马来酸左旋氨氯地平与苯磺酸左旋氨氯地平治疗老年高血压的疗效对比

目的比较马来酸左旋氨氯地平与苯磺酸左旋氨氯地平治疗老年高血压的效果。方法将我院门诊确诊的60例原发性老年高血压患者随机分为马来酸左旋氨氯地平组和苯磺酸左旋氨氯地平组,各30例,马来酸左旋氨氯地平组给予马来酸左旋氨氯地平2.5mg,苯磺酸左旋氨氯地平组给予苯磺酸左旋氨氯地平2.5mg,随访4周,观察两组清晨血压降幅、疗效及不良反应。结果马来酸左旋氨氯地平组清晨血压平均降幅均高于苯磺酸左旋氨氯地平组,差异有统计学意义(P<0.05);两组患者疗效比较,差异无统计学意义(P<0.05);两组患者治疗期间均未出现明显不良反应。结论马来酸左旋氨氯地平和苯磺酸左旋氨氯地平均能起到降压的作用,但马来酸左旋氨氯地平较苯磺酸左旋氨氯地平对于清晨血压的控制表现出明显的优势。     

氯沙坦联合依那普利对高血压心肌肥厚患者左室舒张功能的影响

目的 观察氯沙坦联合依那普利对高血压心肌肥厚患者左心室舒张功能的影响.方法 采用自身对照设计,36例坚持随访均患者给予氯沙坦50mg/次,每天一次;依那普利10mg/次～20mg/次,每天一次,随访24周,期间比较血压的变化;治疗前后作超声心动图检查,比较心肌厚度及左室舒张功能的改变.结果 与治疗前相比,患者左室后壁舒张末期厚度(LVPWT)、室间隔舒张末期厚度(IVST)、均明显下降(P<0.01);反映左室舒张功能的A/E值亦较治疗前下降(P<0.05);收缩压与舒张压均明显降低(P<0.01). 结论 氯沙坦与依那普利联合用药能有效地控制血压、逆转左室肥厚、改善左心室舒张功能.     

用苯磺酸氨氯地平和苯磺酸左旋氨氯地平治疗高血压的效果对比

目的分析比较苯磺酸氨氯地平和苯磺酸左旋氨氯地平对治疗高血压的效果。方法本次研究资料选取我院2014年1月~2015年12月收治的高血压患者70例,按照患者自主用药意愿将其分为A组与B组,各35例。对A组患者采用苯磺酸氨氯地平治疗,给B组患者采用苯磺酸左旋氨氯地平治疗,对比两组治疗效果。结果采用苯磺酸氨氯地平治疗的A组临床治疗总有效率取得88.5%,相较于采用苯磺酸左旋氨氯地平治疗的B组的74.6%,两组对比差异有统计学意义(P0.05);且A组治疗期间的不良反应情况也少于B组,两组对比差异有统计学意义(P0.05)。讨论苯磺酸氨氯地平和苯磺酸左旋氨氯地平对治疗高血压均有明显效果,相较于苯磺酸氨氯地平,苯磺酸左旋氨氯地平治疗期间不良反应更小,更适合临床应用。     

不同剂量比索洛尔对老年高血压病并发舒张性心力衰竭左室舒张功能的影响

目的: 观察不同剂量的比索洛尔对舒张性心力衰竭患者左室舒张功能的影响。方法: 92例高血压病并发左室舒张功能不全但左室射血分数（LVEF）>50%的患者,在氨氯地平控制血压达标（<140/90 mmHg）的基础上,按照加用比索洛尔的剂量随机分为3组:对照组（不用比索洛尔组,n=31）,低剂量组（加用比索洛尔1.25 mg,1次/d,n=30）,高剂量组（加用比索洛尔5 mg,1次/d,n=31）,平均随访观察30周。采用超声多普勒心动图评估治疗前后左室结构和功能参数的变化。结果: 3组治疗后LVEF和收缩压无明显改变,舒张压和心率在低剂量组和高剂量组下降明显（P<0.05）。加用比索洛尔治疗后,患者E峰、A峰、E/A、E峰流速积分（VTIE）、A峰流速积分（VTIA）、流速时间积分比率(E-VTI/A-VTI）有不同程度改善,高剂量组较低剂量组改善更加显著（P<0.05）。左室舒张末内径（LVEDD）、室间隔厚度（IVSD）、左室后壁厚度（PWT）、左室质量指数（LVMI)在高剂量组变化显著(P<0.05),对照组无显著改善。结论: 在氨氯地平降压达标基础上,比索洛尔能够进一步改善高血压病患者左室舒张功能,较大剂量作用更加显著。     

苯磺酸左旋氨氯地平联合氯沙坦治疗2型糖尿病肾病高血压及肾功能的临床疗效分析

目的:观察苯磺酸左旋氨氯地平与氯沙坦单独及联合应用对2型糖尿病高血压的临床疗效,以及长期应用的有效性与安全性.方法:以2008年5月～ 2011年12月收治的90例2型糖尿病肾病伴高血压患者为研究对象,分为3组,每组30例,给药方法如下:氨氯地平组(给予苯磺酸左旋氨氯地平2.5mg)、氯沙坦组(给予氯沙坦50mg)和联合用药组(给予苯磺酸左旋氨氯地平2.5mg和氯沙坦50mg),1次/d,疗程12周.结果:两药单独应用和联合应用均可明显降低糖尿病肾病高血压(P＜0.05),改善肾功能(P＜0.05);联合治疗降压作用和改善肾功能损伤作用明显优于单独治疗(P＜0.05).结论:苯磺酸左旋氨氯地平、氯沙坦治疗2型糖尿病肾病高血压均有较好的降压作用和改善肾功能损害,两药联合应用具有协同作用,值得临床推广应用.     

氨氯地平联合奥美沙坦对高血压病人左室肥厚的影响

目的观察氨氯地平联合奥美沙坦对原发性高血压病人左室肥厚和左室功能的影响。方法入选200例高血压病人,随机分为氨氯地平组和氨氯地平+奥美沙坦组,每组100例。治疗前和随访结束时超声心动图测量病人左心室舒张末期内径(LVEDD)、室间隔厚度(IVS)、左室后壁厚度(PWT)、左室射血分数(LVEF)、舒张早期二尖瓣血流速度与舒张晚期二尖瓣血流速度比值(E/A)。酶联免疫吸附法测定血清Ⅲ型前胶原(PCⅢ)、层黏连蛋白(LN)和透明质酸(HA)。结果两组病人治疗后血压均较治疗前下降(P0.05);两组治疗后收缩压和舒张压差异无统计学意义(P0.05)。与氨氯地平组治疗后比较,氨氯地平+奥美沙坦组病人IVST、LVPWT、LVM、LVMI明显降低(P0.05),LVEF和E/A明显增加(P0.05),血清心肌纤维化指标PCⅢ、LN和HA均进一步降低(P0.05)。结论氨氯地平和氨氯地平联合奥美沙坦治疗均能有效降压和改善左室肥厚,但是联用奥美沙坦逆转左室肥厚和改善心功能作用更明显。     

苯磺酸左旋氨氯地平片与厄贝沙坦/氢氯噻嗪片联合治疗高血压的疗效评价

目的 观察苯磺酸左旋氨氯地平片(2.5mg)与厄贝沙坦/氢氯噻嗪片(含厄贝沙坦150mg,氢氯噻嗪12.5mg)联合治疗高血压的临床疗效.方法 选择高血压患者72例,随机分为3组:A组(n=23)口服苯磺酸左旋氨氯地平片2.5mg,1次/d;B组(n=19)口服厄贝沙坦/氢氯噻嗪片150mg,1次/d;C组(n=30)晨服厄贝沙坦/氢氯噻嗪片150mg,睡前服用苯磺酸左旋氨氯地平片2.5mg,1次/d;疗程均为12周.结果 3组患者血压均有下降,A组总有效率为65.2%,B组为63.1%,C组为93.3%.结论 苯磺酸左旋氨氯地平片联合厄贝沙坦/氢氯噻嗪片用于治疗高血压比单用苯磺酸左旋氨氯地平片或厄贝沙坦/氢氯噻嗪片更有效、安全,值得推广.     

苯磺酸左旋氨氯地平与依那普利治疗肾性高血压65例

为了评价苯磺酸左旋氨氯地平联合依那普利治疗肾性高血压以及对蛋白尿的影响和不良反应,对2005年5月—2007年5月在我院就诊的肾性高血压病病人采用苯磺酸左旋氨氯地平与依那普利联合治疗,现报道如下。1资料与方法1.1临床资料选择我院2005年5月—2007年5月住院的慢性肾小球肾炎合并高血压病人65例,经有关检查排除原发性高血压,其中男40例,女25例,年龄12岁~60岁,平均45岁,全部病例有蛋白尿,52例有血尿,10例有肾功能不全。1.2方法1.2.1治疗方法苯磺酸左旋氨氯地平2.5mg/d,早饭后服用,依那普利(5~10)mg/d,每日2次。从小剂量开始根据血压控制情况…     

苯磺酸左旋氨氯地平与苯磺酸氨氯地平在社区治疗轻中度高血压的成本效果分析

目的探讨苯磺酸左旋氨氯地平与苯磺酸氨氯地平在社区治疗轻中度高血压的成本效果。方法选择100例原发性轻中度高血压患者,随机分为两组,分别给予苯磺酸左旋氨氯地平(Ⅰ组)和苯磺酸氨氯地平(Ⅱ组)治疗,运用药物经济学成本效果分析方法进行评价。结果苯磺酸左旋氨氯地平2.16元/片(2.5mg/片),苯磺酸氨氯地平5.70元/片(5mg/片),两组均为1次/d,1～2片/次,治疗8周后,Ⅰ组总有效率86%,Ⅱ组总有效率80%;8周一疗程用苯磺酸左旋氨氯地平可节约药费396元,按敏感度分析一疗程可节约药费316.8元。结论根据经济性、有效性、安全性,苯磺酸左旋氨氯地平可作为轻中度高血压社区治疗的一线用药。     

卡维地洛与氨氯地平联用治疗舒张功能不全性心力衰竭

目的　观察卡维地洛与氨氯地平联用治疗舒张功能不全性心力衰竭的有效性和安全性。方法　将 10 0例心功能 ～ 级舒张功能不全性心力衰竭者随机分为两组 ,治疗组 :卡维地洛与氨氯地平联用 :对照组 :仅氨氯地平口服。观察心功能改善包括多普勒超声心动图测定左心室等容舒张时间 ( IVRT)、舒张早期和晚期充盈速度及其比值 ( E、A、E/A) ,并观察血压 ( BP)、心率 ( HR)。结果　治疗组在改善心功能包括超声心动图参数 :IVRT、E、A、E/A及 BP、HR方面明显优于对照组 ,P<0 .0 1,有统计学显著性差异 ,且不良反应少。结论　卡维地洛与氨氯地平联用治疗舒张功能不全性心力衰竭的疗效优于单用氨氯地平 ,且安全。     

Altered left ventricular diastolic performance in oncologic patients treated with epirubicin

Anthracyclines confer an increased risk of cardiotoxicity. The authors evaluated left ventricular (LV) performance in patients treated with epirubicin. Sixty-eight patients with malignancies (study group), treated with epirubicin < or = 450 mg/m2, and a matched control group of 68 cancer patients who had not started chemotherapy were evaluated by Doppler echocardiography. The authors assessed LV diastolic function by measuring the transmitral flow: the maximal velocity of the E and A waves, the Emax/Amax ratio, the pressure half time of E wave (PHT), and the isovolumic relaxation time (IVRT). Global LV ejection fraction (LVEF) was estimated to determine the systolic performance. The authors documented alterations of the LV diastolic performance in the study group by finding a significant decrease in Emax, whereas Amax was significantly increased. Prolonged PHT and IVRT were also certified in the epirubicin-treated group compared with controls. No significant variation in LVEF between the 2 groups was detected.     

伊贝沙坦与依那普利联用改善高血压病早期肾损害的观察

目的: 评价伊贝沙坦合用依那普利对原发性高血压患者早期肾功能损害的有效性和安全性。方法: 将110例经血、尿中β2微球蛋白（β2-MG）检测证实具有早期肾功能损害的轻、中度高血压患者,随机分为3组, 即伊贝沙坦组(A组,50例):口服伊贝沙坦150~300 mg/d;依那普利组(B组,26例):口服依那普利5~10 mg/d及伊贝沙坦加依那普利组(C组,34例)。所有入选病例均治疗12周,治疗前后测量血压并采用ELISA法检测血、尿中β2-MG的水平;采用彩色超声多普勒仪检查肾血流量及肾血管重构的情况。结果: 与治疗前相比较,治疗12周后3组患者的收缩压、舒张压均明显下降（P<0.01）;血、尿中β2-MG的水平明显降低（P<0.01）;肾阻力指数（RI）、搏动指数（PI）及平均流速（Vm）明显改善（P<0.01）。治疗后肾血管管壁的厚度及肾动脉的内径与治疗前有显著性差异（P<0.05）。伊贝沙坦与依那普利联合治疗组与单用伊贝沙坦或依那普利治疗组比较,血、尿中β2-MG的水平及肾血管重构指标有显著改善（P<0.01或P<0.05）。 结论: 伊贝沙坦与依那普利联用对有早期肾功能损害的高血压患者,不仅有明显的降压作用,而且有明显改善肾功能的作用。     

H型高血压颈动脉粥样硬化及依那普利叶酸片干预效果及其机制研究

目的 了解H型高血压患者Hcy 水平与颈动脉粥样硬化、血管炎症之间的相关性,探讨依那普利叶酸片对动脉粥样硬化的干预效果及其机制。 方法 400例高血压患者中依据纳入标准,抽取120例患者随机分为对照组与治疗组各60例,测定Hcy、颈动脉粥样斑块及颈总动脉平均内膜中层厚度(IMT),计算斑块crouse积分。对照组常规予以依那普利片10mg/日降压,观察组选用依那普利叶酸片10mg/0.8mg/日,其它治疗包括：常规使用抗血小板、稳定斑块等对症处理,在两组间基本一致。治疗随访1年后复测上述实验室及器械检查指标。 结果 Hcy水平与颈动脉粥样硬化及血管炎症反应指标成正相关,Hcy越高, IMT值越大,Crouse积分越高,反映血管炎症的Hs-CRP越高,说明两者相关性越高。依那普利叶酸片对H型高血压患者的干预效果更佳。两组患者治疗后的收缩压（SBP）及舒张压（DBP）与治疗前比较均有明显下降;治疗后两组Hcy比较,治疗组的Hcy明显低于对照组,差异有统计学意义(P＜0.05)。 结论 Hcy水平是导致颈动脉粥样硬化的重要因素,Hcy参与血管炎症反应,Hcy越高,血管炎症反应越显著,动脉粥样硬化越明显。依那普利叶酸片与依那普利比较,在降压、降低Hcy水平同时,对颈动脉粥样硬化的进展能起到明显的抑制作用。     

Effects of enalapril on heart failure in hypertensive patients with diastolic dysfunction.

Ten hypertensive patients with symptoms of heart failure and normal systolic function but with diastolic dysfunction were treated with 10 mg enalapril twice a day for 9 +/- 3 months to evaluate the effects of this agent alone on heart failure induced by diastolic dysfunction. After therapy, all patients improved and echocardiographic parameters of diastolic dysfunction became normalized. It is concluded that enalapril appears to be useful in the treatment of heart failure in hypertensive patients with normal systolic function and diastolic dysfunction.     

左旋氨氯地平和氨氯地平治疗轻中度高血压的临床观察

目的评价左旋氨氯地平和氨氯地平治疗轻中度高血压的疗效与不良反应。方法选择门诊轻中度高血压患者108例,随机分为3组,每组36例,接受氨氯地平5 mg/d(A组)、左旋氨氯地平2.5 mg/d(B组)、左旋氨氯地平5 mg/d(C组),共治疗8周,观察降压效果和不良反应。结果 3组治疗后收缩压和舒张压较治疗前明显下降(P<0.05)。与A、B组比较,C组血压变化值更高(P<0.01),血压达标率高(P<0.05)。3组治疗后红细胞计数、血红蛋白较治疗前明显增高(P<0.05);B组血K~+明显降低(P<0.05)。结论左旋氨氯地平能有效降低轻中度高血压患者的血压,不良反应低于氨氨地平,左旋氨氯地平2.5 mg治疗后血K+下降。     

Effects of enalapril on left ventricular mass and diastolic function in essential hypertension: special reference to duration of hypertension

Using M-mode and pulsed Doppler echocardiography, the effects of enalapril on left ventricular (LV) hypertrophy and diastolic dysfunction in essential hypertension and the relation between improvement in these two parameters and duration of hypertension were evaluated. The subjects, 30 previously untreated hypertensive patients, were divided into nonhypertrophy (18 patients) and hypertrophy (12 patients) groups. All patients received enalapril at a daily dose of 5 to 10 mg for 6 months. Left ventricular mass by M-mode echocardiography and LV inflow (LVIF) velocity by transthoracic pulsed Doppler echocardiography were measured before and after enalapril therapy. In the nonhypertrophy group, enalapril significantly increased peak early diastolic LVIF (E) velocity (P < .05), slightly lowered peak atrial systolic LVIF (A) velocity, significantly decreased their ratio (A/E) (P < .01), and significantly shortened both the deceleration time, from the peak of the early diastolic wave, and isovolumic relaxation time (P < .05 and P < .01, respectively). In the hypertrophy group, enalapril significantly increased E (P < .05), slightly lowered A, significantly decreased A/E (P < .05), slightly shortened the deceleration time and isovolumic relaxation time, and slightly decreased LV mass. The administration of enalapril correlated significantly and positively with the duration of hypertension and the rates of change in A/E and LV mass in all of the hypertensive patients (P < .01 and P < .05, respectively). These results suggest that long-term administration of enalapril to hypertensive patients improves LV diastolic hemodynamics regardless of the presence or absence of LV hypertrophy and that the effects are most remarkable in patients with the shortest duration of hypertension.     

Additive effect of drospirenone/17-beta-estradiol in hypertensive postmenopausal women receiving enalapril

BACKGROUND: Aldosterone has been implicated in the pathogenesis of progressive cardiovascular disease. Drospirenone (DRSP) is a novel progestin with aldosterone receptor antagonist activity developed for hormone replacement therapy (HRT) as DRSP/17beta-estradiol (DRSP/ E2). We investigated the additive effect of DRSP/E2 versus placebo on 24-h ambulatory blood pressure (BP) in postmenopausal women with hypertension treated with enalapril maleate (ENA). METHODS: This was a double-blind, randomized, two-parallel group trial. Twenty-four nonsmoking postmenopausal women receiving 10 mg of ENA twice a day before study were randomized to DRSP/E2 + ENA (n = 12) or placebo (P) + ENA (n = 12) for 14 days. Twenty-four-hour ambulatory BP, plasma renin activity, and serum aldosterone were determined at baseline and on day 14. RESULTS: Compared to placebo, 24-h mean [SD] BP in the DRSP/E2 + ENA group decreased significantly from baseline (139/80 mm Hg), systolic (-9 [51 mm Hg, P = .014) and diastolic (-5 [4] mm Hg, P = .007). Essentially no change from baseline (139/83 mm Hg) in systolic or diastolic 24-h ambulatory BP were observed in the P + ENA group. Aldosterone (mean [SD]) increased from baseline by 2.6 [4.5] ng/dL in the DRSP/E2 + ENA group, and decreased by 0.3 [5.5] ng/dL in the P + ENA group (P = .08) consistent with an antimineralocorticoid effect. CONCLUSIONS: Our results suggest a significant additive BP-lowering effect of DRSP/E2 on both systolic and diastolic BP in hypertensive postmenopausal women receiving ENA, consistent with an antimineralocorticoid effect. DRSP/E2, a HRT with antimineralocorticoid effects, could offer a novel potential mechanism for reducing cardiovascular end points in postmenopausal women.     

Blood pressure and left ventricular geometric pattern determine diastolic function in hypertensive myocardial hypertrophy

Abnormal left ventricular (LV) diastolic relaxation is an early sign of hypertensive heart disease. Whether LV diastolic dysfunction is caused directly by raised blood pressure, or by structural changes related to LV hypertrophy remains controversial. We examined 115 hypertensive patients with LV hypertrophy, and two age- and gender-matched groups (38 hypertensive patients without LV hypertrophy and 38 normotensive subjects) by echocardiography to assess determinants of LV diastolic function, and the relation between diastolic function and LV geometric pattern. Diastolic function was evaluated by the E/A-ratio, E wave deceleration time (E-dec), isovolumic relaxation time (IVRT), and the atrioventricular plane displacement method (AV-LA/AV-mean). A multivariate analysis (including gender, age and body mass index) shows diastolic function to be inversely related to blood pressure, LV wall thickness and LV mass, but not to LV end diastolic diameter. The E/A-ratio generally showed the strongest relations. Only the E/A-ratio and AV-LA/AV-mean were related to heart rate. By stepwise regression analysis, age was the strongest determinant for the E/A-ratio, E-dec and AV-LA/AV-mean, followed by systolic blood pressure, heart rate and LV wall thickness. For IVRT, however, LV wall thickness appeared strongest, followed by systolic blood pressure and age. In conclusion, blood pressure and LV wall thickness both have independent influence on LV diastolic function. Age and blood pressure are the most important factors to determine the E/A-ratio and E-dec, whereas LV geometry and blood pressure are most important when IVRT is used. AV-LA/AV-mean may not be useful in hypertensive LV hypertrophy.     

Color M-mode flow propagation velocity and conventional doppler indices in the assessment of diastolic left ventricular function during isometric exercise

BACKGROUND AND OBJECTIVE: Color M-mode flow propagation velocity (Vp) was shown to be a preload-independent measure of diastolic function. To study the effects of an increase in afterload induced by isometric handgrip exercise on diastolic function assessment in patients with cardiomyopathy, we measured Vp and conventional Doppler indices at baseline and at 30% of predetermined maximum handgrip strength. METHODS: Twenty-four patients with systolic dysfunction were divided into two groups: Group I comprising 12 patients with E/A < 1 (early filling velocity/atrial contraction velocity) and Group II comprising 12 patients with E/A > 1. All the patients underwent measurement of Vp, E velocity, its deceleration time (DT), A velocity, isovolumic relaxation time (IVRT), and pulmonary atrial flow reversal velocity (PFR) at baseline and at 30% of predetermined maximum handgrip strength. Twelve healthy controls underwent these same measurements. RESULTS: When comparing baseline to peak echocardiographic data, no significant changes were noted in Vp in any of the groups while a shift of pulsed Doppler indices of Group I toward a pattern closer to that of Group II was noted and a decrease in E velocity and E/A ratio with an increase in IVRT occurred in healthy controls. CONCLUSIONS: Color M-mode flow propagation velocity seems to be an afterload-independent measure of diastolic function in patients with moderate to severe cardiomyopathy while pulsed Doppler indices are more sensitive to loading conditions induced by isometric exercise.     

Effects of carvedilol on left ventricular diastolic function and chamber volumes in advanced heart failure

AIM: Carvedilol treatment in chronic heart failure (CHF) demonstrated to reduce mortality and rehospitalisation, and improvement of cardiac systolic function with reduction of left ventricular volumes and remodelling. The effects of the drug on left ventricular (LV) filling are less studied. Systolic dysfunction is often associated to diastolic alteration, pseudonormal and restrictive filling pattern are related with poor prognosis. In this study we evaluated diastolic cardiac modifications during carvedilol therapy at early and long term in patients with advanced CHF and pseudonormal or restrictive filling pattern by echo Doppler method. METHODS: We studied 59 patients with severe but stable CHF (40 in class NYHA III and 19 in class NYHA IV) with both systolic and diastolic dysfunction due to idiopathic or ischemic cardiomyopathy. Group I (n=32) received preceding treatment plus carvedilol and Group II (n=27) continued standard therapy with ACE-inhibitors, diuretics, digossin and vasodilators. In all subjects were evaluated LV volumes mass and ejection fraction (EF). Therefore, we studied transmitral filling parameters: Early filling wave (E), atrial filling wave (A), E/A ratio, deceleration time of E (DT) and isovolumetric releasing time (IVRT) by echo Doppler method. RESULTS: After 4 months of therapy carvedilol group showed a significant increase of A wave (p<0.001) DT (p<0.0001) and IVRT (p<0.0001), and significant reduction of E/A ratio (p<0.0005) respect to Group II. Any significant changes were observed for volumes mass and EF. Transmitral Doppler measurements remained unchanged or further ameliorated at 12 months (A p<0.0005; DT p<0.00002; IVRT p<0.000004; E/A p<0.0008), we also observed E wave reduction (p<0.001) in Group I respect to controls. Besides, after 1 year of follow-up we observed a reduction of systolic volume (p<0.001) pulmonary pressure (p<0.0001) and consequent increase of EF (p<0.001) in group treated with beta-blockers. Multivariate analysis demonstrated that Doppler modification were minimally related to heart rate and blood pressure reduction. CONCLUSIONS: Carvedilol treatment improve diastolic function in CHF with severe diastolic impairment driving restrictive or pseudonormal filling pattern towards altered pattern at early time. These changes remained also after 1 year of therapy and appeared to precede increase of systolic function and improvement of emodynamic status.