冻干重组人脑利钠肽治疗顽固性心力衰竭的护理

目的 观察冻干重组人脑利钠肽治疗顽固性心力衰竭的疗效,并分析其护理上应注意的问题.方法 2008年7月至2009年11月用冻干重组人脑利钠肽治疗顽固性心力衰竭患者32例,观察用药前后血压、心率、无创血氧饱和度、24 h尿量、肺部啰音的变化,水肿及呼吸困难的改善情况,血常规、尿常规、肝肾功能的变化,以及用药后可能出现的不良反应,并在使用冻干重组人脑利钠肽前和使用冻干重组人脑利钠肽后第3天分别测定左室射血分数和血中B型尿利钠肽水平.结果 治疗后患者呼吸困难症状明显改善,水肿减轻,肺部哕音明显减少甚至消失;根据疗效判断标准,显效4例,有效24例,无效4例;治疗前后血压的差异无统计学意义（P〉0.05）,治疗前后心率、血氧饱和度、24 h尿量、左室射血分数、血B型尿利钠肽水平差异均有统计学意义（P〈0.01）.治疗前后血常规、尿常规、肝肾功能无明显变化.出现的副作用有低血压、胸闷、恶心.结论 冻干重组人脑利钠肽治疗心力衰竭疗效好,但也要注意其不良反应.     

重组人脑利钠肽治疗超高龄老年人充血性心力衰竭

目的探讨重组人脑利钠肽治疗超高龄充血性心力衰竭患者的临床疗效及安全性。方法采集在常规治疗基础上加重组人脑利钠肽治疗的14例充血性心力衰竭患者的临床资料,包括呼吸困难及水肿程度、尿量、心率、血压、呼吸频率、左室射血分数、血浆氨基末端脑钠肽前体,以及肾功能、电解质等指标,采用自身对照方法,分析评价重组人脑利钠肽在超高龄老年患者中应用的临床疗效及安全性。结果重组人脑利钠肽能明显改善超高龄心力衰竭患者的呼吸困难程度,增加尿量（P〈0．05）;心率、血压、呼吸频率、左室射血分数、血浆氨基末端脑钠肽前体、水肿程度均有一定程度的改善,但无统计学意义。药物安全性良好,未见‘肾功能恶化及电解质紊乱等并发症。结论重组人脑利钠肽可用于超高龄充血性心力衰竭患者的治疗,具有较好的临床疗效及安全性。     

托拉塞米对心脏瓣膜置换术后患者在ICU中的疗效观察

目的观察静脉给予托拉塞米对风湿性心脏病瓣膜置换术后患者在ICU中的临床疗效。方法以60例使用呋塞米利尿的患者为对照,观察52例风湿性心脏病瓣膜置换术后第3天的患者静脉给予首剂托拉塞米注射液后药物作用时间、血液电解质的变化;同时保持每天入量,静脉补钾、钠量相当,记录不同时段尿量,并测定尿液中钾、钠量。观察患者的症状、心率、呼吸、心电图和血流动力学变化及不良反应。结果两组患者在ICU治疗中均未出现恶心等消化道不良反应,给药前后血压、呼吸、心率、心电图和血流动力学均未出现显著改变。托拉塞米首剂静脉给药较呋塞米首剂给药作用时间明显延长(P<0.01)。当首剂给药后、尿量达到500 mL时,托拉塞米组血液电解质波动范围明显较小(P<0.01,P<0.05)。给药后0～4 h托拉塞米组尿量高于呋塞米组,尿钾、钠低于呋塞米组(P<0.05);0～12 h托拉塞米组尿量明显高于呋塞米组,尿钾、钠显著低于呋塞米组(P<0.01);0～24 h、48～72 h两组比较差异无统计学意义。结论对于风心病瓣膜置换术后早期在ICU中的患者,托拉塞米利尿作用及对机体内环境的稳定性明显优于呋塞米。     

持续静脉速尿并多巴胺微量泵入在老年危重心衰患者中的应用

目的:探讨速尿并多巴胺持续微量泵入对老年危重心力衰竭的疗效。方法:入选对象共49例,均为NYHA标准Ⅲ~Ⅳ级心力衰竭患者,按先后顺序,查随机排列表分为两组,即持续静脉微量泵注入速尿并多巴胺(观察组,25例)和反复多次静脉注射速尿(对照组,24例)。观察组给予速尿120 mg,多巴胺40 mg加入微量泵持续注入24h;对照组则静脉6 h推注速尿40~80 mg。治疗前和治疗48 h后分别检测电解质,治疗中检测血压,并计算24 h、48 h尿量。结果:持续静脉泵注速尿并小剂量多巴胺在24 h及48 h后统计尿量明显高于多次性速尿注射,观察组尿量显著高于对照组(P<0.01),48 h中平均血压波动差值比较观察组明显小于对照组(P<0.05),且血压波动幅度减小,两组电解质比较无统计学差异(P>0.05),患者水肿明显减轻,胸闷、气促症状改善。结论:持续静脉泵注速尿并小剂量多巴胺在老年危重心衰的疗效明显高于多次性速尿静脉注射。     

血管迷走性晕厥儿童24h尿电解质含量变化

目的 探讨血管迷走性晕厥儿童24 h尿电解质含量变化,对临床补盐补液治疗提供依据.方法 2004-06～2007-04在中南大学湘雅二医院晕厥专科门诊就诊或住院的不明原因晕厥或先兆晕厥儿童79例(晕厥组),男31例,女48例,平均年龄(11.18±2.47)岁.匹配健康儿童11例为对照(对照组).研究对象留取24 h尿,测量尿量后,采用日本HITACHI公司7600-020全自动生化分析仪检测24 h尿电解质(钾、钠、氯、钙、磷、镁)含量.结果 ①晕厥组24 h尿量较对照组减少(P>0.05),24 h尿电解质含量变化不明显(P>0.05),每毫升尿钠和尿钙增加(P<0.01或P<0.05).②晕厥儿童HUTT阳性组24 h尿钠、尿钾较HUTT阴性组明显增加(P<0.05),每毫升尿钠增加(P<0.05).③晕厥儿童24 h尿电解质含量和每毫升尿电解质含量在血管抑制型与心脏抑制型 混合型组、男女性别、<12岁组与≥12岁组、晕厥频次<4次组和晕厥频次≥4次组之间比较差异无统计学意义(P>0.05).结论 24 h尿钠含量增加与VVS发病关系密切,临床治疗VVS要强调健康教育,重视补盐补液方案.     

应用利尿剂治疗老年慢性充血性心力衰竭的护理

老年充血性心力衰竭(congestive heart failure,CHF)患者容易发生水、钠潴留,利尿剂是唯一能够完全控制CHF水钠潴留的药物,与其他抗心力衰竭药物相比,能更快地缓解CHF水肿症状.合理应用利尿剂是其他抗心力衰竭药物取得成功的关键因素[1].2003年3月至2004年8月,本院心血管病区对88例CHF患者应用利尿剂,同时监测并记录24 h尿量、体重、心率、心律、血压、电解质等指标的变化,配合其他抗心力衰竭药物等治疗,取得满意疗效,现将观察和护理体会报告如下.     

小剂量肝素对慢性肺心病顽固性心衰的利尿效果观察

我科对38例慢性肺心病顽固性心衰病人经常规应用强心剂、利尿剂、抗感染、血管扩张剂等,7天后心衰无明显改善。水肿明显、尿量少的病人加用小剂量肝素,总疗程为7天,用药后尿量显著增多,心功能明显改善而未见不良反应。现报道如下: 1 临床资料 男24例,女14例,年龄52～70岁。慢性咳嗽、咯痰、喘息均有10年以上,临床症状均有胸闷、心慌、气促、呼吸困难、腹胀、尿少。体征除心脏体征外,均有肝脏肿大、双下肢明显凹陷性水肿,30例病人有腹水征。入院后都采用强心、利尿、抗感染、血管扩张剂、纠正水、电解质紊乱等综合治疗一周后,心衰仍无明显改善,水肿显著、尿量少,再加用小剂量肝素治疗。 2 方法 在原综合治疗的基础上加用肝素100u/kg和5％葡萄糖250ml,每日一次,连续用药一周,用药时间前后查出凝血时间、血小板计数和凝血酶原时间并临床观察出血倾向。     

充血性心力衰竭患者血钠水平与其神经内分泌激素水平、运动耐量及再住院率的关系

目的:探讨充血性心力衰竭患者低钠水平对其相关神经内分泌激素水平、运动耐量的影响,并通过观察比较再入院率,明确低钠水平对心衰患者康复和预后的作用。方法:选择2004年2月—2005年4月我院心内科确诊为充血性心力衰竭、NYHAⅡ—Ⅳ级的住院患者,共106例,包括56例充血性心力衰竭伴低钠血症患者和50例正常血钠的慢性心力衰竭患者,用放射免疫法、心脏超声同时测定106例慢性心力衰竭患者血浆NE、ALD、AngⅡ水平和LVEF。结果:低钠水平的充血性心力衰竭患者血浆NE、ALD、AngⅡ水平均较正常血钠组显著升高,NE(0.92±0.24ng/mlvs0.48±0.15ng/ml,t=3.865,P<0.01),ALD(264.05±42.85ng/Lvs154.56±39.34ng/L,t=2.521,P<0.05),AngⅡ(251.35±70.06ng/Lvs106.08±30.15ng/L,t=3.275,P<0.01)。低钠水平与血浆NE、ALD、AngⅡ水平呈显著负相关(r=-0.33,P<0.05;r=-0.69,P<0.01)。低钠水平组的心衰患者6min步行距离明显短于正常血钠组298.45±26.35mvs390.25±29.65m,P<0.05。6个月内因心衰的再入院率明显高于正常血钠组(χ2=117.96,P<0.05)。结论:低钠水平可能促进充血性心力衰竭患者神经内分泌激素激活水平,明显减低其运动耐量,增加再入院率,影响心衰患者的康复和预后。     

重组人脑利钠肽联合缬沙坦治疗慢性充血性心力衰竭的短期疗效观察

目的观察缬沙坦与重组人脑利钠肽(rhBNP)联合治疗慢性充血性心力衰竭(CHF)的短期临床疗效及安全性。方法前瞻性入选经常规洋地黄、利尿剂、血管扩张剂、血管紧张素转换酶抑制剂(ACEI)治疗1周以上效果欠佳的慢性充血性心力衰竭患者100例,随机分成治疗组和对照组各50例。基础治疗为对照组,治疗组在基础治疗上停用ACEI后加服缬沙坦80 mg/d,rhBNP静脉泵注冲击量2.0μg/kg持续1 h,然后0.01μg·kg-1·min-1维持静脉泵注72 h,观察治疗前后心率、血压、尿量、电解质水平、体重、左心室射血分数(LVEF)、心功能的变化。结果治疗组的心率、体重与对照组比较均明显下降(P<0.05),LVEF、6MWT行走距离、尿量增加(P<0.01),心功能改善更显著(P<0.05)。结论缬沙坦联合rhBNP治疗慢性充血性心力衰竭是一种安全、有效的方法,值得临床进一步推广。     

冻干重组人脑利钠肽治疗顽固性心力衰竭的疗效观察及护理

目的探讨冻干重组人脑利钠肽(rhBNP)治疗顽固性心力衰竭的疗效及护理方法。方法将我院64例顽固性心力衰竭住院患者随机分为观察组和对照组,各为32例。对照组患者按常规抗心衰治疗,在此基础上加用硝酸甘油起始剂量均为25μg/min,连用3d;而观察组在常规抗心衰治疗基础上加用重组人脑利钠肽,首次负荷剂量2.0μg/kg静脉注射后,维持剂量速率0.01μg/(kg.min),连续静脉滴注3d。分别记录两组患者用药3d后心功能改善情况、用药后24h后液体的出入量和血流动力学参数,以及给药后1h、12h及24h的呼吸困难程度以及整体临床情况。结果观察组心功能改善的总有效率、1h和12h观察组呼吸困难好转程度、临床状况好转程度均显著优于对照组(P0.05),而用药24h后两组临床状况的改善差异无显著意义(P0.05);观察组的尿量、尿量与入量的差值、射血分数的增加、肺动脉压和收缩压的降低均明显高于对照组(P0.05)。结论脑利钠肽通过促进尿液排泄、降低肺动脉压及增加左室射血分数等途径明显改善顽固性心力衰竭患者心功能、呼吸困难和整体临床状况,从而提高患者的生存率及生活质量。     

Elevation of plasma atrial natriuretic peptide in rats with chronic heart failure by SCH 39370, a neutral metalloendopeptidase inhibitor

Hormonal, renal and blood pressure effects of SCH 39370, a selective inhibitor of neutral metalloendopeptidase (endopeptidase 24.11, NEP), were studied in a chronic, congestive heart failure (CHF) model produced by coronary artery ligation in the rat. Sham-operated control rats and rats with CHF were treated either with vehicle or SCH 39370, 30 mg/kg s.c. b.i.d. for 2.5 days. Plasma levels of atrial natriuretic peptide (ANP) and urinary excretion of cyclic GMP (cGMP) were clearly raised in rats with CHF as compared with controls during vehicle treatment. SCH 39370 caused a further increase in plasma ANP in CHF rats but not in control rats. Urinary excretion of immunoreactive ANP and cGMP increased during SCH 39370 treatment both in CHF rats and in controls. SCH 39370 treatment resulted in an initial increase in urine volume in rats with CHF whereas urine sodium excretion did not change significantly. No changes in renal function due to SCH 39370 treatment were seen in control rats. Systolic blood pressure, plasma renin activity and urine excretion of catecholamine metabolites (4-hydroxy-3-methoxyphenyl acetic acid and metanephrines) did not change during SCH 39370 treatment either in controls or in CHF rats. We conclude that the NEP-inhibitory compound SCH 39370 is capable of increasing plasma ANP concentration and urinary excretion of cGMP in rats with chronic CHF. In this severe heart failure model, the possible beneficial effects of additional ANP increments may be blunted, however. NEP inhibitors offer a novel approach to study the significance of ANP elevation in chronic CHF.     

Atriopeptin III. A potent natriuretic, diuretic, and hypotensive agent in rats with chronic renal failure.

Chronic renal failure is frequently associated with volume overload, resulting in hypertension and, in some cases, congestive heart failure. Atriopeptin III (AP III), a 24-amino acid atrial peptide, is a potent vasodilator and natriuretic/diuretic agent in normal rats. An infusion of AP III at 0.2 microgram/kg per min for 60 min produced dramatic responses in animals with chronic renal failure (5/6 nephrectomy 4 wk before study). Systemic blood pressure fell 20% by the end of infusion. A pronounced rise in glomerular filtration rate (24%) was maintained during the infusion period when urine flow rate was stable (35-60 min), even though renal blood flow was unchanged from base line. Urinary volume increased 4.4-fold and sodium excretion increased 9 to 12-fold during the infusion. Fractional excretion of sodium ranged between 9 and 15% in those animals whose initial GFR values were lower than 0.5 ml/min. We conclude that AP III is a potent natriuretic/diuretic agent in rats with reduced renal mass, presumably exerting that effect predominantly through increases in GFR. This agent may well be useful in the treatment of volume overload in patients with chronic renal failure.     

Hemodynamic, renal, and hormonal responses to alpha-human atrial natriuretic peptide in patients with congestive heart failure

Hemodynamic, renal, and hormonal effects of intravenous bolus injection of 50 micrograms synthetic alpha-human atrial natriuretic peptide (alpha-hANP) were studied in eight patients with congestive heart failure. alpha-hANP caused significant reductions in mean blood pressure and systemic vascular resistance. These responses were sustained up to 90 minutes and not accompanied by reflex tachycardia. Cardiac index and stroke volume index increased significantly at 90 minutes and pulmonary capillary wedge pressure, pulmonary arterial pressure, and mean right atrial pressure remained unchanged. Urine volume, urinary sodium excretion, creatinine clearance, and fractional excretion of sodium increased significantly, but fractional excretion of potassium and phosphate did not change. Elevated plasma renin activity, plasma aldosterone, and norepinephrine were suppressed after the injection of alpha-hANP. The bolus injection of this peptide has moderately hypotensive, vasorelaxant, and natriuretic effects in patients with congestive heart failure.     

Renal, haemodynamic and hormonal interactions between atrial natriuretic factor and arginine vasopressin in patients with congestive heart failure.

1. Nine patients with compensated heart failure were infused with synthetic arginine vasopressin at a rate of 0.1 m-units min-1 kg-1 for 60 min to increase their plasma arginine vasopressin concentration. Synthetic human atrial natriuretic factor (3 pmol min-1 kg-1) or placebo was co-infused with the arginine vasopressin in random order in a single-blind cross-over design. 2. The resultant plasma concentrations of arginine vasopressin and atrial natriuretic factor fell to within the upper range observed in congestive heart failure. Compared with the infusion of arginine vasopressin alone, atrial natriuretic factor co-infusion enhanced both the urine flow rate and the sodium excretion rate (both P less than 0.05) without significant haemodynamic and hormonal effects. 3. Systematic blood pressure was elevated by arginine vasopressin infusion (P less than 0.05) without any change in heart rate. Co-infusion of atrial natriuretic factor did not affect these haemodynamic parameters. 4. These results suggest that an increased release of atrial natriuretic factor maintains water and sodium excretion in the presence of arginine vasopressin-induced renal modulations, and that the pressor effect of arginine vasopressin is not antagonized by the increased plasma level of atrial natriuretic factor in patients with congestive heart failure.     

Ibopamine in Patients with Congestive Heart Failure and Different Degrees of Renal Function

Following a 1-week placebo run-in phase, 20 patients with congestive heart failure (New York Heart Association class II) were treated orally for 7 days with 100 mg ibopamine t. i. d. Ten subjects had a normal renal function, whereas 10 patients suffered from chronic renal insufficiency (mean creatinine clearance 36 plus minus 3.9 ml min(minus sign1)). Ibopamine significantly increased stroke volume and cardiac output, but only 45 and 90 min after administration. After 7 days of ibopamine treatment, urine output rose significantly in both patient groups by about 400--500 ml per 24 h. The glomerular filtration rate (inulin clearance) and urine osmolality remained nearly unchanged, whereas renal plasma flow (PAH clearance) increased on ibopamine administration. Urinary sodium and potassium excretion were slightly but insignificantly elevated. Pharmacokinetic parameters of ibopamine were unaltered in impaired renal function, both on the first and seventh treatment day. Maximum plasma levels of the active metabolite epinine were achieved after 45 min and were higher on the first as compared with the seventh treatment day in both groups. In conclusion, ibopamine caused a relevant increase in stroke volume and cardiac output associated with a rise in renal perfusion and urine output in patients with normal and with impaired renal function. Ibopamine is an orally active derivative of dopamine and is used for treatment of patients with congestive heart failure, who frequently have an impaired renal function. Therefore, in the present study, the hemodynamic effects and kinetic behavior of ibopamine should be investigated in patients with different degrees of renal function.     

Efficacy and pharmacokinetics of piretanide in patients with congestive heart failure

The efficacy and pharmacokinetics of the diuretic piretanide were studied in two groups of six patients hospitalized for congestive heart failure. A dosage of 2 x 6 mg day-1 to 2 x 12 mg day-1 of intravenous piretanide for 7 days was sufficient to abrogate most symptoms of cardiac insufficiency. When compared with another group of healthy volunteers, patients with congestive heart failure had reduced total body clearance of piretanide of about 50% which was attributable to a diminished renal but not non-renal clearance. The analysis of the interrelationship between urinary piretanide excretion and diuresis by means of a linearized Emax-model revealed a maximal diuresis of 231 ml h-1 and a urinary piretanide excretion to induce half-maximal diuresis of 245 micrograms h-1. Thus patients with congestive heart failure exhibit a decreased renal clearance of piretanide and a good response to this high ceiling diuretic after intravenous dosing.     

Captopril and ANP: changes in renal hemodynamics, glomerular-ANP receptors and guanylate cyclase activity in rats with heart failure.

To define the renal effects of atrial natriuretic peptide (ANP) in heart failure, we studied rats with heart failure after coronary artery ligation. The rats received either captopril (2 milligrams drinking water) or placebo for 4 weeks. Glomerular filtration rate, renal plasma flow, filtration fraction, urine volume, urinary sodium excretion and the percent fractional excretion of sodium were measured before and after an infusion of ANP (0.3 microgram/kg/min). To determine whether changes in ANP receptor binding and responsiveness occur in heart failure and after captopril treatment, we performed radioreceptor binding studies and measured guanylate cyclase activity. Atrial natriuretic peptide in sham-operated rats decreased mean arterial pressure from 118 +/- 5 to 95 +/- 5 mm Hg (P less than .001), increased urine volume from 0.06 +/- 0.02 to 0.16 +/- 0.05 ml/min/kg (P less than .05), urinary sodium excretion, 14.2 +/- 3.1 to 41.4 +/- 8.9 mu eq/min/kg (P less than .02), filtration fraction from 0.30 +/- 0.03 to 0.40 +/- 0.4 (P less than .05), and the percent fractional excretion of sodium from 0.84 +/- 0.19 to 2.85 +/- 0.61 (P less than .02). Atrial natriuretic peptide in untreated rats with heart failure produced no significant systemic or renal hemodynamic effects. In rats with heart failure treated with captopril, ANP decreased mean arterial pressure from 93 +/- 4 to 86 +/- 4 mm Hg (P less than .05) and increased hematocrit from 50 +/- 2 to 52 +/- 1 (P less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Intrarenal effects of ecadotril during acute volume expansion in dogs with congestive heart failure

Neutral endopeptidase 24.11 (NEP) inhibitors are known to have vascular, diuretic, and natriuretic effects that may be helpful in the treatment of congestive heart failure (CHF). Most NEP inhibitors may act principally through intrarenal mechanisms, which are not completely understood. The purpose of this study was to determine the principal renal effects of the NEP inhibitor ecadotril in dogs with progressive CHF induced by rapid ventricular pacing. Renal function was measured before, during, and after acute i.v. infusion of normal saline in a total of six dogs during normal cardiac function, early left ventricular dysfunction, and overt CHF. During overt CHF, each dog was treated with either ecadotril or placebo orally for 1 week. Parameters measured included glomerular filtration rate, renal blood flow, urine output, sodium clearance, sodium fractional excretion, and proximal and distal sodium reabsorption. Ecadotril treatment resulted in increased urine output, sodium clearance, and renal sodium excretion relative to placebo-treated controls. The principal intrarenal effect of ecadotril was decreased distal renal tubular sodium reabsorption. Both glomerular filtration rate and renal blood flow declined during overt CHF and were unaffected by ecadotril treatment. The results of this study are consistent with the principal action of ecadotril occurring by way of intrarenal events as opposed to changes in renal hemodynamics. The principal effect of ecadotril on distal tubular sodium reabsorption suggests that inhibition of NEP activity in the proximal renal tubules may allow increased binding of filtered atrial natriuretic peptide to natriuretic peptide receptor sites in the distal renal tubules and collecting ducts.     

Renal blockade to angiotensin II in acute and chronic sodium-retaining states.

Acute thoracic inferior vena cava constriction results in alterations in renal hemodynamics which may explain the characteristic antinatriuretic response. Since adrenalvein-aldosterone secretion is increased within 30 minutes of acute caval constriction and elevated plasma-renin activity is found in the chronic caval dog, we sought to determine whether the renal hemodynamic alterations observed in acute caval constriction are due to the intrarenal action of angiotensin II. The renal response to acute caval constriction in dogs receiving unilateral renal arterial infusion of a specific competitive antagonist of angiotensin II, 1-sarcosine-8-alanine-agiotensin II, was studied. Effective blockade did not alter the renal hemodynamic or antinatriuretic response to acute caval constriction. As a model of chronic sodium retention, dogs with chronic congestive heart failure produced by tricuspid insufficiency and pulmonary stenosis were similarly studied. Effective renal blockade to antiotensin II did not affect renal hemodynamics or urinary sodium excretion. The renal hemodynamic and antinatriuretic responses to acute caval constriction and chronic congestive heart failure are not dependent on the intrarenal action of angiotensin II.     

Piretanide, a potent diuretic with potassium-sparing properties, for the treatment of congestive heart failure

The diuretic and clinical efficacy and safety of piretanide, a new high-ceiling loop diuretic, was determined in patients with mild to moderately severe congestive heart failure. Piretanide (n = 20) administered orally in a daily dosage of up to 24 mg was compared with placebo (n = 18) for 28 days, using a double-blind, randomized, parallel design. Patients were hospitalized during the first 5 days of the study when dosage titration was established and 24-hour fractionated urine collections were obtained. Piretanide caused significant diuresis for 3 hours after ingestion with a natriuretic response noted for up to 6 hours. While occasional kaliuretic response was noted, it did not significantly increase 24-hour urinary potassium excretion. Only one patient treated with the highest allowed dose of piretanide developed mild hypokalemia. An improvement in New York Heart Association functional class status was noted after piretanide therapy. In contrast, patients who received placebo exhibited no significant improvement. BUN increased in nine piretanide-treated patients; two were discontinued from the study because of progressive azotemia. However, there was no significant increase in serum creatinine levels. Other blood, physical, ECG, and audiometric examinations also revealed no significant abnormalities. The study suggests that oral piretanide is a relatively safe and effective diuretic for treating congestive heart failure with a potential advantage of having potassium-sparing properties.