不同剂量卡维地洛防治高压负荷性心衰幼鼠心室重构

目的 观察不同剂量卡维地洛对高压负荷性心衰幼鼠心室重构的防治作用.方法 采用腹主动脉缩窄术建立慢性心力衰竭(CHF)模型,36只存活雄性5周龄Wistar幼鼠随机分组:(1)CHF对照组(n=8);(2)大剂量卡维地洛组(10 mg·kg-1·d-1,n=10);(3)中剂量卡维地洛组(1 mg·kg-1·d-1,n=10) ;(4)小剂量卡维地洛(0.1 mg·kg-1·d-1,n=8);另设假手术对照组.直接灌胃给药,给药4周后行高频超声、血流动力学、心脏病理分析、心肌细胞凋亡及其检测血清中脂质过氧化物(LPO)和超氧化物歧化酶(SOD)含量.结果 与假手术组比较,CHF组左室收缩末期内径(LVESD)、室间隔舒张末期厚度(IVSTd)、室间隔收缩末期厚度(IVSTs)、左室后壁舒张末期厚(LVPWTd)、左室后壁收缩末期厚度(LVPWTs)左、右心室相对重量(LVRW,RVRW)、收缩压(SBP)、舒张压(DBP)、左室收缩压(LVSP)、左室舒张末压(LVEDP) 、凋亡指数(AI) 、LPO均显著升高(P＜0.01),左室舒张末期内径LVEDD也明显升高(P＜0.05).左室短轴缩短率FS、左室射血分数EF、左室内压最大收缩率( dp/dtmax) 、左室内压最大舒张率(-dp/dtmax) 、SOD均显著降低(P＜0.01).与CHF组比较,卡维地洛组LVEDD、LVESD、IVSTd、IVSTs、LVPWTd、LVPWTs、LVRW、RVRW、SBP、DBP、LVSP、LVEDP、AI、LPO均呈剂量相关性下降,以大中剂量下降明显(P＜0.05或P＜0.01),FS、EF、 dp/dtmax、-dp/dtmax、SOD均显著升高(P＜0.01).结论 卡维地洛大、中、小剂量均能有效防治幼鼠CHF发展中的心室重构,改善血流动力学和心功能,阻止心肌细胞凋亡和清除氧自由基;小剂量有效,大剂量更佳.     

奈比洛尔对血管内皮细胞胰岛素抵抗的影响

目的 观察奈比洛尔改善人主动脉内皮细胞(HAEC)胰岛素抵抗(IR)的作用及机制。方法 HAEC分为空白组(正常培养,胰岛素不刺激),对照组(正常培养,胰岛素刺激),不同浓度奈比洛尔+对照组(对照组基础上加奈比洛尔0.1,1,10μmol·L^-1),IR组(高糖33.3 mmol·L^-1+胰岛素1×10^-7 mol·L^-1),不同浓度奈比洛尔+IR组(IR基础上加奈比洛尔0.1,1,10μmol·L^-1)。48 h后,细胞无血清饥饿处理12 h。以噻唑蓝(MTT)法检测细胞活性,以葡萄糖氧化酶法测HAEC葡萄糖消耗量,以硝基还原酶法检测上清液一氧化氮(NO)水平,以蛋白质印迹法测定蛋白表达。结果 与对照组(100%)比较,IR组细胞活性无显著性改变(95.13±2.10)%,且不同浓度奈比洛尔(0.1、1、10μmol·L^-1)预处理对IR组和对照组细胞活性均无显著性影响。IR组的细胞葡萄糖消耗量和上清液NO水平分别为(0.53±0.17) mmol·L<...     

卡维地洛与美托洛尔对CHF长期疗效的研究

目的：观察卡维地洛与美托洛尔对慢性心力衰竭的长期疗效。方法：86例慢性心力衰竭患者，随机分成卡维地洛组（n=42)、美托洛尔组(n=44)．随访1年，并观察心衰症状和心功能指标以及两药的耐受量及安全性。结果：①卡维地洛及美托洛尔组用药后心衰症状明显改善(P＜0.05)；但两组间无显著差异(P＜0.05)。②卡维地洛组比美托洛尔组用药后左心室射血分数明显增加(P＜0.05)。③两组用药后血压和心率有明显下降(P＜0.05)。但卡维地洛组血压下降较美托洛尔组显著、两组间有显著差异（P＜0.05)。美托洛尔组心率下降较卡维地洛组明显（P＜0．05)。④卡维地洛和美托洛尔组治疗慢性心力衰竭安全性好，耐受性良好。卡维地洛优于美托洛尔。结论：卡维地洛和美托洛尔均能明显改善心功能，提高生活质量，但两者之间对慢性心力衰竭的疗效卡堆地洛更显著。     

卡维地洛治疗慢性心衰对外周血浆肾素及利钠肽的影响

目的:探讨β-受体阻滞剂卡维地洛治疗慢性心力衰竭时对外周血中血浆肾素活性(PRA)、心钠肽(ANP)及脑钠肽(NBNP)水平的影响.方法:60例慢性心衰患者随机分为常规治疗组(血管紧张素转换酶抑制 利尿剂 地高辛)和卡维地洛组(常规治疗药物 卡维地洛),随访12周,采用放射免疫法测定二组治疗前后和30例健康体检者(正常对照组)外周血中PRA、ANP及N-BNP水平.同时使用核素心室显像测定心衰患者左心室射血分数(LVEF).结果:心衰患者外周血中PRA、ANP及N-BNP水平较正常对照组显著升高,其中ANP及N-BNP水平在卡维地洛治疗前与LVEF负相关,在卡维地洛治疗后与LVEF密切相关,但PRA水平与LVEF无关.治疗后卡维地洛组外周血中PRA、ANP及N-BNP水平较常规治疗组下降更明显.结论:外周血中ANP及N-BNP水平在慢性心衰的病理生理机制中起着重要作用,甚至在β-受体阻滞剂治疗后仍可用于指导心衰患者的治疗.β-受体阻滞剂能抑制心衰患者神经内分泌的过度激活.     

卡维地洛对慢性心衰的治疗作用

目的 探讨卡维地洛(CAV)治疗心力衰竭的疗效及机制。方法 对慢性心衰病人76例，随机分为3组：常规治疗组20例(A组)、卡维地洛组30例(B组)、美托洛尔组26例(C组)，治疗前后分别观察心功能变化、测量LVEF、左室质量及血浆脂质过氧化物(LPO)和超氧化物歧化酶(SOD)的水平。结果 (1)B组和C组治疗6个月后患心功能明显好转，且疗效优于A组(P＜0．01)，但B组和C组之间疗效差异无显性(P＞0．05)。(2)B组血浆LPO水平较治疗前下降，红细胞SOD升高(P＜0．01)，而A组和C组治疗前后无明显变化。结论 CAV对慢性心衰有明显治疗作用，可能与其脂质过氧化有关。     

卡维地洛对慢性心力衰竭患者神经内分泌和血流动力学的影响

目的　比较卡维地洛 (Carvedilol)与美托洛尔 (Metoprolol)对慢性心力衰竭 (CHF)患者神经内分泌激素和血流动力学的影响。方法　 80例 CHF患者 ,随机分为卡维地洛组和美托洛尔组。观察治疗前后脑钠素 (BNP)、去甲肾上腺素 (NE)和左室射血分数 (LVEF)、平均肺动脉压(MPAP)、肺楔压 (PCWP)的变化。结果　卡维地洛组较美托洛尔组显著降低 BNP、NE、MPAP和 PCWP(P<0 .0 5) ,较美托洛尔组明显提高 L VEF(P<0 .0 5)。结论　卡维地洛抗交感活性作用强于美托洛尔 ,能显著降低 BNP、NE水平 ,血流动力学改善优于美托洛尔     

雷米普利联合美托洛尔对心衰患者ADM、BNP及Apelin水平的影响

目的:探讨雷米普利联合美托洛尔对心衰患者肾上腺髓质素水平的影响.方法:根据电脑产生随机数字表法将本院82例心衰患者均分成对照、观察两组,在常规治疗基础上,对照组实施美托洛尔治疗,观察组予雷米普利配以美托洛尔治疗.比较两组肾上腺髓质素(ADM)、脑钠肽(BNP)、血管活性肽(Apelin)水平及心功能、疗效.结果:两组治疗后ADM、BNP水平比,观察组均较低(P<0.05);两组Apelin水平比,观察组较高(P<0.05).治疗后,观察组左心室收缩末内径(LVESD)、左室舒张末期内径(LVEDD)较对照组短,左室射血分数(LVEF)较对照组高(P<0.05).两组治疗总有效率比,观察组(95.12％)较对照组(78.05％)高(P<0.05).结论:在心衰患者治疗中雷米普利和美托洛尔的联合运用,可促进患者ADM、BNP、Apelin水平及心功能的改善,优化治疗效果.     

卡维地洛与美托洛尔治疗慢性心功能不全的临床研究

目的 研究比较卡维地洛和美托洛尔治疗慢性心功能不全的临床疗效.方法 将100例慢性心功能不全的病人随机分为两组进行对照,分别为卡维地洛组和美托洛尔组,两组采用一致的基础用药.在左室射血分数(LVEF)、左室舒张末期内径(LVDd)等指标上对两组进行比照,同时检测电解质、尿常规、肾功能、肝功能、血糖、血脂、血压、心率等.结果 两组病人的心功能,在3个月疗程后,均获得明显改善,同时心率、血压、和LVEF升高,LVDd降低,卡维地洛组显效42例,好转6例,美托洛尔组显效34例,好转14例,无效1例,卡维地洛组改善更为明显(P＜0.05).结论 在治疗慢性心力衰竭上卡维地洛比美托洛尔更具优势.卡维地洛是更为理想的治疗慢性心功能不全的药物.     

奈比洛尔对自发性高血压大鼠循环和主动脉肾素-血管紧张素系统的影响

目的：探讨奈比洛尔（Nebivolol）对自发性高血压大鼠循环和主动脉肾素-血管紧张素系统（RAS）的影响。方法：18只自发性高血压大鼠（SHR）和6只同源正常血压大鼠Wistar-Kyoto（WKY）随机分为：（1）奈比洛尔组（n=6）：SHR给予奈比洛尔5mg·kg-1·d-1;（2）卡托普利组（n=6）：SHR给予卡托普利15mg·kg-1·d-1;（3）SHR对照组（n=6）;（4）WKY对照组（n=6）。奈比洛尔、卡托普利溶于蒸馏水中灌胃,对照组给予等体积蒸馏水灌胃。给药8周后测定血浆肾素活性（PRA）,血浆和主动脉血管紧张素Ⅱ（AngⅡ）、一氧化氮（NO）浓度,NO/AngⅡ和血管紧张素转化酶（ACE）活性。结果：与WKY比较,SHR血浆和主动脉NO含量降低,AngⅡ水平显著增加,NO/AngⅡ降低;主动脉ACE活性明显增加,而血浆ACE活性则降低;但PRA在两组间无显著性差异。奈比洛尔治疗对SHR血浆AngⅡ含量和ACE活性无影响,但可降低主动脉AngⅡ水平,抑制主动脉ACE活性,从而增加血浆及主动脉NO含量和NO/AngⅡ。结论：奈比洛尔抑制肾素-血管紧张素系统,可能是其降低血压的机制之一。     

卡维地洛治疗中重度心衰的疗效及对心率变异的影响

充血性心衰是心脏泵功能障碍引起的以神经内分泌紊乱为主要特征的临床综合征。心衰激活神经内分泌系统 ,反过来神经内分泌系统的激活进一步加速心室重塑和心衰的恶化。神经内分泌的激活可表现为心率变异的降低 ,本文观察了卡维地洛对心衰心功能及心率变异的影响 ,试图探讨卡维地洛对心衰病人植物神经功能的影响。1 资料和方法1 1资料　 6 4例慢性心衰病人 ,均为窦性心率 ,年龄 5 9± 12岁 ,心功能Ⅲ～Ⅳ级 ,左室射血分数 (EF值 ) :2 6 5± 5 3,基础疾病 :缺血性心脏病 4 2例 ,扩张性心肌病 10例 ,高血压性心脏病 12例。排除标准 :⑴严重…     

Carvedilol induces biased β1 adrenergic receptor-cGMP signaling in heart

OBJECTIVE To elucidate the potential mechanism of carvedilol in treating heart failure and hypertension. METHODS Obesity and diabetes wild type mice induced by feeding with high fat diet(HFD) were treated with beta-blocker carvedilol or metoprolol. The signaling was detected using fluorescence resonance energy transfer assay and cardiac contractile function was examined both in vivo and in vitro. RESULTS Both carvedilol and metoprolol significantly improves cardiac dysfunction in comparison to control HFD mice treated with vehicle.Importantly, carvedilol treatment induces the phosphorylation of cardiac beta1 adrenergic receptor(beta1AR)thus triggers plasma membrane cAMP-PKA signaling of myocytes and modulates the activity of EC coupling related proteins. Interestingly, carvedilol rescues the contractility of myocytes independent of calcium amplitude but depends on the phosphorylation of myosin binding protein C through beta1 AR-c GMP pathway. CONCLUSION These studies elucidate a novel mechanism by which carvedilol improves cardiac function in diabetic heart.     

Comparison of pharmacodynamics between carvedilol and metoprolol in rats with isoproterenol-induced cardiac hypertrophy: effects of carvedilol enantiomers

A recent clinical study has shown that carvedilol has a significantly more favorable effect than metoprolol on survival rate in patients with heart failure. This may be due to actions of carvedilol such as beta(2)-adrenoceptor blockade, alpha-adrenergic receptor blockade and other properties such as anti-oxidant effects that are not yet fully understood. We compared the effects of racemic carvedilol, metoprolol and carvedilol enantiomers on cardiac hypertrophy at similar heart rate in rats with isoproterenol-induced cardiac hypertrophy. Continuous administration of isoproterenol for 2 weeks produced heart failure, which is characterized by an increased heart rate, cardiac hypertrophy and downregulation of beta-adrenoceptors. The doses of racemic carvedilol and metoprolol were adjusted to obtain a similar heart rate in rats with isoproterenol-induced cardiac hypertrophy. The reduction of left ventricular weight and improvement of cAMP production induced by carvedilol were superior to those induced by metoprolol. Although heart rate, blood pressure and cAMP production were not affected by R-carvedilol, left ventricular weight was significantly reduced as a result of alpha-adrenoceptor blockade. The improvement of cAMP production by S-carvedilol was significantly higher than that induced by coadministration of R-carvedilol and metoprolol, suggesting that beta(2)-adrenoceptor blockade partly contributed to the improvement of signal transduction in rats with isoproterenol-induced cardiac hypertrophy. This study has demonstrated that the effects of carvedilol on cAMP production and cardiac hypertrophy in rats with isoproterenol-induced cardiac hypertrophy are superior to those induced by metoprolol at a similar heart rate.     

Carvedilol versus other beta-blockers in heart failure

Carvedilol is a beta-blocker with ancillary properties. Pilot clinical studies with carvedilol, added to the standard therapy of digoxin, diuretics and ACE inhibitors, showed beneficial effects in mild, moderate and severe heart failure. Patients consistently showed improvement in LV ejection fraction and NYHA functional class. Subsequently large clinical trials showed decreased morbidity and mortality with carvedilol in mild and moderate and more recently, severe heart failure. However, there is little or no improvement in exercise tolerance with carvedilol. The beneficial effects of carvedilol in heart failure are associated with cardiac remodelling. Metoprolol and bisoprolol are selective beta(1)-blockers without ancillary properties. Early studies showed benefits with metoprolol and bisoprolol in heart failure. Large clinical trials established that metoprolol and bisoprolol decreased mortality and morbidity in heart failure. In contrast no benefit has been shown with celiprolol, a selective beta(1)-blocker and beta(2)-stimulant in heart failure. There is a debate as to whether the ancillary properties of carvedilol contribute to its beneficial effect in heart failure, making it a better drug to use than metoprolol. Short-term studies suggested that carvedilol and metoprolol were equivalent in heart failure but short-term is probably not an appropriate way to compare the drugs. A recent long-term study and study in poor responders to metoprolol, suggest that carvedilol may be better than metoprolol in heart failure.     

Acute hemodynamic effects of moderate doses of nebivolol versus metoprolol in patients with systolic heart failure

OBJECTIVES: To determine the acute hemodynamic effect of moderate doses of nebivolol (vasodilating beta1-selective blocker) vs. metoprolol tartrate (non-vasodilating beta1-selective blocker) in systolic heart failure (SHF). MATERIAL AND METHODS: 20 stable patients with SHF (left ventricular (LV) ejection fraction < or = 35%) underwent right heart catheterization. Once a reproducible baseline was obtained, patients were randomized to 5 mg nebivolol PO (n = 10) or metoprolol tartrate 50 mg PO (n = 10). Hemodynamic studies were repeated hourly for the first 4 hours and at 6 hours. RESULTS: Both agents caused bradycardia. Nebivolol caused additionally a decrease in systemic vascular resistance (SVR) and no significant change in pulmonary capillary wedge pressure (PCWP), and cardiac output (CO). In contrast, metoprolol caused a deterioration of LV systolic function characterized by a decrease in cardiac output, and an increase in SVR and PCWP. CONCLUSIONS: Treatment initiation with moderate doses of nebivolol is not associated with the adverse hemodynamic effects of metoprolol in patients with SHF. These findings suggest that a long up-titration period may not be necessary with nebivolol.     

Characterization of beta(1)-selectivity, adrenoceptor-G(s)-protein interaction and inverse agonism of nebivolol in human myocardium

Intrinsic activity and beta(1)-selectivity are important features of beta-blockers in the treatment of patients with coronary syndromes and heart failure. In human myocardium, intrinsic activity and beta(1)-selectivity of the novel beta-adrenoceptor antagonist nebivolol have not yet been determined. The study examines intrinsic activity, beta-adrenoceptor-G-protein coupling and beta(1)-selectivity of nebivolol and bisoprolol in human ventricular myocardium. Furthermore, intrinsic activity of both compounds is compared to the one of bucindolol, carvedilol and metoprolol in human atrial myocardium. Radioligand binding studies ([(125)I]-lodocyanopindolol) were performed on membrane preparations of human failing and nonfailing myocardium and on COS-7 cells transfected with human beta(1)- and beta(2)-adrenoceptors, respectively. Functional experiments were carried out on isolated muscle preparations of human left ventricular and right atrial myocardium from failing and nonfailing hearts. Radioligand binding studies reveal 3 - 4 fold beta(1)-selectivity for nebivolol and 16 - 20 fold beta(1)-selectivity for bisoprolol in human myocardium. In COS-7-cells, beta(1)-selectivity is 3 fold for nebivolol and 15 fold for bisoprolol. Neither the binding of nebivolol nor of bisoprolol is affected by the presence of guanylylimidodiphosphate (Gpp(NH)p). Nebivolol and bisoprolol exert similar inverse agonist activity in human ventricular as well as atrial myocardium. In atrial myocardium, inverse agonism of both compounds is higher compared to bucindolol, equal to carvedilol and lower compared to metoprolol. Favourable haemodynamic effects of nebivolol in humans are not due to beta(1)-selectivity or partial agonist activity of this agent. Other mechanisms, i.e. the production of nitric oxide, may thus be responsible for its unique haemodynamic profile.     

Pediatric heart failure therapy with beta-adrenoceptor antagonists

Management of chronic heart failure in pediatrics has been altered by the adult literature showing improvements in mortality and hospitalization rates with the use of beta-adrenoceptor antagonists (beta-blockers) for routine therapy of all classes of ischemic and non-ischemic heart failure. Many pediatric heart failure specialists have incorporated these agents into their routine management of pediatric heart failure related to dilated cardiomyopathy or ventricular dysfunction in association with congenital heart disease. Retrospective and small prospective case series have shown encouraging improvements in cardiac function and symptoms, but interpretation has been complicated by the high rate of spontaneous recovery in pediatric patients. A recently completed pediatric double-blind, randomized, placebo-controlled clinical trial showed no difference between placebo and two doses of carvedilol over a 6-month period of follow-up, with significant improvement of all three groups over the course of evaluation.Experience with adults has suggested that only certain beta-blockers, including carvedilol, bisoprolol, nebivolol, and metoprolol succinate, should be used in the treatment of heart failure and that patients with high-grade heart failure may derive the most benefit. Other studies surmise that early or prophylactic use of these medications may alter the risk of disease progression in some high-risk subsets, such as patients receiving anthracyclines or those with muscular dystrophy. This article reviews these topics using experience as well as data from all the recent pediatric studies on the use of beta-blockers to treat congestive heart failure, especially when related to systolic ventricular dysfunction.     

Carvedilol versus other β-blockers in heart failure

Carvedilol is a β-blocker with ancillary properties. Pilot clinical studies with carvedilol, added to the standard therapy of digoxin, diuretics and ACE inhibitors, showed beneficial effects in mild, moderate and severe heart failure. Patients consistently showed improvement in LV ejection fraction and NYHA functional class. Subsequently large clinical trials showed decreased morbidity and mortality with carvedilol in mild and moderate and more recently, severe heart failure. However, there is little or no improvement in exercise tolerance with carvedilol. The beneficial effects of carvedilol in heart failure are associated with cardiac remodelling. Metoprolol and bisoprolol are selective ₁-blockers without ancillary properties. Early studies showed benefits with metoprolol and bisoprolol in heart failure. Large clinical trials established that metoprolol and bisoprolol decreased mortality and morbidity in heart failure. In contrast no benefit has been shown with celiprolol, a selective ₁-blocker and ₂-stimulant in heart failure. There is a debate as to whether the ancillary properties of carvedilol contribute to its beneficial effect in heart failure, making it a better drug to use than metoprolol. Short-term studies suggested that carvedilol and metoprolol were equivalent in heart failure but short-term is probably not an appropriate way to compare the drugs. A recent long-term study and study in poor responders to metoprolol, suggest that carvedilol may be better than metoprolol in heart failure.     

A comparison of carvedilol and metoprolol antioxidant activities in vitro

Carvedilol is a vasodilating beta-blocker and antioxidant approved for treatment of mild to moderate hypertension. angina, and congestive heart failure. Metoprolol is a beta1-selective adrenoceptor antagonist. When carvedilol and metoprolol were recently compared in clinical trials for heart failure, each showed beneficial beta-blocker effects such as improved symptoms, quality of life, exercise tolerance, and ejection fraction, with no between-group differences. When thiobarbituric acid reactive substance (TBARS) levels were measured in serum as an indirect marker of free radical activity, there were also no between-group differences. However, we had noted superior cardioprotection by carvedilol in comparison to metoprolol in ischemia and reperfusion models. We therefore examined antioxidant activity directly in cells and tissues. Here we show that in cultured rat cerebellar neurons, and in brain and heart membranes, carvedilol has far greater antioxidant activity than metoprolol, which is essentially inactive as an antioxidant in these model systems. The antioxidant activity of carvedilol could be explained by a greater degree of lipophilicity, as measured by its ClogP value of 3.841 as contrasted to a ClogP value of 1.346 for metoprolol. Alternatively, the molecular structure of carvedilol favors redox recycling, which the structure of metoprolol does not. Therefore, carvedilol could have additional pharmacologic effects that are favorable for long-term therapy.     

Different intrinsic activities of bucindolol, carvedilol and metoprolol in human failing myocardium

1. Clinical studies have shown different effects of beta-blockers on the beta-adrenergic system, tolerability and outcome in patients with heart failure. 2. The study examines beta-adrenoceptor-G-protein coupling and intrinsic activity of bucindolol, carvedilol and metoprolol in human ventricular myocardium. 3. Radioligand binding studies ([(125)I]-Iodocyanopindolol) were performed in membrane preparations of human failing and nonfailing myocardium. Functional experiments were carried out in isolated muscle preparations of human left ventricular myocardium from failing hearts. 4. Bucindolol and carvedilol bound non-selectively to beta(1)- and beta(2)-adrenoceptors and exerted guanine nucleotide modulatable binding. Metoprolol was 35-fold beta(1)-selective and lacked guanine nucleotide modulatable binding. 5. All beta-blockers antagonized isoprenaline-induced enhancement of contractility. 6. In preparations in which the coupling of the stimulatory G-protein to adenylate cyclase was facilitated by forskolin, bucindolol increased force of contraction in three and decreased it in five experiments. Carvedilol increased force in one and decreased it in six experiments. Metoprolol decreased force in all experiments by 89. 4+/-2.2% (P<0.01 metoprolol vs carvedilol and bucindolol). The negative inotropic effect of metoprolol was antagonized by bucindolol. 7. It is concluded that differences in intrinsic activity can be detected in human myocardium and have an impact on cardiac contractility. In human ventricular myocardium, bucindolol displays substantially higher intrinsic activity than metoprolol and carvedilol. Bucindolol can behave as partial agonist or partial inverse agonist depending on the examined tissue. 8. Differences in intrinsic activity may contribute to differences in beta-adrenoceptor regulation and possibly to differences in tolerability and outcomes of patients with heart failure.     

卡维地洛及美托洛尔对慢性心力衰竭合并糖尿病患者的心功能及胰岛素抵抗的影响

目的 观察卡维地洛和美托洛尔对慢性心力衰竭（chronicheart failure,CHF）合并2型糖尿病（type2 diabetesmellitus,T2DM）患者的心功能及胰岛素抵抗的影响。方法CHF合并T2DM患者130例,根据常规治疗基础上加用卡维地洛与美托洛尔分为卡维地洛组（65例）和美托洛尔组（65例）。治疗12个月。结果（1）卡维地洛组及美托洛尔组心功能均较治疗前改善（P〈0．05）。LVEF均高于治疗前（P〈0．05）,舒张末期内径（LVEDd）、舒张末期容积指数（LVEDVI）、收缩末期容积指数（LVESVI）均低于治疗前（P〈0．05）。卡维地洛组疗效优于美托洛尔组（P〈0．05）。（2）卡维地洛组的胰岛素抵抗指数显著低于治疗前（P〈0．05）,而美托洛尔治疗前后无明显变化（P〉0．05）。结论卡维地洛和美托洛尔均能明显改善CHF合并T2DM患者的心功能,卡维地洛可改善胰岛素抵抗。