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充血性心力衰竭复发控制对策
充血性心力衰竭(心衰,congestive heart failure,CHF)是极为常见而严重的临床综合征,是各种病因心血管病的严重阶段,患病率、死亡率高,5年存活率与恶性肿瘤相仿[1].CHF是一个公众健康问题,是导致劳动丧失、病残、死亡的重要原因,是老年人住院的常见原因.据统计约有80%~90%心衰的发生是由于诱因诱发的[1].因此,了解和控制诱因,对防治心衰有重要意义.我们于1999~2000年在我科收治的100例CHF患者复发的诱因进行了分析,现报告如下.
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小儿重症肺炎合并心力衰竭、肺水肿及脑水肿1例
患儿,女,2岁,因颜面青紫6 h,神志不清4 h人院.入院前6 h突然哭闹不安,颜面青紫,呛咳,呼吸急促.无发热、呕吐、腹泻或浮肿.入院体查:T 36℃,P 180次/min,R 54~次/min,BP 92/59 mmHg.急性危重病容,昏迷,面色青紫,双侧瞳孔等大等圆,直径约1.5 mm,对光反射存在,鼻翼扇动,唇发绀,双肺满布中、细湿罗音.心率180次/min,律齐,心音有力,无杂音.四肢肌张力低下.入院后立即予吸氧、拍背吸痰.胸片示右上肺叶不张,行支气管镜检查,呼吸道内有大量分泌物,未发现异物.头部CT检查未见明显异常.入院5.5 h胸片复查,两肺广泛斑片状阴影,诊断为肺水肿、肺出血,与第1次胸片对照,心脏明显扩大.
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AIM:To examine and compare the effects of several ARBs that are widely used in clinics , on the ACE-Ang II-AT1 receptor and the ACE2-Ang(1-7)-Mas axis during the development of cardiac remodeling after pressure overload .METHODS: All of the mice used in the study underwent transverse aortic constriction (TAC) or sham operation for 2 or 4 weeks.A solution of either ARBs or sa-line was administered through a stomach tube 3 days before the operation .Meanwhile , to eliminate the influence of Ang II , a recombi-nant adenovirus expressing small interfering RNAs targeting angiotensinogen ( Ad-ATG siRNA) was injected via the tail vein .The sur-gery was then performed and the drug was administered as mentioned above .Cardiac function and remodeling were evaluated by echo-cardiography , hemodynamic measurements and cardiac histology .Western blotting was used to determine the protein expression levels . Meanwhile , we performed similar experiments using ARBs with or without ATG siRNA in cardiomyocytes induced by mechanical stretch.RESULTS:Although all of the six ARBs , none of which repressed the elevation of left ventricular pressure after TAC , attenu-ated the development of cardiac hypertrophy and heart failure in the wild-type mice, the degree of attenuation by Olmesartan , Candesar-tan and Losartan tended to be larger than that of the other three drugs tested .Additionally , the degree of downregulation of the ACE-Ang II-AT1 axis and upregulation of the ACE2-Ang(1-7)-Mas axis was higher in response to Olmesartan, Candesartan and Losartan administration in vivo and in vitro.Additionally, Olmesartan had a larger influence when administered long term .However, the expres-sion of ACE was not influenced by the administration of ARBs in vivo and in vitro.Moreover, in angiotensinogen-knockdown mice, TAC-induced cardiac hypertrophy and heart failure were inhibited by Olmesartan , Candesartan and Losartan but not by Telmisartan , Valsartan and Irbesartan administration .Furthermore , only Olmesartan and Candesartan could downregulate the ACE-Ang II-AT1 axis and upregulate the ACE2-Ang(1-7)-Mas axis in vitro.CONCLUSION: Olmesartan, Candesartan and Losartan could effectively in-hibit pressure overload-induced cardiac remodeling even when with knockdown of Ang II , possibly through upregulation of the expres-sion of the ACE2-Ang(1-7)-Mas axis and downregulation of the expression of the ACE-Ang II-AT1 axis.In contrast, Telmisartan, Valsartan and Irbesartan only played a role in the presence of Ang II , and Losartan had no effect in the presence of Ang II in vitro.
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AIM:Cytochrome P450 epoxygenase 2J2 and epoxyeicosatrienoic acids ( EETs) are known to protect against cardiac hypertrophy and heart failure, which involve activation of 5′-AMP-activated protein kinase ( AMPK) and Akt.Although the functional roles of AMPK and Akt are well established , the significance of crosstalk between them in the development of cardiac hypertrophy and anti -hy-pertrophy of CYP2J2 and EETs remains unclear .Here, we investigated whether CYP 2J2 and its metabolites EETs protected against cardiac hypertrophy by activating AMPKα2 and Akt1.Moreover, we tested whether EETs enhanced crosstalk between AMPKα2 and phosphorylated Akt1 ( p-Akt1), and stimulated the nuclear translocation of p-Akt1, to exert their anti-hypertrophic effects. METHODS:The recombinant rAAV9 vector was coupled to CYP2J2 and the rAAV9-CYP2J2 construct was injected into the caudal vein of AMPKα2-/-and littermate control mice .AMPKα2 -/-and littermate control mice that overexpressed CYP 2J2 in heart were treated with angiotensin II (Ang II) for 2 weeks.Hemodynamic and cardiac functions were also evaluated after 14 days of infusion with Ang II or saline.RESULTS:Interestingly, the overexpression of CYP2J2 suppressed cardiac hypertrophy , including decreased heart size, cross sectional area of cardiomyocytes , markers of cardiac hypertrophy [ brain natriuretic peptide ( BNP) ,β-myosin heavy chain (β-MHC) and skeletal muscle α-actin (ACTA1)] and increased levels of atrial natriuretic peptide (ANP) in the heart tissue and plasma of wild-type mice but not AMPKα2 -/-mice.Measurement of left ventricular ejection fraction and fractional shortening showed that CYP2J2 overexpression prevented Ang II-induced ventricular systolic dysfunction in mice .Moreover, an Ang II-induced reduction in cardiac function, demonstrated by decreased dp/dtmax and dp/dtmin, was prevented by overexpression of CYP2J2.Mechanistically, the CYP2J2 metabolites 11,12-EET activated AMPKα2 to induce the nuclear translocation of p-Akt1, which increased production of ANP and thereby inhibited the development of cardiac hypertrophy .Furthermore , by co-immunoprecipitation analysis , we found that full-length Akt1 and an Akt1 fragment containing amino acids 150-408, which constitute the protein kinase domain , but not other frag-ments of Akt1, bind to the AMPKγ1 subunit.AMPKα2β2γ1 and p-Akt1 interact through the direct binding of the AMPKγ1 subunit to the Akt1 protein kinase domain.This interaction was enhanced by 11,12-EET.CONCLUSION:Our studies reveal a novel mechanism in which CYP2J2 and EETs enhanced Akt1 nuclear translocation through interaction with AMPKα2β2γ1 and protect against cardiac hy-pertrophy and suggest that overexpression of CYP 2J2 might have clinical potential to suppress cardiac hypertrophy and heart failure .
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AIM:Programmed necrosis ( necroptosis ) and apoptosis are crucially involved in multiple severe cardiac pathological conditions , including myocardial infarction, ischemia/reperfusion (I/R) injury, and heart failure.Whereas apoptotic signaling is well defined, the mechanisms underlying cardiomyocyte necroptosis remain elusive .METHODS AND RESULTS:Here we show that both mRNA and protein levels of receptor-interacting protein 3 (RIP3) in the hearts are increased by I/R injury and doxorubicin (Dox) treatment. In mice, RIP3 deficiency ameliorates myocardial necroptosis and heart failure induced by I /R (30-min ischemia/4-h or 8-week reper-fusion) or Dox treatment (20 mg/kg or 5 mg/kg ×4, i.p.).RIP3 overexpression induces cardiomyocyte necroptosis evidenced by de-creased intracellular ATP level and increased lactate dehydrogenase concentration in cell culture medium .RIP3 triggers myocardial ne-croptosis via activation of Ca2+/calmodulin-dependent protein kinase II (CaMKII), rather than the well-established RIP3 partners, RIP1 and MLKL (mixed lineage kinase domain-like protein).Specifically, our data indicate that I/R and Dox markedly activate myo-cardial CaMKII in wild-type but not RIP3-deficient mice , and that CaMKII inhibition or RIP 3 deficiency protect the heart from I/R-and Dox-induced cardiomyocyte necroptosis , cardiac remodeling and heart failure .Mechanistically , RIP3 activates CaMKII via both di-rect phosphorylation and indirect reactive oxidative species-dependent oxidation , and subsequently triggers opening of the mitochondrial permeability transition pore ( mPTP) and myocardial necroptosis .CONCLUSION: These findings identify CaMKII as a novel RIP 3 substrate and delineate a RIP3-CaMKII-mPTP myocardial necroptosis pathway , a promising target for the treatment of cardiac ischemic and oxidative damage , and heart failure .
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AIM:Mitochondrial DNA (mtDNA) copy number variation (CNV), which reflects the oxidant-induced cell damage, has been observed in a wide range of human diseases .However, whether it correlates with heart failure , which is closely related to oxidative stress, has never been elucidated before .We aimed to systematically investigate the association between leukocyte mtDNA CNV and heart failure risk and prognosis .METHODS: A total of 1 700 hospitalized patients with heart failure and 1 700 age-and gender-matched community population were consecutively enrolled in this observational study , as well as 1 638 ( 96.4%) patients were fol-lowed prospectively for a median of 17 months (12~24 months).The relative mtDNA copy number in leukocyte of peripheral blood or cardiac tissue was measured in triplicate by quantitative real-time PCR method .RESULTS:Patients with heart failure possessed much lower relative mtDNA copy number compared with control subjects (P<0.01), especially for the patients with ischemic etiology (P<0.01).Patients with lower mtDNA copy number exhibited 1.7 times higher risk of heart failure ( P<0.01).Long-term follow-up (median 17 months) showed that decreased mtDNA copy number was significant associated with both increased cardiovascular deaths (P<0.01) and cardiovascular rehospitalization (P<0.01).After adjusted for the conventional risk factors and medications , lower mtDNA copy number were still significantly associated with 50% higher cardiovascular mortality (P <0.05).CONCLUSION:
mtDNA copy number depletion is an independent risk factor for heart failure and predicted higher risk of cardiovascular deaths in patients with heart failure . -
血管紧张素Ⅱ受体拮抗剂治疗充血性心力衰竭的研究进展
血管紧张素Ⅱ受体拮抗剂是近年来国际上研究的热点之一[1,2],目前此类药物已在我国上市,下面对其特点及其治疗充血性心力衰竭(Congesitve Heart Failure,CHF)予以总结. 肾素-血管紧张素系统肾素-血管紧张素系统(Renin-Angiotensin.System,RAS)在血压调节过程中起着重要的作用,肝脏合成血管紧张素原,在肾素作用下,转化为血管紧张素I(Ang I),再在肺脏产生的转换酶作用下,变成血管紧张素Ⅱ(Ang Ⅱ).除循环中的AngⅡ起作用外,通过自分泌/旁分泌的局部AngⅡ在不同器官也起着重要的作用,其结果为血管收缩,血压升高,并引起靶器官的损害.
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卡维地洛在充血性心力衰竭中的应用及可能机制
充血性心力衰竭(congestive heart failure, CHF)是复杂严重的临床综合征,是各种心血管疾病(如高血压、心肌梗死、慢性心肌缺血、瓣膜病等)的终末阶段。随着细胞与分子心脏病学的研究进展,对心力衰竭病理生理机制的认识不断深入,Packer[1]等提出,充血性心力衰竭是心脏泵功能障碍引起的,以神经内分泌紊乱为主要特点的临床综合征,亦即CHF激活了神经内分泌系统,后者又进一步加速CHF的发展。Packer的观点得到了许多同行的认同,并随着社会的进步和医学的发展不断完善,如细胞凋亡、细胞因子及氧自由基在心衰中的作用。
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摘译)XXⅡ届洲心脏学会学术年会专题报道(Ⅸ)Cleland JGF:基层的心衰处理">(转载自中国科学院医学信息研究所"心血管病研究展望”2001年1月第16~17期余国膺摘译)XXⅡ届洲心脏学会学术年会专题报道(Ⅸ)Cleland JGF:基层的心衰处理
心衰常见,致残、致命.但更重要的是,它是可治的.当前,这些病人很在姝医疗工作由基层承担.但准确诊断和有效治疗心衰都是复杂的.所以有些基层医生(PCP)问,他们是否应继续承担这些病的医疗?心脏专科医生是否应承担医院内医疗和基层治疗两部分? ESC会议安排了这问题的专题讨论.由欧洲心脏学会心衰小组中的诊断研究组开展的一项名为IMPROVE-MENT的十分详尽的调查提供了大量资料(the Improvement of HFnmtiative.Fur J Heart Failure.1999;1:139).它观察14个欧洲国家1300名基层医生以及他们的>11000例病人.它补充了目前在26个国家进行着的探讨二级医疗单位心衰治疗的Euro Heart Failure Surrey(Cleland J et al.Tne Euro Heart Failure Survey of the Euro HEART survey Programme:a survey on the quality of pts with heart failure in Europe.Eur JHeart failure2000;2:123).
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能量代谢治疗与心力衰竭
心力衰竭是绝大部分心脏病的后转归,尽管其治疗药物和疗法在不断进步,但其死亡率仍居高不下,预后还很差.1年的再人院率为40%住院病人1年内死亡率40%,尤其是近年心衰发病率在增加目前在美国的心衰病人约有4,500,000(National Health and Nutrition Examination Survey Ⅲ,1988-94)估计每年有400,000新病例(Source:excerpt from NHLBI,Congestive Heart Failure Data Fact Sheet:NHLBI).ESC对47个欧洲国家近10亿人口中心衰发病率约5%即5000万.心衰发生率增加与相关危险因素如吸烟、糖尿病、高血压、高血脂、腹型肥胖增加,冠心病增加,老龄人口增加有关.
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急性心力衰竭治疗的现状和进展
随着慢性心衰人群的不断增加,因失代偿性心衰住院的患者人数也同时增加.超过15万人数的美国急性失代偿性心衰注册研究(ADHERE)的结果表明,导致急性失代偿性心衰(AHF)的病因中缺血性心脏病占60%,大约50%表现为左室功能正常,同时合并糖尿病和房颤的分别占44%和31%.大约90%的AHF患者存在呼吸困难,胸片显示有肺淤血者占74%,外周水肿者占65%,大约30%的患者合并肾功能不全.AHF的预后极为不良,美国住院期间的死亡率为4.7%,6~12月内升至20%~40%,而30天内再住率院为20%.
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失代偿性心衰治疗研究进行时
目睹近在降低与慢性心衰相关的死亡率方面取得极大进展的同时,人们似乎忽略了失代偿性心衰(decompensated heart failure,DHF)治疗方法的进步,这一点可以从有限的治疗设备以及同样不多见的有根据的文献报道中得到证实.
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回眸2009年心力衰竭诊断与治疗的进展
随着大多数心血管疾病患者的生存期延长和人类社会的老龄化倾向,心力衰竭(以下简称心衰)的患病率和致死率均不断增高,防治工作越来越重要.本文回眸2009年度中心衰诊断与治疗的进展.
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β受体阻滞剂在慢性心力衰竭治疗中的应用进展
慢性充血性心力衰竭(Chronic Heart Failure,CHF)是由于各种病因导致的心肌损害而引起心脏结构和功能的改变,终导致心脏泵功能衰竭所形成的一组严重的临床综合征.是各种器质性心脏病终末阶段的主要临床表现,是心血管疾病患者住院或死亡的主要原因,也是心血管疾病治疗的重点和难点.
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每天短时透析在慢性肾脏病合并难治性心力衰竭治疗中的应用
心肾综合征(cardiorenal syndrome,CRS)是一类心功能不全与肾功能衰竭共存的严重的、致命的疾病.大多数心肾综合征患者处于心力衰竭(以下简称心衰)的难治性终末期,过重的容量负荷是导致难治性心力衰竭(refractory heart failure,RHF)的主要原因,但因合并肾功能不全,利尿效果欠佳,临床处理非常棘手,往往需要行肾脏替代疗法以减轻容量负荷.其中常用的肾脏替代疗法有常规血液透析(con-ventional hemodialysis,CHD)、连续肾脏替代疗法(continuous renal replacement therapy,CRRT)或腹膜透析(peritoneal dialy-sis,PD).上述透析方式均有其各自优劣,而每天短时透析(short daily hemodialysis,SDHD)因其具有更好的透析效能、稳定的血流动力学及患者耐受性好等特点,近年来被重新认识,可能成为慢性肾脏病(chronic kidney disease,CKD)合并RHF的一种更有效的透析方式.本文将对每天短时透析对慢性肾脏病合并RHF治疗的应用情况作一综述.
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血尿酸与慢性心力衰竭关系的研究进展
自Gertler等1951年首次提出尿酸(uric acid,UA)与心血管疾病存在相互关系后[1],大量的流行病学研究表明高尿酸血症(hyperuricemia,HUA)是高血压、高血脂、冠心痛及心力衰竭等心血管疾病的独立危险因素,慢性心力衰竭(chronic heart failure,CHF)作为心血管疾病的共同转归,与其发生、发展、预后有着密切的关系.
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调控细胞凋亡治疗慢性心力衰竭
慢性心力衰竭(chronic heart failure,CHF)是指各种原因引起心脏泵功能受损,致使心输出量减少,不能满足机体组织代谢需要,通常又称充血性心力衰竭.随着冠心病急性期病死率的下降和人口的老龄化,CHF的发病率显著上升,CHF已经成为严重影响老年人生活质量的疾病,也是导致老年人死亡的重要原因之一.
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中枢性睡眠呼吸暂停与慢性心衰
中枢性睡眠呼吸暂停(central sleep apnea, CSA)是指在睡眠中出现口鼻无气流、并且胸腹呼吸运动停止10 s以上.纯粹的CSA(即CSA指数大于5/h,且无其他类型呼吸暂停)远不如阻塞性睡眠呼吸暂停(OSA)常见,CSA常与其他形式呼吸暂停同时出现但可以是CSA占优势型.许多CSA以陈-斯氏呼吸(Cheyne-Stokes respiration, CSR)的形式出现,CSR、CSA在慢性心衰(chronic heart failure, CHF)的患者中常见,CHF患者CSR-CSA的发病率高达40%~50%[1],由于老年人群更易患多种慢性疾患,如CHF、脑血管疾病、神经肌肉疾病及呼吸肌疲劳等,故CSR-CSA在老年人群中的发病率可能更高.
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心力衰竭的起搏治疗
充血性心力衰竭(congestive heart failure,CHF)是常见而难治的心脏疾病,是各种心脏疾病的主要死亡原因.尽管药物治疗,尤其是ACEI和β受体阻滞剂的应用已使CHF患者的生存期和生活质量得到明显改善,但对心功能NYHA Ⅲ~Ⅳ级患者预后仍差;心脏移植由于供体的缺乏和排斥反应限制了它的应用;人工心脏仍处于实验和计划阶段;近年来双心室起搏的应用,为治疗CHF提供了新的途径,取得了初步成果.
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正性肌力药物和利尿剂在治疗心力衰竭中的应用
正性肌力药物和利尿剂是治疗心力衰竭的传统用药.在强调充分应用血管紧张素转换酶抑制剂(ACEI)和β受体阻滞剂的基础上,合理应用正性肌力药物和利尿剂,对控制心力衰竭的症状和体征,降低住院率有重要的作用.