DNA损伤及氧化应激在放射性心脏损伤中的作用

 放射性心脏损伤（RIHD）是放射诱导的一种进行性加重的疾病,它几乎影响心脏所有结构,从而产生一系列心脏并发症。从早期的无症状到慢性心力衰竭,常需几年至十几年时间。近年来文献报道心脏在正常组织耐受剂量控制下,常规胸部放疗所致的心脏损伤,特别是迟发型心肌损伤问题日益突出。本文综述了DNA损伤及氧化应激在RIHD的发生发展中的作用,现有研究认为RIHD可使心脏僵硬度增加、心肌收缩及舒张功能下降,引起心肌电生理紊乱、心律失常、心功能不全甚至猝死。但目前尚缺乏对RIHD的有效治疗,其根本原因在于对RIHD的原因及发病机制尚未完全阐明。     

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。     

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.     

老年人肺心病多器官衰竭84例分析

分析84例老年人肺心病呼吸衰竭患者并发多器官衰竭、累及器官数目与病死率是正相关关系，累及2—5个器官死亡率分别为34．3％、65．4％、86．7％、100％，其中并发肺性脑病最多，但病死率较低。而肾功能进行性加重预后不佳。揭示老年肺心病患者病程较长，各器官功能减退、免疫功能低下，是导致肺心病多器官衰竭的重要死亡原因。     

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.     

Dystrophic heart failure blocked by membrane sealant poloxamer

Dystrophin deficiency causes Duchenne muscular dystrophy (DMD) in humans, an inherited and progressive disease of striated muscle deterioration that frequently involves pronounced cardiomyopathy. Heart failure is the second leading cause of fatalities in DMD. Progress towards defining the molecular basis of disease in DMD has mostly come from studies on skeletal muscle, with comparatively little attention directed to cardiac muscle. The pathophysiological mechanisms involved in cardiac myocytes may differ significantly from skeletal myofibres; this is underscored by the presence of significant cardiac disease in patients with truncated or reduced levels of dystrophin but without skeletal muscle disease. Here we show that intact, isolated dystrophin-deficient cardiac myocytes have reduced compliance and increased susceptibility to stretch-mediated calcium overload, leading to cell contracture and death, and that application of the membrane sealant poloxamer 188 corrects these defects in vitro. In vivo administration of poloxamer 188 to dystrophic mice instantly improved ventricular geometry and blocked the development of acute cardiac failure during a dobutamine-mediated stress protocol. Once issues relating to optimal dosing and long-term effects of poloxamer 188 in humans have been resolved, chemical-based membrane sealants could represent a new therapeutic approach for preventing or reversing the progression of cardiomyopathy and heart failure in muscular dystrophy.     

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.     

前列腺素E1治疗肺心病合并心力衰竭40例疗效观察

目的：探讨前列腺素E1在肺心病心衰中的治疗作用。方法：对本院1997年6月至200l年6月80例肺心病心衰患进行随机对比性研究、分析。结果：治疗一疗程后，治疗组总有效率92．5％，对照组总有效率72．5％，两组的临床疗效有显性差异。结论：肺心病心衰患使用外源性前列腺素E1可获得较好疗效。     

缺血性心脏病和扩张型心肌病患者心肺运动负荷研究

 缺血性心脏病是心力衰竭的常见病因,峰运动VO2已经广泛用于心力衰竭患者心脏储备能力的评估。本研究通过心肺运动试验（Cardiopulmonary Exercise Test,CPET）心脏储备指数、通气效能指数来评价缺血性心脏病和扩张型心肌病的心衰患者运动心肺储备功能变化。选择170例心力衰竭病人（包括100 例缺血性心脏病、70例扩张型心肌病患者）及75例正常人,进行症状限制性CPET。于运动前、运动高峰和运动后,分别测定心率和血压、峰氧耗量（Peak VO2）和VO2与预测最大VO2比例、无氧代谢阀、VE/VCO2斜率（通气效能指数）。结果显示,缺血性心脏病和扩张型心肌病患者左室射血分数相似,血压和静态心率无明显差异, 运动心率明显下降,峰氧摄取量、无氧阈值、VE/VCO2斜率与扩张型心肌病患者相比有显著差别（P＜0.05）,峰心率明显低于扩张性心肌病。但峰氧耗量/预测峰氧耗量比例无明显差别。45例病人运动心率未达到标准。研究表明,缺血性心脏病患者心肺运动负荷测定的运动高峰VO2、无氧阀值及VE/VCO2斜率提示缺血性心脏病患者运动时通气效能和运动耐力下降比扩张型心肌病患者更为显著。     

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。     

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．     

Fulminant hypertension in transgenic rats harbouring the mouse Ren-2 gene

PRIMARY hypertension is a polygenic condition in which blood pressure is enigmatically elevated; it remains a leading cause of cardiovascular disease and death due to cerebral haemorrhage, cardiac failure and kidney disease. The genes for several of the proteins involved in blood pressure homeostasis have been cloned and characterized, including those of the renin-angiotensin system, which plays a central part in blood pressure control. Here we describe the introduction of the mouse Ren-2 renin gene into the genome of the rat and demonstrate that expression of this gene causes severe hypertension. These transgenic animals represent a model for hypertension in which the genetic basis for the disease is known. Further, as the transgenic animals do not overexpress active renin in the kidney and have low levels of active renin in their plasma, they also provide a new model for low-renin hypertension.     

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。     

Atherosclerosis

Atherosclerosis, a disease of the large arteries, is the primary cause of heart disease and stroke. In westernized societies, it is the underlying cause of about 50% of all deaths. Epidemiological studies have revealed several important environmental and genetic risk factors associated with atherosclerosis. Progress in defining the cellular and molecular interactions involved, however, has been hindered by the disease's aetiological complexity. Over the past decade, the availability of new investigative tools, including genetically modified mouse models of disease, has resulted in a clearer understanding of the molecular mechanisms that connect altered cholesterol metabolism and other risk factors to the development of atherosclerotic plaque. It is now clear that atherosclerosis is not simply an inevitable degenerative consequence of ageing, but rather a chronic inflammatory condition that can be converted into an acute clinical event by plaque rupture and thrombosis.     

多维时序模型及其在人口死亡预报中的应用

本文讨论了多维时序模型的四个最基本的系统特性和统计特性的表述形式,建立了人口总死亡数、心脏病患者和肿瘤患者死亡数的“多输入-单输出”形式的多维时序模型,并进行了预报.结果表明,前两者受气象因素的影响,而后者基本与气象因素无关.     

Myocardial gene therapy.

Gene therapy is proving likely to be a viable alternative to conventional therapies in coronary artery disease and heart failure. Phase 1 clinical trials indicate high levels of safety and clinical benefits with gene therapy using angiogenic growth factors in myocardial ischaemia. Although gene therapy for heart failure is still at the pre-clinical stage, experimental data indicate that therapeutic angiogenesis using short-term gene expression may elicit functional improvement in affected individuals.     

87例肺心病死亡原因分析

本文对87例慢性肺原性心脏病(简称肺心病)死亡原因做了回顾性分析,结果表明:全部死亡病例的诱发因素均为呼吸道的反复感染,且死亡之前均有水电解质和酸碱平衡紊乱:直接死亡原因以肺性脑病为最多,占54.0％;休克次之,占24.1％;消化道出血占18.4％。因此在治疗肺心病的全过程中,在积极抗炎的同时要时刻注意调整内环境的稳定,防止上述重要并发症的发生,对阻抗肺心病的恶向演变至关重要。     

老年冠心病合并退行性心瓣膜病对左室重构的影响

本文探讨合并退行性心瓣膜病对老年冠心病患者心脏结构与功能的影响.作者测定了80例老年冠心病合并退行性心瓣膜病者和80例老年冠心病患者的心脏超声指标结果,方差分析两组上述指标的差异,卡方检验比较两组心衰和左室重构的发生率.结果表明,两组在心脏结构和功能及心律失常等方面存在统计学差异,合并退行性瓣膜病组的左室重量指数较大,心功能较差,心衰发生率高.从而得到退行性心瓣膜病变能促进老年冠心病患者心脏重构的发生,促进心衰的发生的结论.