卡托普利合用利尿剂治疗充血性心力衰竭128例短期疗效观察

以卡托普利合用利尿剂治疗各种病因所引起的充血性心力衰竭128例，显效52例（40．63％），总有效率达93．75％，心衰控制时间3－6d．认为卡托普利合用利尿剂治疗心衰效果明显，适用于各种病因引起的充血性心衰患者．     

治疗肺心病顽固性心衰30例

慢性肺原性心脏病顽固性心衰的临疗治疗是非常困难的,其死亡率也是比较高的。在临床上通过应用生脉注射液和多巴酚丁胺联合用药治疗肺心病顽固性心衰取得较好的疗效。通过对30例病人的治疗,总有效率为93．33％,值得在临床上推广应用。     

别嘌呤醇对慢性心力衰竭患者心功能的影响

目的观察别嘌呤醇治疗慢性心力衰竭的临床效果。方法选择2007年1月至2008年1月在我院住院的慢性：心力衰竭患者56例,随机分成治疗组（别嘌呤醇组）和对照组（常规治疗组）。常规治疗组：标准抗心衰治疗。别嘌呤醇组在常规治疗的基础上加用别嘌呤醇0．3g／d,观察12周。两组均于治疗前以及治疗12周后由专人用超声心动图测左室射血分数（LVEF）、左室收缩末容量指数（LVESVI）,测量治疗前及治疗12周后血清尿酸浓度。结果别嘌呤醇组在血清尿酸浓度明显减少,心功能得到明显改善,而常规治疗组无显著变化。结论在标准抗心衰治疗的基础上加用别嘌呤醇（0．3g／d）能给慢性心力衰竭患者带来益处。     

Stem-cell therapy for cardiac disease

Heart failure is the leading cause of death worldwide, and current therapies only delay progression of the disease. Laboratory experiments and recent clinical trials suggest that cell-based therapies can improve cardiac function, and the implications of this for cardiac regeneration are causing great excitement. Bone-marrow-derived progenitor cells and other progenitor cells can differentiate into vascular cell types, restoring blood flow. More recently, resident cardiac stem cells have been shown to differentiate into multiple cell types present in the heart, including cardiac muscle cells, indicating that the heart is not terminally differentiated. These new findings have stimulated optimism that the progression of heart failure can be prevented or even reversed with cell-based therapy.     

Heart regeneration

Heart failure plagues industrialized nations, killing more people than any other disease. It usually results from a deficiency of specialized cardiac muscle cells known as cardiomyocytes, and a robust therapy to regenerate lost myocardium could help millions of patients every year. Heart regeneration is well documented in amphibia and fish and in developing mammals. After birth, however, human heart regeneration becomes limited to very slow cardiomyocyte replacement. Several experimental strategies to remuscularize the injured heart using adult stem cells and pluripotent stem cells, cellular reprogramming and tissue engineering are in progress. Although many challenges remain, these interventions may eventually lead to better approaches to treat or prevent heart failure.     

双曲美他嗪治疗60例心肌梗死后心力衰竭临床观察

目的观察曲美他嗪治疗心肌梗死后心力衰竭的临床疗效。方法60例心肌梗死后心力衰竭患者随机分为观察组与治疗组。观察组行常规药物治疗,治疗组在常规治疗的基础上加用曲美他嗪20mg／次,3次／d,30d为1疗程。观察治疗前后心功能改变与心脏超声多普勒心功能指标变化。结果治疗后治疗组心功能改善总有效率为93．3％,观察组心功能改善总有效率为80．0％,两组差异有统计学意义（P〈0．05）。左心室射血分数（LVEF）及左心室短轴缩短率（FS）,治疗后治疗组较观察组明显增加,自身对照两组治疗后左心室收缩末期内径（LVSD）、左心室舒张末期内径（LVDD）明显降低,但治疗后两组间对比,差异无统计学意义（P〉0．05）。结论曲美他嗪治疗心肌梗死后心力衰竭可获得较好的临床疗效。     

Cardiac channelopathies.

Genetic alterations of various ion channels produce heritable cardiac arrhythmias that predispose affected individuals to sudden death. The investigation of such 'channelopathies' continues to yield remarkable insights into the molecular basis of cardiac excitability. The concept of channelopathies is not restricted to genetic disorders; notably, changes in the expression or post-translational modification of ion channels underlie the fatal arrhythmias associated with heart failure. Recognizing the fundamental defects in channelopathies provides the basis for new strategies of treatment, including tailored pharmacotherapy and gene therapy.     

门冬氨酸钾镁治疗心律失常疗效评价

为评价门冬氨酸钾镁治疗各种心律失常的临床疗效。方法：用常规１２导联心电图监测门冬氨酸钾镁治疗组和常规治疗组的心率和心律的变化，同时观察病人临床症状和体征。结论门冬氨酸闰是治疗各种心律失常包括心力衰竭伴心律失常有效而安全的药物。     

心血管疾病的基因治疗

基因治疗在先天遗传性以及后天获得性心血管疾病治疗中均具有广阔的发展前景. 对心血管疾病致病机理的深入认识和疾病基因组学研究的发展, 进一步促进了临床前基因治疗的研究进展. 但基因治疗过程中存在的机体细胞免疫反应、外源基因表达水平不足、在体基因转导效率低下等因素都成为基因治疗临床应用转化的瓶颈. 近年来, 基因导入载体和基因组编辑技术的发展为上述问题的改善和解决提供了新的思路. 目前成族规律间隔短回文重复序列(clustered regularly interspaced short palindromic repeats, CRISPR)/Cas9 基因组编辑技术已经成功应用于动物模型的在体基因编辑, 达到了显著改善血脂指标的疗效. 进一步研究体内组织特异和高效的基因导入方式, 提高基因编辑的靶向效率和特异性, 并建立全面有效的安全评估实验体系, 将推动基因治疗向临床应用的转化. 针对心血管疾病基因治疗中基因导入载体的研究以及CRISPR/Cas9 基因组编辑技术的应用展开讨论.     

老年慢性肺源性心脏病合并多脏器功能衰竭87例的临床分析

目的 探讨慢性肺源性心脏病的病死率与多脏器功能衰竭的相关性．方法 收集87例老年慢性肺源性心脏病并发两个以上受损脏器患者的临床资料，并进行分析．结果 慢性肺心病的病死率因受损或衰竭脏器数目的增多而增高．结论 及时诊断多脏器功能衰竭，积极治疗并控制感染，逆转多脏器功能衰竭，是降低病死率的重要措施．     

伊伐布雷定的临床研究进展

伊伐布雷定是高度特异性超极化激活的环核苷酸门控通道（I f通道）阻滞剂,以剂量依赖性方式抑制If电流降低窦房结节律,由此减慢心率,而对心内传导、心肌收缩力、左室收缩功能或心室复极化无影响。目前许多临床研究表明,伊伐布雷定对冠状动脉粥样硬化性心脏病（冠心病）、心力衰竭患者的临床症状以及预后有明确的改善作用,对快速型窦性心律失常疗效确切。现对伊伐布雷定在冠心病的诊断及治疗、心力衰竭和不适当性窦性心动过速中的应用进行综述。     

33例风湿性心脏病合并妊娠的剖宫产麻醉处理

目的：探讨风湿性心脏病（以下简称风心病）合并妊娠剖宫产的麻醉处理及围术期的综合治疗。方法：对33例妊娠合并风心病剖宫产的临床资料进行回顾性分析。28例产妇选用腰麻-硬脊膜外联合麻醉（简称硬脊麻），2例选用硬膜外麻醉（简称硬外麻），1例因术前出现严重心衰及2例需同时行瓣膜置换＋取栓术而行全身麻醉（全麻）。术前、术中积极防治心衰，对已行换瓣术后的产妇围术期合理应用抗凝剂。结果：麻醉过程多数平稳，新生儿除全麻的2例病例Apgar评分在2—3分外，其余均在8分以上，母婴均安全度过围手术期，无1例死亡。仅一例因宫腔出现活动性出血，止血效果差而行全宫切除术，余病例无出现围术期大出血危情。结论：硬脊麻用于风心病合并妊娠剖宫产手术是安全有效的，术前、术中积极正确地防治心衰、改善心功能等综合治疗及围术期合理应用抗凝剂，可降低母婴死亡率。     

SUMO1-dependent modulation of SERCA2a in heart failure

The calcium-transporting ATPase ATP2A2, also known as SERCA2a, is a critical ATPase responsible for Ca(2+) re-uptake during excitation-contraction coupling. Impaired Ca(2+) uptake resulting from decreased expression and reduced activity of SERCA2a is a hallmark of heart failure. Accordingly, restoration of SERCA2a expression by gene transfer has proved to be effective in improving cardiac function in heart-failure patients, as well as in animal models. The small ubiquitin-related modifier (SUMO) can be conjugated to lysine residues of target proteins, and is involved in many cellular processes. Here we show that SERCA2a is SUMOylated at lysines 480 and 585 and that this SUMOylation is essential for preserving SERCA2a ATPase activity and stability in mouse and human cells. The levels of SUMO1 and the SUMOylation of SERCA2a itself were greatly reduced in failing hearts. SUMO1 restitution by adeno-associated-virus-mediated gene delivery maintained the protein abundance of SERCA2a and markedly improved cardiac function in mice with heart failure. This effect was comparable to SERCA2A gene delivery. Moreover, SUMO1 overexpression in isolated cardiomyocytes augmented contractility and accelerated Ca(2+) decay. Transgene-mediated SUMO1 overexpression rescued cardiac dysfunction induced by pressure overload concomitantly with increased SERCA2a function. By contrast, downregulation of SUMO1 using small hairpin RNA (shRNA) accelerated pressure-overload-induced deterioration of cardiac function and was accompanied by decreased SERCA2a function. However, knockdown of SERCA2a resulted in severe contractile dysfunction both in vitro and in vivo, which was not rescued by overexpression of SUMO1. Taken together, our data show that SUMOylation is a critical post-translational modification that regulates SERCA2a function, and provide a platform for the design of novel therapeutic strategies for heart failure.     

心力衰竭大鼠建模常用方法

在研究心力衰竭的药物治疗当中,建立可重复且贴近临床的心衰模型是非常重要的,它可以帮助我们了解药物对疾病的防治机制、药物效应和不良反应,为药物的临床应用提供依据。文献报道心衰动物模型构建方法有多种,但各具优缺点,所以根据不同的情况选择合适的方法就显得极为重要。本文就国内常用的几种实验性心力衰竭大鼠建模方法的特点做一综述。     

阿托伐他汀对冠心病慢性心力衰竭患者的心功能和预后的影响

目的:观察阿托伐他汀对冠心病慢性充血性心力衰竭患者的心功能和预后的影响.方法:选取2004年1月～2008年6月江汉大学附属医院心内科病区冠心病慢性充血性心力衰竭患者132例,随机分成治疗组(67例)和对照组(65例).两组患者均行冠心病慢性充血性心力衰竭的常规基础治疗.治疗组在常规治疗的基础上,加用阿托伐他汀10mg,每晚一次.总疗程26周.治疗前后检测血脂全套、左室射血分数(LVEF)、C反应蛋白(CRP),观察所有患者治疗后两年的住院次数、住院总日数和病死率.结果:治疗组与对照组比较,治疗6个月后,血清总胆固醇(TC),低密度脂蛋白胆固醇(LDL-C),CRP均有不同程度降低,LVEF明显提高,治疗后两年的住院次数和总日数相对减少,差异无显著性;病死率明显降低,差异有非常显著性(P<0.01).结论:阿托伐他汀治疗能改善冠心病慢性心衰患者的心功能和预后.     

p53-induced inhibition of Hif-1 causes cardiac dysfunction during pressure overload

Cardiac hypertrophy occurs as an adaptive response to increased workload to maintain cardiac function. However, prolonged cardiac hypertrophy causes heart failure, and its mechanisms are largely unknown. Here we show that cardiac angiogenesis is crucially involved in the adaptive mechanism of cardiac hypertrophy and that p53 accumulation is essential for the transition from cardiac hypertrophy to heart failure. Pressure overload initially promoted vascular growth in the heart by hypoxia-inducible factor-1 (Hif-1)-dependent induction of angiogenic factors, and inhibition of angiogenesis prevented the development of cardiac hypertrophy and induced systolic dysfunction. Sustained pressure overload induced an accumulation of p53 that inhibited Hif-1 activity and thereby impaired cardiac angiogenesis and systolic function. Conversely, promoting cardiac angiogenesis by introducing angiogenic factors or by inhibiting p53 accumulation developed hypertrophy further and restored cardiac dysfunction under chronic pressure overload. These results indicate that the anti-angiogenic property of p53 may have a crucial function in the transition from cardiac hypertrophy to heart failure.     

基因治疗及其研究进展

基因治疗作为一种新型的疾病治疗手段 ,正在广泛用于血友病、糖尿病、癌症、心血管病、爱滋病等多种疾病的治疗领域 .基因治疗的一般步骤包括 :目的基因的转移和目的基因的表达两个方面 .其中目的基因的导入和目的基因表达的精确调控是两个关键步骤 .新发展的还有反义疗法以及应用核酶进行基因治疗等 .本文就基因治疗的基本步骤、基因治疗的对象、方式及基因治疗的现状和前景作一个简单介绍     

曲美他嗪联合麝香保心丸治疗慢性心力衰竭疗效的系统评价

目的：系统评价常规治疗基础上加用曲美他嗪联合麝香保心丸治疗慢性心功能不全的疗效。方法：系统检索CochraneLibrary、ProQuestResearchLibrary、MEDLINE、Embase、PEDro、OpenSIGLE、Na—tionalTechnicalInformationService（NTIS）、ScienceDirect、CNKI、VIP、WanfangData、CBM,文献检索日期截止于2013年4月30日。收集常规治疗基础上加用曲美他嗪联合麝香保心丸治疗慢性心功能不全的随机对照试验（RCT）,按纳入和排除标准由2名评价者独立选择试验提取资料,交叉核对并进行方法学质量评估,对纳入研究的文献采用RevMan5．2软件进行Meta评价。结果：共纳入6项研究387例患者,Meta分析4个主要结局的结果显示：左心室射血分数（LVEF）改善方面、左室舒张末期内径（LVEDD）改善方面、左室收缩末期内径（LVESD）改善方面、6min步行距离改善方面的比较,其差异均有统计学意义。WMD（95％CI）分别为5．99（5．90,6．08）、-5．04（-5．90,-4．19）、-4．6（-8．59,-0．64）、42．73（32．48,52．97）,均无不艮反应。4个主要结局的倒漏斗图显示左右不对称,提示可能存在发表性偏倚。结论：现有证据显示曲美他嗪联合麝香保心丸治疗慢性心力衰竭的疗效明显,左心室射血分数、左室舒张末期内径、6min步行距离、左室收缩末期内径的改善明显。受纳入文献质量的限制,其治疗慢性心力衰竭疗效的评价期待更多高质量的随机对照双盲研究,以进行进一步的评价。     

基因治疗及其研究进展情况

本文综述了基因治疗的步骤,基因治疗的对象及基因治疗的现状及前景。基因治疗的步骤包括基因诊断;治疗基因与载体的连接;基因转移。其中载体是基因治疗中的一个重大关键技术问题。目前基因治疗已进入理性化阶段,世界上许多国家对基因治疗前景看好,投资加强。     

HSVTK gene therapy for carcinoembryonic antigen-producing human lung cancer cells

The long-term success of gene therapy for cancer relies heavily on the development of effective targeting systems. We investigate the possibility of targeted gene therapy using promoter of carcinoembryonic antigen (CEA) gene. By using luciferase reporter gene, we found that CEA promoter exhibit 16 times high activity in CEA-producing lung cancer cells, A549 than in nonproducing cells, Hela. We also constructed a recombinant expression plasmid pCEATK, in which CEA promoter drives the effector gene, thymidine kinase gene of Herpes Simplex Virus (HSVTK). A549 cells transfected with pCEATK became 865 times more sensitive to ganciclovir (GCV) than the control cells. However, Hela cells transfected with this plasmid remained resistant to GCV. These data indicate the potential for targeted gene therapy using the CEA promoter against CEA-producing tumor cells, such as lung cancer cells. Foundation item: Supported by the National Natural Science Foundation of China Natural Science Foundation of Hubei Province Biography: XIAO Geng-fu(1966-), male, phD graduate candidate, Lecturer.