美托洛尔与卡维地洛在慢性心力衰竭中耐受性的比较

目的 :探讨美托洛尔与卡维地洛在慢性心力衰竭中的耐受性。方法 :186例慢性心力衰竭患者随机分成美托洛尔组与卡维地洛组 ,在常规抗心力衰竭治疗基础上从小剂量开始逐渐加用美托洛尔与卡维地洛 ,直至目标剂量维持。结果 :美托洛尔组平均维持剂量为 (81.1± 33.5 )mg/d ,坚持维持量者 80例 (84 .2 % ) ,卡维地洛组平均维持剂量为 (34.9± 14 .6 )mg/d ,坚持维持量者 78例 (85 .7% ) ,卡维地洛组较美托洛尔组更易达最大靶剂量 (5 8.2 %∶2 .1% ,P <0 .0 1) ,且剂量调整时间短 [(31.6± 9.4 )d∶(4 6 .7± 17.2 )d ,P <0 .0 1]。美托洛尔组降低心率 (16 .2± 3.5 )次 /min ,卡维地洛组为 (13.8± 4 .1)次 /min(P <0 .0 1)。美托洛尔组降低收缩压 (12 .9± 3.7)mmHg(1mmHg =0 .133kPa) ,舒张压 (6 .7± 2 .6 )mmHg ,卡维地洛组分别为 (14 .4± 4 .1)mmHg和 (7.9± 2 .9)mmHg (P <0 .0 5 )。结论 :慢性心力衰竭患者对美托洛尔和卡维地洛都具有良好的耐受性 ,美托洛尔对心率的影响较大 ,而卡维地洛对血压的影响较大 ,卡维地洛比美托洛尔更易达到最大靶剂量 ,且剂量调整时间短     

卡维地洛、美托洛尔治疗慢性心力衰竭疗效比较

β受体阻滞剂可阻断神经内分泌系统的激活,阻断心肌重塑,已成为治疗心力衰竭的一线药物.本试验选取卡维地洛与美托洛尔进行比较,以便了解二者对心力衰竭治疗效果的差异.     

卡维地洛与美托洛尔治疗心力衰竭的疗效对比观察

目的:比较卡维地洛与美托洛尔治疗充血性心力衰竭(CHF)的疗效及对神经激素、细胞因子的影响。方法:选择CHF患者120例,随机分3组。A组为对照组:予以血管扩张剂、利尿剂、地高辛等常规心力衰竭治疗。B、C组在上述治疗基础上分别予以美托洛尔50mg,bid、卡维地洛25mg,bid口服,维持该剂量至6个月。用药前后分别观察左室射血分数(LVEF)、每搏输血量(SV)、短轴缩短率(FS)、左室舒张末期内径(LVEDD)、左室收缩末期内径(LVESD)、相对室壁厚度(RWT)及醛固酮(ALD)、肿瘤坏死因子-α(TNF-α)、内皮素(ET)、心钠素(ANP)等指标变化情况。结果:6个月后B组及C组LVEDD、LVESD缩小,RWT增厚,LVEF、FS、SV明显提高,而ALD、ET、TNFα、ANP水平明显降低,与治疗前及A组比较均差异有统计学意义。B、C组再入院率及病死率均明显低于A组,同时C组LVEF改善优于B组。结论:美托洛尔、卡维地洛均可明显降低CHF患者神经激素、细胞因子的水平,逆转心室重塑,改善心脏功能。卡维地洛疗效及耐受性略优于美托洛尔。     

卡维地洛对慢性心力衰竭患者左心功能的影响

目的观察卡维地洛对慢性充血性心力衰竭患者左心室收缩功能的影响。方法117例慢性心力衰竭患者分为卡维地洛组和对照组,用心脏超声诊断仪测量治疗前和治疗后1个月、3个月的心脏结构及功能。结果两组患者治疗1个月后左心室舒张末径、左心室舒张末容积、左心室收缩末容积,左心室射血分数与治疗前比较差异均无统计学意义(P>0.05);3个月及6个月时的上述指标与治疗前比较差异均有统计学意义(P<0.05)。结论卡维地洛可明显改善慢性心力衰竭左心室收缩功能。     

卡维地洛与美托洛尔治疗心力衰竭的对比研究进展

美托洛尔 (Ｍｅｔｏｐｒｏｌｏｌ)是一种选择性的第二代 β 受体阻滞剂 ,而卡维地洛 (Ｃａｒｖｅｄｉｏｌｏ)是一种无内在拟交感活性的非选择性的第三代 β 受体阻滞剂 ,同时具有α受体的阻滞作用 ,并且是一种强效自由基清除剂。卡维地洛已在一些大规模的临床试验中 ,试用于慢性心力衰竭 (ＣＨＦ)的治疗 ,被认为是一种非常有前途的药物。本文重点介绍卡维地洛与美托洛尔在治疗慢性心力衰竭中的对比研究进展。1　β 受体阻滞剂用于ＣＨＦ的治疗现状近年的研究发现 ,心力衰竭时由于交感神经活性增强 ,儿茶酚胺 (ＣＡ)的浓度增高 ,心肌细胞膜上…     

卡维地洛与美托洛尔治疗缺血性心脏病心力衰竭的疗效观察

目的:观察卡维地洛和美托洛尔对缺血性心脏病心力衰竭患者的临床疗效。方法:缺血性心脏病心力衰竭患者80例,左室射血分数（LVEF）≤0.45,心功能（NYHA）ⅡⅣ级,常规治疗基础上随机分为卡维地洛组和美托洛尔组,治疗3月后,观察两种药物对心功能及运动耐量的影响。应用心脏彩色超声仪测定心功能基线值及3月后的变化。用6 m in步行距离测定运动耐量的改善程度。结果:经过3月的治疗,卡维地洛组与美托洛尔组心率、血压、运动耐量改善程度及心功能均有明显改善,且卡维地洛组6 m in步行试验结果,收缩压、舒张压变化及左室收缩末容积（LVESV）、左室舒张末容积（LVEDV）、LVEF改善程度明显优于美托洛尔组（P<0.01）。结论:在常规治疗基础上卡维地洛、美托洛尔对缺血性心脏病的治疗均有显著效果,前者在改善运动耐量、LVEDV、LVESV及心室射血方面更优。     

卡维地洛与美托洛尔治疗慢性心力衰竭的临床疗效对比

目的比较卡维地洛与美托洛尔治疗慢性心力衰竭的临床效果。方法选取2011年1月—2013年1月我院收治的慢性心力衰竭患者120例,按照就诊顺序将其分为A组和B组,各60例。A组在常规治疗的基础上给予卡维地洛治疗,B组在常规治疗的基础上给予美托洛尔治疗,均治疗6个月。比较两组治疗前后心功能指标变化、治疗后临床疗效及不良反应发生情况。结果 B组治疗总有效率为73.3%(44/60),低于A组的90.0%(54/60)(P0.05)。治疗前两组患者左室射血分数(LVEF)、左室舒张末期内径(LVEDD)及左室收缩末期内径(LVESD)比较,差异均无统计学意义(P0.05);治疗后A组LVEF高于B组,LVEDD和LVESD低于B组(P0.05)。两组均未发生严重不良反应。结论卡维地洛与美托洛尔治疗慢性心力衰竭,均有较好的临床疗效,能改善患者心功能指标,但卡维地洛效果更明显。     

美托洛尔与卡维地洛治疗充血性心力衰竭疗效及安全性比较

将108例非瓣膜性慢性充血性心力衰竭（CHF）患者随机分为两组,各54例。卡维地洛组予非选择性β受体阻断剂卡维地洛治疗,美托洛尔组予高选择性β受体阻断剂美托洛尔治疗。结果卡维地洛组总有效率高于美托洛尔组（P〈0．05）,出现心衰加重及房室传导阻滞例数（AVB）低于美托洛尔组（P〈0．05）。认为非选择性β受体阻断剂治疗CHF疗效优于高选择性β受体阻断剂,且安全性高。     

卡维地洛治疗老年慢性心力衰竭的临床疗效观察

目的：观察卡维地洛治疗老年慢性充血心力衰竭（CHF）的临床疗效及副作用。方法：72例老年CHF患者随机分为卡维地洛组（治疗组）和常规治疗组（对照组），各36例。对照组使用洋地黄、利尿剂、血管紧张素转换酶抑制剂、硝酸酯类等药物治疗。治疗组在常规治疗的基础上加用卡维地洛5mg／d，只要能耐受尽可能递增到10～20mg／d，疗程20周。每周测量血压、心率，评定心功能，治疗前后检查超声心动图。结果：治疗组左室射血分数（LVEF）明显升高（P〈0．001），心功能分级、左室舒张末期内径（LVEDD）、心肌耗氧指数和收缩末期内径（LVESD）明显降低（P〈0．01），心率减慢，血压降低（P〈0．01）．与对照组比较差异有显著性（P〈0．05）。结论：卡维地洛治疗心力衰竭改善心功能，改善左室重塑，安全有效。     

卡维地洛对慢性心力衰竭患者心肌重构和炎性细胞因子的影响

目的探讨卡维地洛对慢性心力衰竭(心衰)患者心肌重构和血浆肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)和白细胞介素-6(IL-6)的影响。方法72例心衰患者随机分为治疗组和对照组各36例。对照组给予洋地黄、利尿剂及血管紧张素转换酶抑制剂。治疗组在此基础上加用卡维地洛。随访半年,治疗前后采用超声心动图、胸部X线和化学发光法测定心功能、心胸比率和血浆TNF-α、IL-1β和IL-6的变化。结果两组治疗后心功能改善,总有效率为77.8%和50%,P<0.01;心胸比率分别为(0.55±0.07和0.58±0.06,P<0.05)。治疗组治疗后左室舒张期末内径和左室收缩期末内径分别为(58.7±6.9)mm和(44.7±7.2)mm,显著低于对照组(61.3±2.7)mm和(50.9±9.2)mm;左室射血分数为(46.3±9.7)%,显著高于对照组(39.9±6.8)%,P<0.01;血浆TNF-α、IL-1β和IL-6分别为(46.08±13.27)pg/ml、(31.32±4.06)pg/ml和(30.26±10.59)pg/ml,显著低于对照组(59.23±18.65)pg/ml、(39.58±11.38)pg/ml和(54.96±20.21)pg/ml,P<0.01)。副作用发生率,两组相比较差异无统计学意义。结论慢性心力衰竭在常规治疗基础上加用卡维地洛安全有效,可以改善心功能,逆转心肌重构,降低血浆主要细胞因子水平。     

卡维地洛、美托洛尔对心衰大鼠心功能及体液因子的影响

目的探讨β受体阻滞剂卡维地洛、美托洛尔对心衰大鼠体液因子及心功能的影响。方法建立心衰大鼠模型,随机分为三组,B组为安慰剂组;C组给予卡维地洛,D组给予美托洛尔;同时设假手术组(A组)。观察6周后行心脏超声、血流动力学检查,以及血清尿钠素(ANP)、血管紧张素(Ang)、肿瘤坏死因子α(TNF-α)、白介素6(IL-6)及去甲基肾上腺素(NE)测定。结果β受体阻滞剂能显著降低心衰大鼠的左室舒张末压,增加左室短轴缩短率、左室压力最大上升及下降速率,以及ANP、TNF-α、IL-6、NE(均P<0.05),减小室间隔厚度及左室质量指数(LVWI)(P<0.05);其中卡维地洛降低Ang、减小左室舒张末期直径、降低LVWI的作用明显优于美托洛尔(P<0.05)。结论β受体阻滞剂能较全面地降低神经内分泌、细胞因子,这可能是其改善心脏功能,抑制左室重塑的机制之一。卡维地洛降低神经内分泌、细胞因子,减轻心肌重塑的作用优于美托洛尔。     

The effects of chronic carvedilol therapy on QT dispersion in patients with congestive heart failure.

BACKGROUND: Carvedilol therapy reduces mortality from sudden cardiac death and progressive pump failure in congestive heart failure (CHF). However, the effect(s) of carvedilol on ventricular repolarization characteristics is unclear. AIM: The aim of the study was to investigate the effects of chronic carvedilol therapy on ventricular repolarization characteristics as assessed by QT dispersion (QTd) in patients with CHF. METHOD: Nineteen patients (age 53+/-12 years; 16 male, three female) with CHF (eight ischemic, 11 non-ischemic dilated cardiomyopathy) were prospectively included in the study. Carvedilol was administered in addition to standard therapy for CHF at a dose of 3.125 mg bid and uptitrated biweekly to the maximum tolerated dose. From standard 12-lead electrocardiograms the maximum and minimum QT intervals (QTmax, QTmin), QTd, corrected QT intervals (QTcmax, QTcmin) and corrected QTd (QTcd) values were calculated at baseline, after the 2nd and the 16th month of carvedilol therapy. RESULTS: A significant reduction was noted in the QTd and QTcd values with carvedilol therapy after the 16th month (QTd: 81+/-22 ms vs. 40+/-4.3 ms P<0.001; QTcd: 91+/-25 ms vs. 51+/-7 ms P<0.001), but not after the 2nd month (P>0.05). The resting heart rate was also significantly reduced after a 16-month course of carvedilol therapy (78+/-13 bpm vs. 66+/-15 bpm, P<0.05). Carvedilol therapy did not alter QTmax and QTcmax intervals (P>0.05), however, QT min and QTcmin significantly increased with carvedilol at the 16th month (P<0.001 and P<0.01, respectively). CONCLUSION: Long-term carvedilol therapy was associated with a reduction in QTd, an effect that might contribute to the favorable effects of carvedilol in reducing sudden cardiac death in CHF.     

Differing beta-blocking effects of carvedilol and metoprolol

BACKGROUND: Metoprolol is a beta(1)-selective beta-adrenergic antagonist while carvedilol is a non-selective beta-blocker with additional blockades of alpha(1)-adrenoceptors. Administration of metoprolol has been shown to cause up-regulation of beta-adrenoceptor density and to decrease nocturnal melatonin release, whereas carvedilol lacks these typical effects of beta-blocking drugs. AIMS: To compare beta-blocking effects of metoprolol and carvedilol when applied orally in healthy subjects. Methods: We investigated the effects of single oral doses of clinically recommended amounts of metoprolol (50, 100 and 200 mg) and carvedilol (25, 50 and 100 mg) to those of a placebo in a randomised, double-blind, cross-over study in 12 healthy male volunteers. Two hours after oral administration of the drugs heart rate and blood pressure were measured at rest, after 10 min of exercise, and after 15 min of recovery. RESULTS: Metoprolol tended to decrease heart rate during exercise (-21%, -25% and -24%) to a greater extent than carvedilol (-16%, -16% and -18%). At rest, increasing doses of metoprolol caused decreasing heart rates (62, 60 and 58 beats/min) whereas increasing doses of carvedilol caused increasing heart rates (62, 66 and 69 beats/min), 50 and 100 mg carvedilol failed to differ significantly from the placebo (71 beats/min). CONCLUSIONS: We conclude that clinically recommended doses of carvedilol cause a clinically relevant beta-blockade in humans predominantly during exercise where it appears to be slightly (although not significantly) less effective than metoprolol. On the other hand, the effects of carvedilol on heart rate at rest appear rather weak, particularly in subjects with a low sympathetic tone. This might be caused by a reflex increase on sympathetic drive secondary to peripheral vasodilation resulting from the alpha-blocking effects of the drug. These results might be helpful in explaining why carvedilol, in contrast to metoprolol, may fail to cause up-regulation of beta-adrenoceptor density and does not decrease nocturnal melatonin release. This, in turn, may be a reason for the weak side-effects of carvedilol resulting from the beta-blockade. In addition, our data might be of interest in the interpretation of the forthcoming results of the COMET trial, although it has to be emphasised that they were derived from healthy subjects and, therefore, cannot be directly extrapolated to patients with heart failure.     

β受体阻滞剂对心力衰竭大鼠基质金属蛋白酶-13及其组织抑制因子-1的影响

目的探讨不同β受体阻滞剂对心力衰竭模型大鼠基质金属蛋白酶-13(MMP-13)及金属蛋白酶组织抑制因子-1(TIMP-1)的影响。方法取SD雄性大鼠,结扎左冠状动脉前降支建立慢性心力衰竭模型,将37只大鼠随机分为心力衰竭组(9只)、卡维地洛组(10只)、美托洛尔组(8只)和假手术组(10只),观察各组大鼠的左心室参数和丙二醛(MDA)水平,并行MMP-13及TIMP-1的Westernblot检测。结果与假手术组比较,心力衰竭组MDA水平显著升高(P<0.05),经卡维地洛和美托洛尔干预后下降,其中卡维地洛组MDA下降显著(P<0.05);心力衰竭组TIMP-1蛋白水平表达降低,药物干预后TIMP-1蛋白水平表达上调,卡维地洛组更为明显;心力衰竭组MMP-13蛋白水平表达明显增加,药物干预后MMP-13蛋白水平表达下调,卡维地洛组更为明显。结论卡维地洛有调节MMP-13和TIMP-1蛋白表达的作用,可部分解释心肌梗死模型胶原重构的机制。     

卡维地洛对慢性心力衰竭患者血浆脑钠肽水平的影响

目的观察卡维地洛对慢性心力衰竭患者血浆脑钠肽水平的影响。方法将123例慢性心力衰竭患者随机分为卡维地洛组(62例)和对照组(61例)。治疗后观察脑钠肽和超声心动图的结果。结果卡维地洛组较对照组治疗后血浆脑钠肽水平显著降低(P<0.05);卡维地洛组治疗后左心室射血分数(LVEF)、每搏量以及每分排血量明显增加(P<0.05,P<0.01);卡维地洛组治疗前后患者血浆脑钠肽的下降水平与LVEF增加呈负相关(△LVEF:r=-0.86,P<0.01)。结论卡维地洛能明显改善慢性心力衰竭患者血流动力学,抑制神经内分泌因素的过度激活,改善心功能;血浆脑钠肽水平可作为评价β受体阻滞剂治疗慢性心力衰竭疗效的监测指标之一。     

Impact of concurrent amiodarone treatment on the tolerability and efficacy of carvedilol in patients with chronic heart failure

OBJECTIVE—To assess the safety and efficacy of carvedilol when administered to heart failure patients already receiving amiodarone.
DESIGN—Retrospective analysis of the clinical outcome of 230 patients treated with carvedilol for chronic heart failure, stratified according to whether they were already receiving amiodarone (amiodarone group, 80 patients) or not (non-amiodarone group, 130 patients) at baseline.
SETTING—Heart failure clinic at a university affiliated public teaching hospital.
MAIN OUTCOME MEASURES—Incidence of adverse events; changes in functional status and echocardiographic dimensions at three months.
RESULTS—Adverse reactions to carvedilol occurred in 33 (41%) of the amiodarone group and 43 (29%) of the non-amiodarone group (p = 0.049). Carvedilol was discontinued in 21 (26%) of the amiodarone group and 37 (25%) of the non-amiodarone group (NS). The clinical outcome at three months did not differ significantly between the two groups; 31 (39%) of the amiodarone group improved their New York Heart Association status, 28 (35%) were unchanged, and 21 (26%) deteriorated compared with 67 (45%), 51 (34%), and 32 (21%), respectively, for the non-amiodarone group (NS). Both groups had highly significant decreases in heart rate and left ventricular end systolic dimension, and a significant increase in left ventricular ejection fraction after three months of carvedilol treatment, with no significant differences between the groups.
CONCLUSIONS—The beneficial effects of carvedilol on left ventricular remodelling, systolic function, and symptomatic status are not affected by concurrent treatment with amiodarone. Adverse reactions necessitating cessation of carvedilol are no more frequent in patients receiving amiodarone.


Keywords: carvedilol; amiodarone; heart failure     

Low-dose combination therapy with metoprolol and captopril for congestive heart failure in mice

Summary We assessed the therapeutic efficacy of a low-dose combination of metoprolol and captopril given orally to C3H/Hej mice that developed dilated and hypertrophied hearts after being inoculated with the encephalomyocarditis virus. Mice were randomly assigned to one of six 8-week oral regimens: 1 mg/kg/day of metoprolol (group 1); 10 mg/kg/day of metoprolol (group 2); 1.2 mg/kg/day of captopril (group 3); 12 mg/kg/day of captopril (group 4); 1 mg/kg/day of metoprolol plus 1.2 mg/kg/day of captopril (group 5); or distilled water (control group). Group 4 exhibited a significantly lower survival rate and body weight than the control group (p<0.01). Survival rates and body weights were similar in groups 1, 2, 3, 5, and the control group. Low-dose metoprolol plus captopril is superior to low-dose metoprolol, high-dose metoprolol, and low-dose captopril with regard to heart weight and the heart weight/body weight ratio. The left and right ventricular cavity dimensions as well as myocardial necrosis, calcification, and fibrosis were less severe in groups 4 and 5 than in the control group. The left ventricular free wall showed significantly more thinning in group 4 than in the control group (p<0.01). Our results show that the administration of low-doses of metoprolol and captopril given in combination was effective in this animal model of congestive heart failure and was associated with a reduction in biventricular cavity dimensions and myocardial necrosis.     

美托洛尔联合非诺特罗对心力衰竭大鼠Fas及FasL的影响

目的评价β1肾上腺素受体(AR)阻滞剂美托洛尔联合β2AR激动剂非诺特罗对扩张型心肌病大鼠Fas、FasL表达的影响。方法将异丙基肾上腺素诱导的心力衰竭大鼠32只随机分为美托洛尔组(11只),联合治疗组(11只),安慰剂组(10只)。治疗8周后有创血流动力学评价心功能,TUNEL法检测心肌细胞凋亡指数,Westernblot测定Fas及FasL表达。另外随机选取9只雄性Wistar大鼠作为对照组。结果美托洛尔组较安慰剂组左心室收缩末压(PES)、左心室压力最大上升速率(dp/dtmax)明显增高(P<0.05),左心室舒张末压(PED)、凋亡指数明显降低(P<0.01)。美托洛尔组较联合治疗组PES、dp/dtmax、左心室压力最大下降速率(dp/dtmin)进一步增高(P<0.05),PED、凋亡指数进一步降低(P<0.01)。安慰剂组Fas、FasL表达明显高于对照组(P<0.01),美托洛尔组及联合治疗组较安慰剂组Fas、FasL表达明显减低(P<0.01),联合治疗组较美托洛尔组进一步减低(P<0.05)。结论Fas、FasL信号系统的充分抑制很可能是β1AR阻滞剂联合β2AR激动剂使心肌细胞凋亡率进一步降低的重要机制之一。