面积.结果 与对照组相比,AngⅡ能够刺激心肌细胞上调ANP、BNP和β-MHC表达(P＜0.05),刺激LDH释放(P＜0.05)、增加细胞凋亡比率和心肌细胞横截面积(P＜0.05);与AngⅡ组相比,褪黑素可以浓度依赖性显著抑制AngⅡ诱导的ANP、BNP和β-MHC的上调和LDH的积累,抑制心肌细胞的横截面积增加,降低细胞凋亡,并抑制诱导的PERK-ATF4-CHOP通路的激活(P＜0.05);与对照组相比,AngⅡ显著增加PERK、ATF4和CHOP的表达水平(P＜0.05),但给予褪黑素后,激活的PERK-ATF4-CHOP则被明显抑制(P＜0.05).结论 褪黑素可能通过抑制内质网应激PERK-ATF4-CHOP信号通路激活,改善AngⅡ诱导的乳鼠心肌细胞肥厚,为未来褪黑素的进一步临床研究拓展新思路.

目的 探讨左主干闭塞患者的心电图表现及其临床特点.方法 回顾性分析2017年3月至2018年3月就诊于唐都医院经冠状动脉造影检查确诊为左主干闭塞患者21例的临床资料,根据患者入院心电图中有无"6+2"表现分为两组,其中A组(有"6+2"表现)9例,B组(无"6+2"表现)12例.比较两组患者的一般临床资料、发病急慢情况、有无室性心动过速发作、有无侧支循环、有无新增束支阻滞、ST段改变总和、是否合并右冠脉病变及死亡率等.结果 两组患者一般资料均无显著差异(P>0.05);A组急性心肌梗死、室性心动过速、新增束支传导阻滞、ST段改变总和≥18 mm发生率均显著高于B组,差异有统计学意义(P<0.05);A组存在侧支循环的患者占比明显低于B组,差异有统计学意义(P<0.05);21例患者经冠状动脉造影确诊为左主干闭塞的患者,且A组冠状动脉造影确诊合并右冠脉病变的发生率较B组无显著差异(P>0.05);A组患者死亡率高于B组,差异有统计学意义(P<0.05).结论 典型"6+2"心电图表现的左主干闭塞患者往往是急性闭塞,ST段改变总和≥18 mm发生率高,易合并室性心动过速及新增束支阻滞的特点,死亡率高;没有"6+2"典型心电图表现的左主干闭塞患者往往是慢性闭塞患者,多有侧支循环,死亡率低.

Objective To investigate the clinical efficacy of Qishen Yiqi Dropping Pills combined with Discornin Tablets in treatment of angina pectoris of coronary heart disease. Methods Patients (104 cases) with angina pectoris of coronary heart disease in the Second Affiliated Hospital of the Fourth Military Medical University from February 2016 to February 2017 were divided into control (52 cases) and treatment(52 cases)groups according to different treatments.Patients in the control group were po administered with Discornin Tablets,160 mg/time,twice daily.Patients in the treatment group were po administered with Qishen Yiqi Dropping Pills on the basis of the control group, 0.5 g/time, three times daily. Patients in two groups were treated for 2 weeks. After treatment, the clinical efficacy was evaluated, and the ECG curative effect, the frequency and duration of angina pectoris, serological indexes and cardiac function indexes in two groups before and after treatment were compared. Results After treatment, the clinical efficacy in the control group was 80.77%, which was significantly lower than 96.15% in the treatment group, and the difference was statistically significant between two groups (P < 0.05). After treatment, the ECG curative effect in the control and treatment groups were 69.23% and 90.38%, respectively, and there were differences between two groups (P < 0.05). After treatment, the frequency and duration of angina pectoris in two groups were significantly decreased (P < 0.05). And the frequency and duration of angina pectoris in the treatment group was significantly less than those in the control group (P < 0.05). After treatment, the serum IL-1β, IL-18, PAPP-A and NF-κB level in two groups was significantly decreased (P < 0.05). And the serological indexes in the treatment group were significantly lower than those in the control group (P < 0.05). After treatment, the LVEF and CO in two groups was significantly increased, but LVESD was significantly decreased, and the difference was statistically significant in the same group (P < 0.05). And these cardiac function indexes in the treatment group improved more obviously than that in the control group (P < 0.05). Conclusion Qishen Yiqi Dropping Pills combined with Discornin Tablets can effectively reduce the frequency of angina pectoris and inflammation reaction and improve cardiac function in treatment of angina pectoris of coronary heart disease, which has a certain clinical application value.

[Objective] To explore the prognostic value of serum sirtuin-1 (SIRT1) in short-term follow-up (3 months) of inpatients with heart failure.[Methods] A total of 86 inpatients with heart failure from December 2015 to December 2016 in our hospital were selected as the subjects.They were followed up for 3 months and the follow-up rate was 100％.According to the prognosis of the patients,they were divided into two groups:poor prognosis group (n=41) and good prognosis group (n=45).The serum levels of SIRT1 were compared between the two groups at admission and after 3 months of follow-up,and the predictive value of serum SIRT1 level in the short-term follow-up of patients with heart failure was analyzed.[Results] (1) Compared with the good prognosis group,the serum SIRT1 level was significantly decreased in the poor prognosis group (P＜0.05),and the level of left ventricle ejection fraction (LVEF) was significantly decreased (P＜0.05).(2) At admission,the serum SIRT1 level in the good prognosis group was significantly higher than that in the poor prognosis group (P＜0.05).Compared with those at admission,serum SIRT1 levels in the poor and good prognosis groups after 3 months of treatment were significantly increased (P＜0.05),and the serum SIRT1 level in the good prognosis group was significantly higher than that in the poor prognosis group (P＜0.05).(3) The median of serum SIRT1 level in 86 patients with heart failure was 5.37 ng/ml,which was as the cut-off point.The nurnbers of readmission and death of heart failure in patients with serum SIRT1 level ≥ 5.37 ng/ml were significantly lower than those in patients with serum SIRT1 level ＜5.37 ng/ml (P＜0.05).(4) The results of COX regression analysis showed that serum SIRT1 level and LVEF were the independent risk factors for 3-month follow-up in patients with heart failure.[Conclusion] The lower the level of serum SIRT1,the poorer the prognosis.It is speculated that serum SIRT1 can be used as an effective reference indicator for predicting poor prognosis of heart failure.

Objective To evaluate the clinical efficacy of interventional therapy in pediatric patients with complex congenital heart disease of diminished pulmonary blood flow after palliative surgery.Methods One hundred and forty nine complex congenital heart disease pediatric patients with diminished pulmonary blood flow after palliative surgery were admitted in our hospital from January 2012 to June 2015.All patients received percutaneous balloon pulmonary artery dilatation,the pulmonary transvalvular gradient(PTG),right ventricle systolic pressure(RVSP),pulmonary arterial systolic pressure(PASP),and oxyhemoglobin saturation (SaO2) were measured by right cardiac catheterization before and after the intervention.Patients were followed up for 12 months,pulmonary artery development index (Nakata index,McGoon ratio),SaO2 and PTG were measured by the end of follow-up.Results The interventional procedures underwent smoothly in all 149 patients.There were 3 patients with arrhythmia and 2 patients with fever after operation with a perioperative complication rate of 3.36％.The PTG,RVSP,PASP and SaO2 of patients were significantly improved after operation(P＜0.05);Nakata index,McGoon ratio and SaO2 of patients increased significantly at 1,3,6 and 12 months after operation;and PTG of patients was significantly decreased compared with preoperative value (P＜0.05).Conclusion Interventional therapy after palliative surgery can reduce postoperative complications,and promote pulmonary vascular development and improve ventricular function effectively for children with complex congenital heart disease of diminished pulmonary blood supply.

Purpose The mean pulmonary artery (MPAP) has been widely used as an important parameter to diagnose and evaluate pulmonary hypertension (PH).The purpose of this paper is to compare the efficacy of two methods in evaluating PH,including estimating pulmonary artery systolic pressure (PASP) using Doppler ultrasonography to measure tricuspid regurgitation (TR) velocity,and directly using the peak velocity of TR.Materiasl and Methods From January 2012 to June 2013,eighty patients with left-to-right shunt congenital heart diseases (CHD) planned for closure procedure in Tangdu Hospital of the Fourth Military Medical University and the General Hospital of Shenyang Military region were included in this prospective study,who underwent right heart catheterization to measure pulmonary artery pressure,and underwent Doppler ultrasonography to measure the peak velocity ofTR.Results Using catheter-measured MPAP of≥ 25 mmHg as diagnostic reference,the false positive rate was 62.96％,and the false negative rate 0％ when the estimated PASP of ＞30 mmHg determined by TR method was used to diagnose PH.There was high diagnostic agreement when peak velocity of TR was used to diagnose PH.When 320 cm/s and 340 crn/s were used as diagnostic cutoff values,false positive rates were 14.81％ and 7.41％,and false negative rates were 15.91％ and 20.45％,respectively.Conclusion In patients with left-to-right shunt CHD,peak velocity of TR measured on echocardiography can be used to diagnose PH which overcomes the high false positive rate in estimation method.It is more suitable to diagnose PH when the MPAP is used as the diagnostic criterion.

目的:探讨不同剂量瘦素预处理对糖尿病大鼠心肌缺血再灌注损伤的保护作用.方法:将72只大鼠随机分为对照组、假手术组、心肌梗死组以及大、中、小剂量瘦素预处理组.对照组给予普通饲料喂养,其余各组均给予高糖高脂喂养.1个月后,采大鼠静脉血,检测其血清FBG、FTNS、瘦素、HOMA、TNF-α、MDA及血脂水平.结果:与对照组相比,其余各组FBG、FINS、瘦素水平及HOMA-IR均明显升高(P＜0.05);心肌梗死组及大、中、小剂量瘦素预处理组FBG及瘦素水平与假手术组相比均明显升高,心肌梗死组、高剂量瘦素预处理组FINS及HOMA-IR与之相比亦明显升高,小、中剂量瘦素预处理组FINS及HOMA-IR与之相比均明显降低(P＜0.05);小、中剂量瘦素预处理组FBG、FINS、瘦素水平及HOMA-IR与心肌梗死组相比均明显降低(P＜0.05).与对照组相比,其余各组大鼠TNF-α、MDA水平均明显升高(P＜0.05);与假手术组相比,心肌梗死组、大、中、小剂量组大鼠TNF-α、MDA水平明显升高(P＜0.05);与心肌梗死组相比,中、小剂量组大鼠TNF-α、MDA水平均明显降低(P＜0.05).与对照组相比,其余各组大鼠TG、TC、LDL-C水平均明显升高,HDL-C水平均明显降低(P＜0.05);大、中、小剂量组HDL-C值与假手术组相比均明显升高,TG、TC、LDL-C值与之相比均明显降低(P＜0.05);与心肌梗死组相比,小、中剂量组大鼠TG、TC、LDL-C水平均明显降低(P＜0.05),HDL-C水平均明显升高(P＜0.05).结论:瘦素预处理能够保护糖尿病大鼠心肌缺血再灌注损伤,可能与其减轻炎症、氧化应激、血脂紊乱及胰岛素抵抗有关.