组织多普勒技术对美托洛尔治疗前后的左室舒张功能的评价

目的应用组织多普勒成像(TDI)技术测量室间隔、侧壁等的舒张、收缩速度,评价美托洛尔对左室舒张功能的影响。方法原发性高血压(EH)左室肥厚患者23例,在服用美托洛尔2mg·kg-1·d-1前后,用TDI法分别测其二尖瓣环水平间隔、侧壁、前壁、下壁的收缩期峰值速度(Sm),舒张早期峰值速度(Em),舒张晚期峰值速度(Am),比较用药前后各部位Em/Am比值。结果服用美托洛尔3个月后,患者舒张功能均有明显改善。EH组左室各部位心肌Em增大,Am减少,Em/Am均明显提高。结论美托洛尔能够改善肥厚心肌的舒张功能,二尖瓣环水平的Em、Am的测定能克服二尖瓣血流的假性正常化,对用药后的变化也能够敏感地表现出来,可作为定量无创评价左室舒张功能的良好指标。     

新建中复脉汤治疗舒张性心力衰竭的临床观察

目的观察新建中复脉汤对舒张性心力衰竭病人的临床疗效。方法 60例舒张性心力衰竭病人随机平均分成两组,治疗组在对照组基础上加用新建中复脉汤。观察两组临床疗效,超声心动图检测舒张早期二尖瓣血流峰值/舒张晚期二尖瓣血流峰值(E/A比值);E峰减速时间(Dt值)和等容舒张时间(IVRT);收缩期S波/舒张期D波;二尖瓣口血流频谱E峰速度/二尖瓣环舒张早期E’峰速度(E/E’比值);左房容积指数(LAVI)等左室舒张功能参数。结果两组治疗后临床症状及左室舒张功能参数均有明显改善,与治疗前比较,差异有统计学意义(P0.05)。而治疗组疗效明显优于对照组(P0.01)。结论新建中复脉汤联合常规西药治疗气虚血瘀型舒张性心力衰竭,能改善临床症状及超声心动图左室舒张功能参数,对舒张性心力衰竭有良好的治疗效果。     

新西兰兔腹主动脉缩窄术后心肌收缩和舒张功能的变化

目的观察新西兰兔腹主动脉缩窄术后不同时间点心肌收缩和舒张功能的变化。方法30只新西兰兔随机分为2组:手术组(20只)行腹主动脉缩窄术,假手术组(10只)作为对照。术后观察兔精神状态、饮食、活动等变化。手术前后监测血流动力学变化并定期行超声心动图检查。结果术后4周,手术组出现心室肥厚,等容舒张时间延长。术后8周,组织多普勒提示二尖瓣舒张早期血流峰速与舒张晚期血流峰速比值和心肌收缩期血流峰速降低,左心室舒张末压升高(P<0.05);而射血分数无显著差异。结论腹主动脉缩窄术后可造成舒张功能的损伤,同时也伴有轻度收缩功能的损伤。     

组织速度成像技术评价糖尿病患者左室舒张功能的临床应用

目的探讨组织速度成像技术评价糖尿病患者左室舒张功能的临床应用。方法66例糖尿病患者分为单纯糖尿病组(DM组,36例)与糖尿病合并左室肥厚组(DM LVH组,30例)两组,设正常健康人38名为对照组。应用组织速度成像技术于二尖瓣环与侧壁交界处测量二尖瓣环舒张早期峰值运动速度(Em)与舒张晚期峰值运动速度(Am);应用常规超声心动图脉冲多普勒超声检查,测量二尖瓣口舒张早期血流速度(E)、舒张晚期血流速度(A);计算Em/Am、E/A和E/Em比值。结果①两组糖尿病患者Em显著低于正常对照组(P<0.01),DM LVH组Em又显著低于DM组(P<0.05);②两组糖尿病患者的E/A≤1与Em/Am≤1检出率显著高于正常对照组,而且各组应用组织速度成像方法检出率明显高于应用常规脉冲多普勒方法(P<0.01);③两组糖尿病患者E/Em显著高于正常对照组,而DM LVH组E/Em又显著高于DM组(P<0.01)。结论组织速度成像技术通过测量二尖瓣环运动速度可以评价糖尿病患者的左室舒张功能,结合传统脉冲多普勒测量二尖瓣口血流速度,可以提高评价糖尿病患者左室舒张功能的准确性。     

慢性心力衰竭的左心室舒张功能检测

目的探讨舒张性心力衰竭(心衰)与收缩性心衰的超声特点。方法选择舒张性心衰患者40例为舒张性心衰组,并选择基本情况与之匹配的收缩性心衰患者40例为收缩性心衰组。应用多普勒技术进行舒张功能的检测,进而评价2组在心房、心室容积,二尖瓣口血流舒张早期流速(E)与二尖瓣口血流舒张晚期流速(A)及其比值(E/A)和E峰减速时间,二尖瓣环舒张早期峰值速度(e)和二尖瓣环舒张晚期峰值速度(a)及其比值(e/a),左心房反流入肺静脉血流速度,P波终末电势等方面的差异。结果舒张性心衰组与收缩性心衰组比较,E/A、e/a倒置。舒张性心衰组E峰减速时间延长,左心房反流入肺静脉血流速度增宽。舒张性心衰组左心房增大,左心室舒张末径正常。P波终末电势负值增大。结论肺静脉血流频谱和二尖瓣环组织多普勒可作为二尖瓣血流频谱重要补充。     

组织多普勒成像联合血浆N末端B型钠尿肽原评价左心室舒张功能

目的应用组织多普勒成像技术结合血浆N末端B型钠尿肽原（NT—proBNP）共同评价左心室舒张功能。方法随机选择120例左心室舒张性心力衰竭患者为研究组,120例心功能rF常且无心力衰竭症状和依据的患者为对照组。分别测取患者血浆NT—proBNP水平、左心室射血分数（排除收缩性心力衰竭患者）,二尖瓣血流频谱舒张早期速度（E）和二尖瓣血流频谱舒张晚期速度（A）并计算其比值E／A,二尖瓣环室间隔舒张早期峰值速度（Esep）和左心室游离壁舒张早期峰值速度（Elat）,两者的均值作为二尖瓣环舒张早期速度（Em）,并计算二尖瓣血流频谱舒张早期速度E和二尖瓣环舒张早期速度Em的比值E／Era,综合评价左心室舒张功能。结果研究组与对照组比较,平均血浆NT—proBNP水平增高（P〈0．01）,E／Era增大（P〈0．01）,E／A减小（P〈0．01）。研究组、对照组患者的平均血浆NT—proBNP水平与E／Era呈正相关。利用E／Em检出左心率舒张性心力衰竭阳性率高于E／A,联合NT—proBNP和E／Em诊断左心室舒张性心力衰竭阳性预测值为94％,阴性预测值为83％。结论血浆NT—proBNP水平与组织多普勒成像左心室舒张功能参数E／Em之间存在明显的相关性,联合NT—proBNP和E／Em较E／A能更好的诊断左心室舒张忡心力衰竭。     

原发性干燥综合征对左心结构及功能影响

目的探讨原发性干燥综合征对左心结构及功能的影响。方法选取成都市第三人民医院2010年10月至2014年2月收治的原发性干燥综合征患者120例。另外,选择与患者组年龄及性别匹配的健康对照组120例。经胸超声心动图检测左心大小、左心室收缩功能、舒张功能、肺动脉压、瓣膜反流及心包积液。结果病例组与对照组相比,左心房(LAD)增大,差异有统计学意义(P0.05);两组左心室(LVD)比较,差异无统计学意义(P0.05);两组二尖瓣口舒张晚期血流速度峰值(A)、二尖瓣口舒张早期血流速度峰值/二尖瓣口舒张晚期血流速度峰值(E/A)、二尖瓣环舒张早期运动速度峰值(Em)、二尖瓣环舒张晚期运动速度峰值(Am)、Em/Am、E/Em比较,差异均有统计学意义(P0.05);两组左心室射血分数比较,差异无统计学意义(P0.05)。病例组心包积液及肺动脉高压较对照组发病率增高;二、三尖瓣反流发生率大于对照组,差异有统计学意义(P0.05)。结论原发性干燥综合征易导致左心结构及功能受累。左心室舒张功能不全、肺动脉高压、心包积液、瓣膜反流、左心房增大是常见受损表现。需重视其潜在的心血管风险。     

组织多普勒超声评价冠状动脉狭窄患者左心室舒张功能

目的探讨组织多普勒超声评价冠状动脉不同狭窄程度对左心室舒张功能的影响。方法在我院行冠状动脉造影检查的患者219例,根据造影结果分为3组,冠状动脉病变严重组(至少1支血管狭窄≥70%,A组),冠状动脉病变轻微组(血管狭窄70%,B组)和冠状动脉造影检查正常组(C组)。应用超声测量冠心病患者二尖瓣舒张早期血流峰值(E)与组织多普勒成像二尖瓣环舒张早期峰值(Em)的比值(E/Em)。结果 A组的E/Em较B、C组高,差异有统计学意义(P0.05,P0.01),B组与C组比较,E/Em差异无统计学意义(P0.05)。结论E/Em可检测出冠状动脉高度狭窄引起的左心室功能障碍。     

组织多普勒成像技术对2型糖尿病病人心脏舒张功能的评价

目的应用组织多普勒成像技术(TDI)评价2型糖尿病病人心脏舒张功能。方法选择80例2型糖尿病病人为糖尿病组,同期80名正常健康人作为正常对照组,采用脉冲多普勒技术检测二尖瓣口血流频谱测量舒张早期峰值流速(E)、舒张晚期峰值流速(A)、E/A值,使用TDI检测二尖瓣环获取瓣环运动频谱,并测量其舒张早期运动速度峰值(Em)、舒张晚期运动速度峰值(Am)及Em/Am。结果与对照组比较,糖尿病病人E峰减少,A峰增加,E/A的值减少,差异有统计学意义(P0.05)。与对照组比较,糖尿病病人Em减少,Am增加,Em/Am的值减少,差异有统计学意义(P0.05)。对照组均E/A1,Em/Am1。糖尿病组,E/A1所占比例67.5%,Em/Am1所占比例91.25%。结论与测量E/A相比,使用TDI技术检测糖尿病病人Em/Am,可简单快捷、无创有效地评价糖尿病病人左心室舒张功能。     

超声心动图评价慢性间歇性低氧兔左心室功能的实验研究

目的建立慢性间歇性低氧(CIH)健康雄性新西兰大白兔动物模型,应用超声心动图评价不同左心室几何构型的左心室收缩和舒张功能。方法 65只健康雄性新西兰兔置于CIH舱内建立模拟阻塞性睡眠呼吸暂停综合征(OSAS)动物模型。造模后8周(51只兔)将左心室几何构型分为正常左心室构型(NG)组、向心性左心室重构(CR)组、向心性左心室肥厚组(CH)组和离心性左心室肥厚(EH)组,比较4组左心室收缩、舒张功能参数。结果左心室收缩功能参数:左心室射血分数(LVEF)在CR组、NG组、CH组、EH组依次降低,等容收缩时间(IVCT)、射血时间(ET)在CR组、NG组、CH组、EH组依次增加;二尖瓣环组织多普勒收缩期速度(Sm)在NG组、CR组、CH组、EH组中依次降低。左心室舒张功能参数:舒张期二尖瓣舒张早期峰值流速(E峰)、E/A、二尖瓣环组织多普勒舒张早期速度(IVS-Em)在NG组、EH组、CR组、CH组依次降低,二尖瓣环组织多普勒舒张期晚期速度(IVS-Am)、等容舒张时间(IVRT)、E峰减速时间(DT)在NG组、EH组、CR组、CH组依次升高;Em/Am在CR组、NG组、EH组、CH组依次减低,E/Em依次升高;舒张早期左室内血流播散速度(Vp)在NG组、CR组、EH组、CH组依次降低。结论 CIH早期可影响左心室收缩及舒张功能,EH左心室收缩功能受损明显,CH左心室舒张功能受损明显。     

脑钠肽结合超声多普勒评价舒张性心力衰竭患者的心功能

目的 采用血浆脑钠肽(BNP)浓度测定结合超声多普勒心动图的参数来评价舒张性心力衰竭患者的心功能,为临床提供判断舒张性心力衰竭及其严重程度的敏感和特异的客观指标.方法 选择舒张性心力衰竭患者85例(心力衰竭组),按纽约心脏病学会(NYHA)心功能分级,Ⅱ级31例、Ⅲ级36例、Ⅳ级18例,以及健康对照组30例.测定血浆BNP浓度,超声多普勒结合组织多普勒显像(TDI)测定左室结构、左室舒张功能及左室舒张末压.结果 舒张性心力衰竭患者血浆BNP浓度明显高于对照组(P<0.001),且随心力衰竭程度加重而逐渐升高(P<0.001).舒张性心力衰竭组左房内径(LA)、室间隔厚度(IVS)、左室后壁厚度(LVPW)、舒张早期流速峰值/舒张早期速度峰值(E/Em)较对照组升高,E/舒张晚期流速峰值(A)降低(P<0.01),血浆BNP浓度与E/A比值呈负相关(r=-0.634,P<0.01),与E/Em比值呈正相关(r=0.728,P<0.01).结论 血浆BNP浓度测定结合超声多普勒心动图的参数判断舒张性心力衰竭患者的心功能简便准确.     

β1肾上腺素能受体阻断剂与β2肾上腺素能受体激动剂联用对心力衰竭大鼠心功能及心肌细胞凋亡的影响

目的 在一定范围内激活β2肾上腺素能受体（AR）可以在不加重心室重构的前提下改善心力衰竭（心衰）大鼠心功能,推测β1AR阻断剂联合β2AR激动剂有可能进一步改善心衰大鼠心功能并减轻心肌细胞凋亡,该实验对此进行了研究并探讨了其机制。方法 随机选取9只雄性Wistar大鼠为对照组。将异丙基肾上腺素诱导的心衰大鼠随机分为美托洛尔组（n=11）,联合治疗组（n=11）,安慰剂组（n=10）。美托洛尔组给予美托洛尔50mg／kg,一日两次灌胃。联合治疗组给予非诺特罗125μg／kg,美托洛尔50mg／kg一日两次灌胃。安慰剂组给予等量生理盐水一日两次灌胃。对照组不予处理。治疗8周后应用超声心动图评价心功能,TUNEL法检测心肌细胞凋亡指数,测定Caspase-3酶活性,Westernblot测定bcl-2及bax蛋白质表达,测定脏器重量／体重,组织病理学测定胶原容积分数（CVF）。结果 （1）美托洛尔组及联合治疗组均较安慰剂组左室舒张末期直径（LVEDd）、左室收缩末期直径（LVESd）、E峰A峰比值（E／A）明显下降,短轴缩短率（FS）、射血分数（EF）则有明显增高。联合治疗组较美托洛尔组LVEDd、LVESd有进一步降低（均为P〈0．05）,FS、EF则有进一步增高（均为P〈0．01）。（2）美托洛尔组及联合治疗组较安慰剂组左室重量体重比（LVW／BW）、肺脏重量体重比（PW／BW）及CVF明显降低（均为P〈0．01）。联合治疗组LVW／BW及PW／BW较美托洛尔组进一步降低（P〈0．01）,但两组之间CVF无显著差异。（3）美托洛尔组及联合治疗组较安慰剂组心肌细胞凋亡指数（AI）及Caspase．3活性均有明显减低。联合治疗组较美托洛尔组有进一步减低（均为P〈0．01）。（4）与安慰剂组相比,美托洛尔组及联合治疗组bax蛋白表达有明显下降而bcl-2／bax显著升高,并且以联合治疗组改善更为显著（均为P〈0．01）。结论 β1AR阻断剂联合β2AR激动剂较单用β1AR阻断剂进一步改善心衰大鼠的心功能,减轻心室重构。明显降低bax蛋白表达及bcl-2／bax,减轻心肌细胞凋亡很可能是其疗效提高的机制之一。     

超声心动图对老年舒张性心力衰竭患者心脏结构和功能改变的评价

目的通过超声心动图检查探讨老年舒张性心力衰竭(diastolic heart failure,DHF)患者心脏结构及舒张和收缩功能的变化情况。方法对129例老年DHF患者(DHF组)和79例年龄匹配的健康老年人(对照组)进行超声心动图检查,测量左心室容积、左心房容积、左心室质量,获取二尖瓣血流、右上肺静脉血流频谱,用组织多普勒测量二尖瓣环心室长轴方向的收缩期心肌峰值运动速度(Sm)、舒张早期心肌峰值运动速度(Em)等值,并进行分析。结果与对照组比较,DHF组患者左心室舒张末容积指数轻度增大,左心室质量指数明显增大,左心房容积指数明显增大,Sm和Em均明显下降,差异均有统计学意义(P0.01)。相关分析显示,Sm与左心室质量指数独立相关(β=-0.018,P0.01),左心房容积指数与老年DHF患者舒张功能不全程度独立相关(β=0.002,P0.01)。结论老年DHF患者总体表现为显著的向心性增厚,左心房的大小与舒张功能受损程度相关;收缩与舒张功能的损害,可能共同参与老年DHF发生和发展的过程。     

Improvements in left ventricular diastolic function after cardiac resynchronization therapy are coupled to response in systolic performance.

OBJECTIVES: To determine the short-term effects of cardiac resynchronization therapy (CRT) on measurements of left ventricular (LV) diastolic function in patients with severe heart failure. BACKGROUND: Cardiac resynchronization therapy improves systolic performance; however, the effects on diastolic function by load-dependent pulsed-wave Doppler transmitral indices has been variable. METHODS: Fifty patients with severe heart failure were evaluated by two-dimensional Doppler echocardiography immediately prior to and 4 +/- 1 month after CRT. Measurements included LV volumes and ejection fraction (EF), pulsed-wave Doppler (PWD)-derived transmitral filling indices (E- and A-wave velocities, E/A ratio, deceleration time [DT], diastolic filling time [DFT], and isovolumic relaxation time). Tissue Doppler imaging was used for measurements of systolic and diastolic (Em) velocities at four mitral annular sites; mitral E-wave/Em ratio was calculated to estimate LV filling pressure. Color M-mode flow propagation velocities were also obtained. RESULTS: After CRT, LV volumes decreased significantly (p < 0.001) and LVEF increased >5% in 28 of 50 patients (56%) and were accompanied by reduction in PWD mitral E-wave velocity and E/A ratio (both p < 0.01), increased DT and DFT (both p < 0.01), and lower filling pressures (i.e., E-wave/Em septal; p < 0.01). Patients with LVEF response < or =5% after CRT had no significant changes in measurements of diastolic function; LV relaxation (i.e., Em velocities) worsened in this group. CONCLUSIONS: In heart failure patients receiving CRT, improvement in LV diastolic function is coupled to the improvement in LV systolic function.     

贝拉普利与琥珀酸美托洛尔治疗左室射血分数正常的心力衰竭临床观察

目的:探讨贝拉普利与琥珀酸美托洛尔单用及联用对左室射血分数正常的心力衰竭(HFNEF)的疗效及其对左室肥厚的逆转和舒张功能的改善作用。方法:选取符合HFNEF诊治中国专家共识(CHFS 2010)诊断标准的患者120例。随机双盲分为3组,每组各40例。分别给予贝拉普利(A组),琥珀酸美托洛尔(B组)或两药合用(C组)进行治疗。随访6个月,比较各组患者血压,临床症状[6min步行试验(6MWT)]以及前体脑钠肽(NT-proBNP)的变化,超声心动图检测舒张早期二尖瓣环运动速度比值(E/E')、左室舒张期充盈速度比值(E/A)、组织多普勒E峰减速时间(DT)、左房容积指数(LAVI)等指标,观察心室舒张功能的改变。结果:与治疗前相比,治疗6个月后6MWT:A组[(342.2±67.1)∶(399.7±62.5)m,P<0.05],B组[(328.3±58.4)∶(495.5±82.2)m,P<0.05],C组[(337.3±45.1)∶(534.5±77.3)m,P<0.05]。DT:A组[(297.1±74.1)∶(256.6±75.7)ms,P<0.05],B组[(302.6±83.2)∶(237.4±61...     

Role of heart rate reduction in the prevention of experimental heart failure: comparison between If-channel blockade and β-receptor blockade

To investigate whether heart rate reduction via I(f)-channel blockade and β-receptor blockade prevents left ventricular (LV) dysfunction, we studied ivabradine and metoprolol in angiotensin II-induced heart failure. Cardiac dysfunction in C57BL/6J mice was induced by implantation of osmotic pumps for continuous subcutaneous dosing of angiotensin II (1.8 mg/kg per day SC) over a period of 3 weeks. Ivabradine (10 mg/kg per day) and metoprolol (90 mg/kg per day), which resulted in similar heart rate reduction, or placebo treatments were simultaneously started with infusion of angiotensin II. After 3 weeks, LV function was estimated by conductance catheter technique, cardiac remodeling assessed by estimation of cardiac hypertrophy, fibrosis, and inflammatory stress response by immunohistochemistry or PCR, respectively. Compared with controls, angiotensin II infusion resulted in hypertension in impaired systolic (LV contractility, stroke volume, end systolic elastance, afterload, index of arterial-ventricular coupling, and cardiac output; P<0.05) and diastolic (LV relaxation, LV end diastolic pressure, τ, and stiffness constant β; P<0.05) LV function. This was associated with a significant increase in cardiac hypertrophy and fibrosis. Increased cardiac stress was also indicated by an increase in cardiac inflammation and apoptosis. Both ivabradine and metoprolol led to a similar reduction in heart rate. Metoprolol also reduced systolic blood pressure. Ivabradine led to a significant improvement in systolic and diastolic LV function (P<0.05). This was associated with less cardiac hypertrophy, fibrosis, inflammation, and cardiac apoptosis (P<0.05). Metoprolol treatment did not prevent the reduction in cardiac function and adverse remodeling, despite a reduction of the inflammatory stress response. Behind heart rate reduction, additional beneficial cardiac effects contribute to heart failure prevention with I(f)-channel inhibition.     

超声评价氯沙坦单用或与美托洛尔联用对逆转原发性高血压左室肥厚心肌的影响

目的:应用多普勒超声心动图技术观察氯沙坦、美托洛尔联合应用与单用氯沙坦在逆转原发性高血压(EH)患者左室肥厚(LVH)及改善左室舒张功能方面的疗效。方法:对EH伴LVH患者68例采用随机、单盲、彩色多普勒超声心动图测量左室重量指数(LVMI)、左室舒张功能等指标。结果:经过≥6个月治疗后,氯沙坦组(A组)、氯沙坦加美托洛尔组(B组)的血压、LVMI及左室舒张功能指标均明显改善(P<0.01),两组间结果比较:B组左室舒张功能指标较A组有统计学意义(P<0.01)。结论:氯沙坦加美托洛尔联合应用,对EH患者降压、逆转LVH的作用并不优于单用氯沙坦,但改善左室舒张功能却明显优于后者,且不良反应轻,值得临床推广应用。     

Myocardial fibrosis and diastolic dysfunction in patients with hypertension: results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA)

OBJECTIVES: Hypertensive left ventricular hypertrophy (LVH) is associated with cardiomyocyte hypertrophy and an excess in myocardial collagen. Myocardial fibrosis may cause diastolic dysfunction and heart failure. Circulating levels of the carboxy-terminal propeptide of procollagen type I (PICP), an index of collagen type I synthesis, correlate with the extent of myocardial fibrosis. This study examines myocardial fibrosis in relation to blood pressure, left ventricular mass (LVM), and diastolic function. METHODS: We examined PICP levels in 115 patients with hypertensive LVH, 38 with hypertension but no hypertrophy, and 38 normotensive subjects. Patients with LVH were subsequently randomly assigned to the angiotensin II type 1 receptor blocker irbesartan or the beta1 receptor blocker atenolol for 48 weeks. Diastolic function was evaluated by tissue velocity echocardiography (n=134). We measured basal septal wall velocities of early (Em) and late (Am) diastolic myocardial wall motion, Em velocity deceleration time (E-decm), and isovolumic relaxation time (IVRTm). RESULTS: Compared with the normotensive group, PICP was elevated and left ventricular diastolic function was impaired in the hypertensive groups, with little difference between patients with and without LVH. PICP related to blood pressure, IVRTm, Em, and E/Em, but not to LVM. Irbesartan and atenolol reduced PICP similarly. Only in the irbesartan group did changes in PICP relate to changes in IVRTm, and LVM. CONCLUSION: Myocardial fibrosis and diastolic dysfunction are present in hypertension before LVH develops. The findings with irbesartan suggest a role for angiotensin II in the control of myocardial fibrosis and diastolic function in patients with hypertension with LVH.     

Cardiac beta ARK1 inhibition prolongs survival and augments beta blocker therapy in a mouse model of severe heart failure

Chronic human heart failure is characterized by abnormalities in beta-adrenergic receptor (betaAR) signaling, including increased levels of betaAR kinase 1 (betaARK1), which seems critical to the pathogenesis of the disease. To determine whether inhibition of betaARK1 is sufficient to rescue a model of severe heart failure, we mated transgenic mice overexpressing a peptide inhibitor of betaARK1 (betaARKct) with transgenic mice overexpressing the sarcoplasmic reticulum Ca(2+)-binding protein, calsequestrin (CSQ). CSQ mice have a severe cardiomyopathy and markedly shortened survival (9 +/- 1 weeks). In contrast, CSQ/betaARKct mice exhibited a significant increase in mean survival age (15 +/- 1 weeks; P < 0.0001) and showed less cardiac dilation, and cardiac function was significantly improved (CSQ vs. CSQ/betaARKct, left ventricular end diastolic dimension 5.60 +/- 0.17 mm vs. 4.19 +/- 0.09 mm, P < 0.005; % fractional shortening, 15 +/- 2 vs. 36 +/- 2, P < 0.005). The enhancement of the survival rate in CSQ/betaARKct mice was substantially potentiated by chronic treatment with the betaAR antagonist metoprolol (CSQ/betaARKct nontreated vs. CSQ/betaARKct metoprolol treated, 15 +/- 1 weeks vs. 25 +/- 2 weeks, P < 0.0001). Thus, overexpression of the betaARKct resulted in a marked prolongation in survival and improved cardiac function in a mouse model of severe cardiomyopathy that can be potentiated with beta-blocker therapy. These data demonstrate a significant synergy between an established heart-failure treatment and the strategy of betaARK1 inhibition.     

美托洛尔治疗慢性心力衰竭的临床疗效观察

目的：观察酒石酸美托洛尔治疗慢性心力衰竭（CHF）的临床疗效及安全性。方法：将66例慢性心力衰竭患者随机分成两组,治疗组33例给予内科常规抗心力衰竭治疗,对照组33例在常规治疗的基础上加用酒石酸美托洛尔治疗。治疗前后观察静息心率（HR）、收缩压（SBP）、舒张压（DBP）、心功能级别、左室舒张末内径（LVEDD）、左室收缩末期内径（LVESD）左室射血分数（LVEF）。结果：两组患者的各项指标在治疗后均较治疗前有明显改善,但治疗组较对照组改善更为显著,其临床疗效优于对照组（P〈0．05）。结论：酒石酸美托洛尔可明显改善CHF患者心功能,提高生存率,是一种安全、有效的临床治疗方法。