川芎嗪与环磷腺苷葡胺治疗肺心病失代偿期

目的观察川芎嗪与环磷腺苷葡胺治疗肺心病失代偿期患者之疗效。方法60例肺心病失代偿期患者随机分为对照组和治疗组,两组常规治疗相同,治疗组加用川芎嗪和环磷腺苷葡胺,疗程7～10d。比较两组心率、尿量、血气变化。结果治疗组和对照组心率分别为(79.7±7.18)次/min和(84.4±7.88)次/min;尿量分别为(1445.6±161.7)ml/24h和(1332.8±156.8)ml/24h;血气分析PaO2分别增加了(6.33±1.76)mmHg和(5.39±1.39)mmHg。两组比较有统计学差异(P<0.05)。结论川芎嗪与环磷腺苷葡胺联合治疗肺心病失代偿期疗效明显,未见明显副作用。     

环磷腺苷葡胺辅助治疗慢性肺源性心脏病心力衰竭疗效观察

目的观察环磷腺苷葡胺辅助治疗慢性肺源性心脏病(简称肺心病)心力衰竭的疗效及安全性。方法将80例慢性肺心病心力衰竭患者随机分为观察组和对照组,各40例,两组给予抗感染、利尿、纠正电解质及酸碱平衡紊乱、低流量吸氧等常规治疗,观察组静滴环磷腺苷葡胺,连续治疗7 d,观察治疗前后咳嗽、咳痰、活动耐力、肺部体征及动脉血气检查结果。结果观察组总有效率92.50%,对照组70.00%,P<0.05;与治疗前比较,两组治疗后Pa O2、Sa O2明显增加、Pa CO2明显降低(P均<0.05)。与对照组比较,观察组治疗后Pa O2、Sa O2、Pa CO2变化更显著(P均<0.05)。观察组药物不良反应发生率5.00%,对照组2.50%,P>0.05。结论环磷腺苷葡胺治疗慢性肺心病心力衰竭安全、有效。     

川芎嗪联合环磷腺苷葡胺治疗肺尘埃沉着病合并肺心病患者的临床效果

目的探讨川芎嗪联合环磷腺苷葡胺对肺尘埃沉着病(尘肺)合并肺心病患者的临床效果。方法选择92例尘肺合并肺心病,按抽签法分为对照组和试验组,每组46例。对照组予以环磷腺苷葡胺治疗,静脉滴注150 mg环磷腺苷葡胺和250 ml 5%葡萄糖注射液,1次/d,持续治疗14 d。试验组基于对照组联合川芎嗪治疗,静脉滴注120 mg川芎嗪和250 ml 5%葡萄糖注射液,1次/d,持续治疗14 d。比较两组临床疗效,血清白细胞介素(IL)-6、脑钠肽(BNP)、D-二聚体(D-D)、纤维蛋白原(FIB)、心肺功能及不良反应发生情况。结果两组有效率差异有统计学意义(P0.05)。治疗后,两组血清IL-6、BNP、FIB水平比较差异有统计学意义(P0.05)。试验组心肺功能显著优于对照组(P0.05)。两组均有腹泻、呕吐、恶心发生,药物不良反应发生率差异无统计学意义(P0.05)。结论川芎嗪联合环磷腺苷葡胺对尘肺合并肺心病患者的效果优于环磷腺苷葡胺,能够降低血清IL-6、BNP、D-D、FIB水平,缓解病情。     

环磷腺苷葡胺联合丹参酮ⅡA磺酸钠治疗肺心病42例观察

目的观察环磷腺苷葡胺联合丹参酮ⅡA磺酸钠治疗肺心病的疗效。方法将84例肺心病急性发作期患者随机分为两组,各42例。两组均采用抗感染、扩张支气管、利尿及吸氧等治疗。治疗组在此基础上使用丹参酮ⅡA磺酸钠联合环磷腺苷葡胺,疗程为10d。结果治疗组总有效率为95.2%,对照组总有效率为85.7%;两组治疗后血液流变指标有改善,治疗组改善较对照组更明显(P<0.05)。结论丹参酮ⅡA磺酸钠联合环磷腺苷葡胺可以有效改善患者血液流变指标,改善心肺功能。     

环磷腺苷葡胺治疗尘肺结核心功能不全的观察

环磷腺苷葡甲胺是我国自行合成的环磷腺苷（cAMP）的衍生物,为环磷腺苷与葡甲胺结合形成的化合物,它能加强心肌收缩,具有一定的强心作用,可显著增加心肌细胞的搏动强度,并能扩张心血管,降低外周血管阻力,营养心肌﹑改善循环﹑改善心肌泵血功能,改善心肌细胞代谢,减少心肌氧耗量和改善左室功能等作用。现就对20例煤工尘肺结核合并肺心病患者应用环磷腺苷葡胺治疗改善慢性肺源性心脏病的临床观察结果报告如下。     

环磷腺苷葡甲胺治疗重度充血性心力衰竭的临床研究

目的观察环磷腺苷葡甲胺注射液治疗重度充血性心力衰竭(CHF)的临床疗效.方法将62例CHF病人随机分为治疗组32例和对照组30例.对照组应用常规治疗,治疗组在常规治疗基础上,以环磷腺苷葡甲胺注射液60 mg加入5%葡萄糖注射液250 ml中缓慢静脉输注2 h,两组均以10 d为1个疗程,1个疗程后观察疗效.结果两组治疗后心功能较治疗前有明显好转,治疗组与对照组的总有效率分别为97%和70%(P＜0.05);两组治疗前后左心室射血分数(LVEF)、每分心排血量(CO)、每搏量(SV)比较均有统计学意义(P＜0.05～P＜0.01),且治疗组优于对照组(P＜0.05～P＜0.01).结论环磷腺苷葡甲胺注射液对CHF有良好的治疗效果.     

环磷酸腺苷葡甲胺对慢性肺心病肺动脉高压的影响

目的:观察环磷酸腺苷葡甲胺静滴对肺心病心衰时肺动脉高压的影响。方法:对30例肺心病心衰肺动脉高压患者,应用环磷酸腺苷葡甲胺120 mg静滴,1次/d,疗程14天。治疗前后用彩色多普勒超声诊断仪测定平均肺动脉压力(mPAP)。结果:静滴环磷酸腺苷葡甲胺治疗10天及14天后mPAP均显著降低(P<0.01),治疗10天后与14天后相比:mPAP无明显变化(P>0.05)。结论:环磷酸腺苷葡甲胺静滴对降低肺动脉压力有显著作用,持续静滴之则肺动脉压力可维持在较低水平,对治疗肺心病心衰及改善预后有重要意义。     

环磷腺苷葡胺联合米力农与洋地黄治疗慢性肺心病心力衰竭的疗效

目的比较环磷腺苷葡胺联合米力农与洋地黄类强心剂治疗慢性肺心病心力衰竭的疗效与安全性。方法采用随机、平行对照的研究方法,对108例慢性肺心病心力衰竭随机分成两组:治疗组(54例)在常规治疗的基础上加用环磷腺苷葡胺和米力农;观察组(54例)在常规治疗的基础上加用洋地黄(西地兰针),12天一疗程。结果治疗组总有效率94.4%,明显优于观察组66.6%(P<0.01),治疗组心功能指标右室内径、右心室流出道/左心房内径及心胸比例的改善明显优于观察组(P<0.01),肺功能、PaO2、PaCO2及脑钠肽改善明显优于观察组(P<0.01),而心率、血压无明显差异(P>0.05);治疗组不良反应主要有心悸、出汗、头痛,减慢静滴速度症状消失,观察组主要不良反应心律失常,常需停药。结论环磷腺苷葡胺联合米力农治疗慢性肺心病心力衰竭有更好的疗效,更少的副作用,值得临床上进一步推广应用。     

环磷腺苷葡甲胺治疗充血性心力衰竭疗效观察

目的观察环磷腺苷葡甲胺治疗充血性心力衰竭的疗效。方法将68例充血性：心力衰竭患者分为治疗组（34例）与对照组（34例），两组常规治疗相同，治疗组给予环磷腺苷葡甲胺150mg加入5％葡萄糖注射液250ml中静滴，每天1次，疗程15天，比较两组治疗前后心功能改善情况。结果治疗组与对照组的临床总有效率分别为94．1％（32／34）和73．5％（25／34），经统计学分析差异有非常显著性（P〈0．01）。结论环磷腺苷葡甲胺治疗充血性心力衰竭有较好疗效。     

氯沙坦联合环磷腺苷葡胺治疗肺心病临床观察

目的探讨氯沙坦联合环磷腺苷葡胺治疗肺心病的效果。方法选取2015年2月~2016年2月在我院接受治疗的肺心病患者60例,随机分成观察组和对照组,各30例。对照组患者采用常规肺心病治疗方式,观察组在常规治疗基础上采用氯沙坦联合环磷腺苷葡胺治疗。两组患者均连续治疗2周,比较两组患者疗效。结果治疗后,观察组用力呼吸容积(FEV1)、FEV1/用力肺活量(FVC)指标明显优于对照组,差异有统计学意义(P0.05);观察组左心室射血分数(LVEF)、心输出量(CO)、每搏量(SV)指标明显优于对照组,差异有统计学意义(P0.05);两组患者lg G、lg A以及C3治疗前后无显著变化(P0.05)。结论氯沙坦联合环磷腺苷葡胺治疗肺心病能够修复患者心肺功能损伤,恢复肺功能,缓解患者病情,具有较高的临床应用价值。     

Lack of improvement of lung diffusing capacity following fluid withdrawal by ultrafiltration in chronic heart failure

OBJECTIVES: We sought to investigate the possibility that lung diffusing capacity reduction observed in chronic heart failure is reversible in the short term. BACKGROUND: Mechanical properties of the lung usually ameliorate with antifailure treatment including drugs, ultrafiltration and heart transplantation, whereas lung diffusion rarely improves. METHODS: We studied the mechanical properties of the lung (pulmonary function tests with determination of alveolar volume, extravascular lung fluids and lung tissue), lung diffusion for carbon monoxide (DLco), including membrane diffusing capacity (Dm), pulmonary capillary blood volume (Vc) and pulmonary hemodynamics, in 28 patients with stable chronic heart failure, before a single session of extracorporeal ultrafiltration (3,973 +/- 2200 ml) and four days thereafter. Lung mechanics and diffusion were also evaluated in 18 normal subjects. RESULTS: Vital capacity, forced expiratory volume (1 s) and maximal voluntary ventilation were lower in patients when compared with normal subjects, and increased after ultrafiltration from 2.1 +/- 0.7 to 2.5 +/- 0.7(1)*, 1.7 +/- 0.5 to 2.0 +/- 0.6(1)* and 67 +/- 25 to 79 +/- 26 (1/min)*, respectively (* p < 0.02 vs. pre-ultrafiltration). Post-ultrafiltration alveolar volume was augmented, while lung tissue, body weight (approximately 6 kg), chest X-ray extravascular lung water score and pulmonary vascular pressure were reduced. Heart dimensions (echocardiography) remained unchanged. DLco, Dm and Vc were 29.0 +/- 5.0 ml/min/mm Hg, 47.0 +/- 11.0 ml/min/mm Hg, 102 +/- 20 ml in normal subjects and 17.1 +/- 4.0#, 24.1 +/- 6.5#, 113 +/- 38 and 17.0 +/- 5.0#, 24.8 +/- 7.9#, 100 +/- 39 in patients before and after ultrafiltration, respectively (# = p < 0.01 vs. controls). CONCLUSIONS: In chronic heart failure, ultrafiltration improves volumes and mechanical properties of the lung by reducing lung fluids. Diffusion is unaffected by ultrafiltration, suggesting that, in chronic heart failure, the alveolar-capillary membrane abnormalities are fluid-independent.     

Pulmonary circulation hemodynamics in patients with post-infarct left ventricular aneurysm

The catheterization of right and left compartments of the heart and cinecoronaroventriculography were carried out in 92 patients with chronic post-infarction left-ventricular aneurysm. Fifty-four patients (group 1) showed no clinical signs of heart failure or just a first-stage failure, and 38 patients (group 2) had heart failure at stages IIA and IIB. Highly significant intergroup differences were demonstrated between pressure values in the pulmonary artery (28.7 +/- 1.3 and 48.0 +/- 3.6 mm Hg in groups 1 and 2, respectively), pulmonary capillaries (13.5 +/- 0.7 and 21.4 +/- 2.0 mm Hg), the right atrium (7.1 +/- 0.4 and 9.7 +/- 0.7 mm Hg) as well as right-ventricular end diastolic pressure (6.6 +/- 0.5 and 10.6 +/- 1.0 mm Hg). It is suggested that pulmonary circulation adequately reflects the clinical stage of chronic heart failure in patients with post-infarction left-ventricular aneurysm. Impaired blood outflow from pulmonary veins due to reduced ventricular pump function and inadequate elasticity of the ventricular wall is the primary link in the pathogeny of pulmonary hypertension in patients with left-ventricular aneurysm.     

Systemic and regional hemodynamic effects of captopril and milrinone administered alone and concomitantly in patients with heart failure

The effects of milrinone and captopril on ventricular performance, renal blood flow, and femoral vein oxygen content were compared in 11 patients with severe chronic heart failure. The increase in stroke volume index was greater with milrinone than with captopril (28 +/- 7 vs 24 +/- 7 ml/m2; p less than .05), while pulmonary capillary wedge pressures fell similarly (19 +/- 10 vs 21 +/- 7 mm Hg). Mean systemic arterial pressure decreased significantly from 84 +/- 10 to 73 +/- 11 mm Hg (p less than .05) with captopril but did not with milrinone. Neither drug changed heart rate significantly. Although milrinone produced a greater improvement in ventricular performance than captopril, renal blood flow increased similarly with both drugs from 289 +/- 78 to 417 +/- 111 ml/min (p less than .05) and from 278 +/- 77 to 441 +/- 115 ml/min (p less than .05), respectively. Femoral vein oxygen content was increased by milrinone from 7.9 +/- 2.6 to 9.8 +/- 3.0 ml/100 ml (p less than .05) and was not changed by captopril. In seven additional patients, intravenous milrinone, administered at the peak effect of captopril, further augmented stroke volume index from 24 +/- 6 to 32 +/- 6 ml/m2 (p less than .05) and tended to reduce pulmonary capillary wedge pressure further from 20 +/- 8 to 18 +/- 9 mm Hg (p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of chronic pressure and volume stress on the function of the right ventricle

Biplane right ventricular angiography was performed in 36 patients with chronic pressure overload of the right ventricle; 12 patients additionally had tricuspid insufficiency (TI). There were 4 subgroups: patients with systolic pulmonary artery pressure less than or equal to 40 mm Hg without (group I, n = 10) and with TI (group II, n = 6), as well as patients with systolic pulmonary artery pressure greater than 40 mm Hg without (group III, n = 14) and with TI (group IV, n = 6). Compared with the normal volumes of groups I and III, a significant increase in end-diastolic right ventricular volumes (p less than 0.01) was found in groups II and IV with 112.2 +/- 22.3 ml/m2 and 116.3 +/- 27.4 ml/m2, respectively. In both groups II and IV end-systolic volumes were also significantly increased, with 51.0 +/- 10.3 ml/m2 in group II and 49.7 +/- 11.3 ml/m2 in group IV. Right ventricular ejection fraction was 53.8 +/- 11.9% in group II, 57.3 +/- 8.5% in group III and 57.8 +/- 7.3% in group IV. There was no significant difference between the ejection fraction of these groups in comparison to the normal ejection fraction of group I with 63.4 +/- 10.9%. The results suggest that the right ventricle can compensate for moderate chronic pressure and volume overload using the Frank-Starling mechanism. Overall right ventricular dysfunction is not determined primarily by the loading conditions alone. Local myocardial and septal involvement is suspected to be an important determinant of right ventricular function.     

Early improvement in left ventricular diastolic function after relief of chronic right ventricular pressure overload

Chronic right ventricular pressure overload is associated with left ventricular diastolic dysfunction. Whether or not an abrupt reduction in pulmonary artery pressure in patients with chronic pulmonary hypertension results in early improvement of left ventricular diastolic function is unknown. To assess this, the Doppler indexes of left ventricular diastolic function and echocardiographic measures of left ventricular volume were analyzed in 22 patients (age, 41 +/- 14 years, mean +/- SD) before and within 1 week after pulmonary thromboendarterectomy for chronic thromboembolic pulmonary hypertension. Mean duration of cardiopulmonary symptoms was 37 months (range, 4 months to 9 years). After operation, mean pulmonary artery pressure and pulmonary vascular resistance decreased (50 +/- 13 to 29 +/- 9 mm Hg and 904 +/- 654 to 283 +/- 243 dynes.sec/cm5, respectively, both p less than 0.001), pulmonary artery wedge pressure was unchanged (11 +/- 5 to 12 +/- 5 mm Hg), and cardiac index increased (2.0 +/- 0.5 to 2.8 +/- 0.7 l/min/m2 p less than 0.001). Left ventricular end-diastolic volume and stroke volume increased significantly (58.5 +/- 18.0 to 76.6 +/- 25.0 ml and 30.3 +/- 12.3 to 41.8 +/- 12.5 ml, respectively, both p less than 0.001) after surgery.(ABSTRACT TRUNCATED AT 250 WORDS)     

急性肺栓塞大鼠肺表面活性物质的变化

目的探讨急性肺栓塞大鼠肺表面活性物质的变化情况。方法32只雄性SD大鼠以随机数字表法分为对照组、栓塞24h组、栓塞1周组、栓塞2周组,每组8只;以明胶海绵溶液经大鼠颈静脉注入制备大鼠肺栓塞模型,经右心导管测定肺动脉压、心率、呼吸频率,并行动脉血气分析。上述4组大鼠分别于肺动脉栓塞后2周、24h、1周、2周时处死,取肺组织制备病理切片,HE染色光镜下观察肺组织病理变化;逆转录聚合酶链反应、Western-blot法测定肺表面活性物质相关蛋白A(SPA)mRNA及蛋白水平。结果对照组、栓塞24h组、栓塞1周组、栓塞2周组大鼠肺动脉压平均值分别为(14.2±4.1)、(26.1±7.5)、(26.1±6.8)、(29.0±8.2)mm Hg(1mm Hg=0.133kPa),肺栓塞后大鼠肺动脉压升高(F值为3.09,P<0.05);心率分别为(415±15)、(451±35)、(463±29)、(446±14)次/min(F值为2.24,P<0.05);动脉血氧分压分别为(94.1±8.8)、(80.5±5.8)、(80.4±13.8)、(73.4±14.3)mm Hg(F值为1.25,P<0.05)。实验大鼠肺组织病理切片光镜检查,栓塞24h组可见肺组织多个血管腔有明胶海绵栓塞,栓塞1周组栓子部分溶解,栓塞2周组栓子基本溶解。大鼠肺栓塞后2周内肺组织SPA mRNA及蛋白水平显著下降,对照组、栓塞24h组、栓塞1周组、栓塞2周组肺组织SPA mRNA水平分别为1.43±0.51、0.83±0.33、0.91±0.33、0.87±0.35(F值为2.92,P<0.05);蛋白水平分别为1.00±0.00、0.44±0.18、0.44±0.33、0.52±0.32(F值为3.49,P<0.05)。结论大鼠急性肺栓塞后SPA水平显著降低,这可能与急性肺栓塞大鼠动脉低氧血症的发生有关。     

Repetitive hemodilution in chronic obstructive pulmonary disease and pulmonary hypertension: effects on pulmonary hemodynamics, gas exchange, and exercise capacity.

BACKGROUND: In cor pulmonale associated with severe chronic obstructive pulmonary disease (COPD), disturbances of pulmonary microcirculation may contribute significantly to hypoxemia, pulmonary hypertension, and exercise intolerance. OBJECTIVE: It was tested whether reduction of blood viscosity induced by repetitive hemodilution might improve pulmonary hemodynamics and oxygen uptake. METHODS: Seven patients with stable COPD (forced expiratory volume in 1 s 33 +/- 3 % of predicted, means +/- SE) and pulmonary hypertension were phlebotomized 5-6 times over a period of 3 months with substitution of 6% hydroxyethyl starch (molecular weight 40, 000). This resulted in a stepwise reduction of the hematocrit from 53.3 +/- 2.6 to 45.8 +/- 3.1% and a reduction of whole blood viscosity from 9.8 +/- 0.6 to 8.8 +/- 0.7 mPa x s at a shear rate of 2.0 s-1. Before and after the treatment period, patients underwent cardiopulmonary exercise testing and right heart catheterization. RESULTS: Mean pulmonary artery pressure (PAm) decreased from 30 +/- 3 to 22 +/- 2 mm Hg and arterial oxygen partial pressure (PaO2) increased from 63.2 +/- 2.2 to 71.8 +/- 3.7 mm Hg at rest. During peak exercise, PAm decreased from 59 +/- 7 to 53 +/- 7 mm Hg and PaO2 increased from 54.0 +/- 5.7 to 63.2 +/- 2.4 mm Hg after hemodilution. Peak oxygen consumption rose from 573 +/- 84 to 750 +/- 59 ml x min-1, corresponding to an increase in cardiac index from 4.25 +/- 0.5 to 5.88 +/- 0.76 liters x min-1 x m-2. Pulmonary vascular resistance fell from 345 +/- 53 to 194 +/- 32 dyn x s x cm-5. The patients' peak exercise capacity increased from 9.2 +/- 2. 0 before to 13.5 +/- 3.2 kJ at the end of the study (p < 0.05 for all differences, paired t test). CONCLUSION: The findings suggest that a prolonged improvement of pulmonary microcirculation by reducing blood viscosity may improve pulmonary gas exchange, central hemodynamics, and exercise tolerance in patients with severe COPD and pulmonary hypertension.     

Long-term results of balloon pulmonary valvuloplasty of valvar pulmonic stenosis

The purpose of this paper is to document long-term results of percutaneous balloon pulmonary valvuloplasty. Forty-one patients, aged 7 days to 20 years, underwent pulmonary valvuloplasty over a 3 1/2-year period ending in April, 1987. Balloon valvuloplasty resulted in immediate reduction in the pulmonary valvar pressure gradient from 92 +/- 45 to 30 +/- 22 mm Hg (p less than 0.001). Follow-up (3 to 34 months) clinical, ECG, and echo Doppler data were available in 35 patients. Follow-up (6 to 34 months) cardiac catheterization data were available in 29 of the 35 patients. Short ejection systolic murmurs were heard in all 35, but an early diastolic decrescendo murmur was heard in only 12 patients. Based on the catheterization and Doppler data, the patients were divided into two groups: group I (30 patients) with excellent results and group II (five patients) with poor results (gradients greater than 50 mm Hg). In group I ECG right ventricular hypertrophy regressed. The echocardiographic right ventricular end-diastolic dimension (21 +/- 6 vs 15.9 +/- 4.6 mm) decreased (p less than 0.001) while the left ventricular dimension increased (p less than 0.02). Peak Doppler flow velocity in the main pulmonary artery fell from 4.0 +/- 0.8 m/sec to 2.3 +/- 0.5 m/sec (p less than 0.001). Doppler evidence for pulmonary insufficiency was present in 21 patients. Catheterization-determined pulmonary valvar gradients (24 patients) also fell from 95.6 +/- 50.3 mm Hg to 18.3 +/- 12.5 mm Hg (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Milrinone in congestive heart failure: acute and chronic hemodynamic and clinical evaluation

Acute and chronic hemodynamic and clinical responses to milrinone, a new oral inotrope-vasodilator agent, were evaluated prospectively in 37 patients with severe congestive heart failure. The majority of patients (n = 31) had not responded to prior vasodilator therapy, with a substantial number (n = 8) requiring intravenous inotropic support at the time of initial study. All patients showed acute hemodynamic improvement with oral milrinone, and an optimal maintenance dose was chosen for each patient during dose-ranging studies (average dose 48 mg/day). Milrinone was discontinued before follow-up hemodynamic study in 12 patients (because of worsening congestive heart failure in 6 patients, sudden death in 3 patients, arrhythmia in 1 patient and refusal by 2 patients). Hemodynamic effects of milrinone both acutely and after chronic therapy (average 37 days) were compared in the remaining 25 patients. Acutely, mean cardiac index increased from 1.9 +/- 0.5 to 2.5 +/- 0.5 liters/min per m2 (p less than 0.001), and mean pulmonary capillary wedge pressure decreased from 28 +/- 9 to 18 +/- 8 mm Hg (p less than 0.001). When oral milrinone was readministered after chronic therapy, mean cardiac index increased from 1.9 +/- 0.5 to 2.5 +/- 1.7 liters/min per m2 (p less than 0.001), and pulmonary capillary wedge pressure decreased from 27 +/- 8 to 20 +/- 8 mm Hg (p less than 0.001) at 1 hour. New York Heart Association functional class improved in 18 of the 25 patients treated over a long-term period (mean 5.5 +/- 2.3 months).(ABSTRACT TRUNCATED AT 250 WORDS)     

Clinical, hemodynamic and neurohumoral effects of long-term therapy of patients with severe chronic heart failure with beta-adrenoblocker bisoprolol

The use of beta-adrenoblockers in conjunction with angiotensin converting enzyme inhibitors improves quality of life and prognosis of patients with chronic heart failure. However basic mechanisms of these positive effects in severe heart failure remain to be elucidated. METHODS: Patients (n=54) with NYHA class III-IV heart failure and left ventricular ejection fraction < or =35% were randomized either to treatment with bisoprolol (1.25-10 mg/day) (n=30) or in control group (n=24) and were followed up for 12 months. RESULTS: The use of bisoprolol was associated with significant improvement of heart failure functional class, lowering of heart rate (by 14%, p<0.01), elevation of systolic blood pressure (by 7.2+/-12.3 mm Hg, p<0.01) and increase of walking distance (by 30.1+/-29.0 m, p<0.01). No significant changes of these parameters occurred in control group. After 12 months increases of left ventricular end diastolic and end systolic volumes (by 85+/-69.2 and 71+/-51.5 ml, respectively, p<0.001) and of ejection fraction (by 5.7+/-7.3%, p<0.01) took place in bisoprolol treated patients. These changes were significantly (p<0.001) higher than those in control group. After 6 months of treatment with bisoprolol noradrenaline concentration fell from 533 to 402 pg/ml (p<0.05) while in controls it rose from 369 to 474 pg/ml, p<0.01). Decreases of plasma renin activity (from 1.2 to 0.42 ng/ml/h), plasma concentrations of angiotensin II (from 17.1 to 13.1 pg/ml) and aldosterone (from 173 to 148 pg/ml, p<0.05) were also observed in bisoprolol group. No substantial dynamics of activity of main components of renin angiotensin system took place in controls. There were no significant changes of atrial natriuretic peptide in both groups. Significant positive dynamics of parameters of heart rate variability was registered only in bisoprolol group: SDNN increased by 25% (p<0.05), high frequency spectrum by 106% (p=0.03), LF/HF ratio from 2.18+/-1.41 to 1.82+/-0.7. CONCLUSION: Long term use of bisoprolol was associated with improved clinical and hemodynamic status, increased systolic BP, blocked processes of pathological left ventricular remodeling, lowered activity of not only sympathetic-adrenal but also of main components of renin-angiotensin system and improved heart rate variability.