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At least 1,135 records · Page 63Linked to original sources
PubMed1998

Effects of combination therapy with an angiotensin converting enzyme inhibitor and thiazide diuretic on insulin action in essential hypertension.

OBJECTIVE: To determine whether combination of an angiotensin converting enzyme inhibitor with a high dose of thiazide diuretic avoids adverse metabolic consequences of thiazide diuretics. DESIGN: Double-blind randomized crossover study of two 12-week treatment periods with captopril (up to 100 mg/day) either alone or in combination with 5 mg bendrofluazide given after a 6-week placebo run-in period. Treatment periods were separated by a 6-week placebo washout period. SETTING: Outpatient clinics in greater Belfast. PATIENTS: Fifteen white non-diabetic essential hypertensives (seven male) aged < 65 years recruited from general practices in greater Belfast. MAIN OUTCOME MEASURES: Systolic and diastolic blood pressures and peripheral and hepatic insulin action. RESULTS: Two patients failed to complete the study. Blood pressure was lowered (139/89+/-18/7 mmHg combination versus 160/97+/-21/7 mmHg captopril; P < 0.001). Fasting insulin level was raised (7.9+/-3.6 mU/l combination versus 6.2+/-3.2 mU/l baseline; P < 0.001). There were no differences between treatments for glucose, urate, cholesterol and triglyceride levels. Serum potassium level was lowered (3.8+/-0.4 mmol/l combination versus 4.2+/-0.4 mmol/l captopril, P < 0.05). Postabsorptive endogenous glucose production was raised (10.8+/-1.7 micromol/kg per min combination versus 10.0+/-1.5 micromol/kg per min captopril; P < 0.01) and was greater than baseline (9.7+/-2.1 micromol/kg per min, P < 0.05). Suppression of glucose production by insulin was similar with both treatments. Exogenous glucose infusion rates required to maintain euglycaemia did not differ (32.4+/-7.6 micromol/kg per min captopril, 32.7+/-6.2 micromol/kg per min combination, 31.5+/-7.2 micromol/kg per min baseline). CONCLUSIONS: Combination therapy increased glucose production (compared with captopril alone), indicating hepatic insulin resistance. It cannot be assumed that combined preparations with angiotensin converting enzyme inhibitors will ameliorate adverse effects of high doses of thiazide diuretics on insulin action.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2001

High and low serum potassium associated with cardiovascular events in diuretic-treated patients.

OBJECTIVE: To determine the relationship of moderately high and low concentrations of serum potassium with cardiovascular disease events among treated hypertensive patients. DESIGN: An observational cohort study with prospectively collected data. SETTING: A worksite treatment program for mild hypertension. PATIENTS: All program participants with baseline and at least one annual follow-up measure of serum potassium; 7,653 individuals with 6.7 years mean follow-up met these criteria. MAIN OUTCOME MEASURES: Outcome events were admissions to hospital because of cardiovascular disease, and deaths. The research question regarding serum potassium categories was formulated after data collection. The serum potassium concentration (mean +/- 2SD) of the study population was used to define low (3.0-3.5 mmol/l), high (5.1-5.9 mmol/l) and middle (3.6-5.0 mmol/l) categories. RESULTS: Individuals with low (n = 146) and high (n = 226) serum potassium had significantly greater risk for cardiovascular disease events than those in the middle category (n = 7,281). Multivariate adjusted hazard ratios from Cox models were 2.6 [95% confidence intervals (CI) 1.5-4.4] for the low potassium group and 1.7 (95% CI 1.0-2.7) for the high potassium group, with the middle group as reference. Among 1,679 individuals who regularly took diuretics, hazard ratios were 4.3 (95% CI 2.4-7.9) for the low potassium group and 6.7 (95% CI 2.8-15.9) for the high group. Neither low nor high potassium was significantly associated with outcome events for those not regularly using diuretics. CONCLUSIONS: These data confirm an association of mild hypokalemia with increased cardiovascular events among diuretic-treated hypertensive patients. In addition, we have found a similar increased cardiovascular risk associated with modest hyperkalemia among these patients. Whether modification of these serum potassium concentrations would alter that risk remains to be determined.

Cardiovascular Diseases↗
PubMed2004

Foot volume increase on nifedipine is not prevented by pretreatment with diuretics.

OBJECTIVE: Despite their natriuretic effects, dihydropyridine calcium-channel blockers (CCBs) often induce ankle oedema, probably due to vasodilation in the dependent legs. Since concomitant administration of frusemide does not prevent the acute increase in foot volume on nifedipine, we investigated whether diuretic pretreatment attenuates foot swelling on CCBs. METHODS: In four separate experiments, 10 healthy volunteers received: (i) 20 mg of nifedipine without active pretreatment (pretreatment with placebo only); (ii) 20 mg of nifedipine after 5 days' treatment with amiloride 5 mg twice daily; (iii) 20 mg of nifedipine after 5 days' treatment with chlorthalidone 50 mg once daily; and (iv) no active drugs (pretreatment with placebo and placebo in place of nifedipine) as the control. Foot volumes were measured using an accurate water displacement technique (intra-individual coefficient of variance 0.27%). RESULTS: Amiloride and chlorthalidone pretreatment induced marked volume depletion, with a 2-3% reduction in body weight, a 5-10% increase in haematocrit and a 14-23% increase in plasma colloid osmotic pressure. In addition, the mean +/- SEM foot volume after both chlorthalidone (1282 +/- 37 ml) and amiloride (1289 +/- 40 ml) was lower than without pretreatment (1315 +/- 38 ml) (P < 0.05). Neither amiloride nor chlorthalidone significantly influenced the acute increase in foot volume on nifedipine. However, due to pretreatment effects, the foot volume after nifedipine was higher (P < 0.05) without pretreatment (1356 +/- 36 ml) than after amiloride (1318 +/- 38 ml) or chlorthalidone (1319 +/- 37 ml). Amiloride significantly attenuated the natriuretic effect of nifedipine, whereas chlorthalidone prevented the nifedipine-induced rise in colloid osmotic pressure and haematocrit. CONCLUSIONS: Diuretic pretreatment and the concomitant volume depletion did not prevent acute foot swelling on nifedipine, although the absolute foot volume remained lower after such pretreatment. Therefore diuretics mitigate the oedema of CCBs, but do not directly interfere with oedema formation.

Adult↗
PubMed1987

SQ 27,786 and SQ 28,853: two angiotensin converting enzyme inhibitors with potent diuretic activity.

SQ 27,786 and SQ 28,853 were designed to possess both angiotensin converting enzyme (ACE) inhibitory and diuretic properties. Both compounds were given to conscious male Sprague-Dawley rats and mongrel female dogs to determine ACE inhibitory and diuretic activities. All animals had previously been equipped with indwelling arterial and venous catheters. Both compounds resulted in dose-related inhibition of an angiotensin I pressor response in rats after i.v. administration. The maximum response and duration of effect of both compounds were similar to that seen with equimolar doses of captopril. Oral doses of SQ 28,853 (50.0 mumol/kg) and SQ 27,786 (15.0 mumol/kg) resulted in 15 and 64% inhibition of ACE, respectively. In conscious normotensive dogs, both compounds (2.0 mg/kg, i.v.) resulted in complete inhibition of ACE. Urine volume was increased by 153 and 667% after SQ 27,786 and SQ 28,853, respectively. Similarly, sodium excretion was increased by 336% after SQ 27,786 and by 650% after SQ 28,853. SQ 27,786 and SQ 28,853 increased potassium excretion by 54 and 115%, respectively. No significant changes in blood pressure were observed with either compound in either species. These results demonstrate that both SQ 27,786 and SQ 28,853 are potent ACE inhibitors and diuretic agents in vivo.

Administration, Oral↗
PubMed1987

Antihypertensive effects and pharmacokinetics of felodipine combined with a beta-blocker and a diuretic.

The antihypertensive effect of felodipine, a new calcium antagonist with dihydropyridine structure, was investigated in 25 patients with essential hypertension that was not controlled on standard triple therapy (a beta-blocker, a diuretic, and a vasodilator). After substituting the previous vasodilator with felodipine, blood pressure was reduced and remained well controlled during a 2 year follow-up period. After about 1 1/2 years of treatment, felodipine was compared double-blind with placebo in a subgroup of 10 patients while keeping the same beta-blocker and diuretic therapy. Compared with the placebo, felodipine lowered blood pressure during a 12 h interval, which supports a twice-daily dosage in clinical practice. Determination of the plasma concentrations of felodipine during steady-state conditions showed a mean elimination half-life of 23.4 +/- 11.1 h. During long-term therapy, tolerance was good, and felodipine seems to be a safe and efficient antihypertensive agent in combination with a beta-blocker and a diuretic in patients whose hypertension is not adequately controlled on standard triple therapy.

Adrenergic beta-Antagonists↗
PubMed1988

Additive effects of diuretics or sodium restriction with calcium channel blockers in the treatment of hypertension.

The role of dietary sodium intake and diuretic administration on the blood pressure response to calcium channel blockers (CCB) is reviewed. CCB has been shown to have a natriuretic effect irrespective of sodium balance state. Sodium-sensitive hypertensives often have lower blood pressure levels after dietary sodium restriction or diuretic therapy, making the additive benefit of CCB on blood pressure more difficult to discern. The majority of studies including appropriate controls suggest that CCBs of the dihydropyridine class (nifedipine and nitrendipine) and also verapamil have an antihypertensive effect that can be augmented by diuretic administration.

Calcium Channel Blockers↗
PubMed1992

Long-term diuretic therapy: effects of dose reduction on antihypertensive efficacy and counterregulatory systems.

In the present study, the effects of a dose reduction on antihypertensive efficacy and metabolic side effects of diuretic therapy were investigated in 36 hypertensive patients. During the first treatment period of 1 year, the patients were treated with 25 mg of the thiazide diuretic bemetizide (n = 18) or 25 mg bemetizide plus 50 mg of the potassium-sparing agent triamterene (n = 18). Mean blood pressure (BP) values decreased significantly (p less than 0.01) during the first year of the trial. Thereafter, doses were reduced to 10 mg bemetizide or 10 mg bemetizide plus 20 mg triamterene in patients whose BP became normal during the first year (n = 16 in both groups). At the end of the second year, equal BP control was achieved with doses more than twice smaller than those used during the first year. During the second year of the trial, activation of the renin-angiotensin system (RAS) was significantly less pronounced as compared with the first year and the percentage of patients with hypokalemia (less than 3.5 mM) decreased from 62.5 to 25% in the bemetizide group. Thus, this long-term study provides additional evidence that diuretics have a flat dose-response curve with respect to their antihypertensive efficacy, whereas lower doses might cause less pronounced activation of counter-regulatory systems. Furthermore, our results indicate that long-term studies might be necessary to assess the full antihypertensive potential of low doses of antihypertensive agents.

Aldosterone↗
PubMed1993

Recent studies on the characterization of loop diuretics.

This article provides a survey of transport mechanisms in the loop of Henle and of secondary effects on electrolyte excretion of loop diuretics. Results are presented of experiments that define ion transport in the thick ascending limb. New data on ion channels and transport regulation in this tubule segment are summarized. In addition, the mechanisms underlying enhanced sodium chloride and water transport after diuretics in tubule segments that are located downstream of the loop of Henle are surveyed. Finally, the effects of K depletion and chronic metabolic acidosis on diuretic potency of torasemide as well as possible antialdosterone effects of torasemide are evaluated.

Animals↗
PubMed1995

Diuretic effectiveness of hydrochlorothiazide and furosemide alone and in combination in chronic renal failure.

In the absence of formal clinical trials, the efficacy of thiazide diuretics in patients with renal impairment remains in doubt. Our study was therefore designed to evaluate the separate and combined effects of single and multiple doses of hydrochlorothiazide (HCTZ) and furosemide (FU) on the glomerular filtration rate (GFR) and electrolyte excretion in 19 patients with chronic renal insufficiency and in six normal control subjects by a randomized single-blind protocol. After establishment of a steady state of urinary electrolyte excretion, a single oral dose of HCTZ (25 mg) induced increases in the urinary excretion of Na+, K+, Cl-, Ca2+, and Mg2+ over the subsequent 12 h, which was significantly inversely related to the GFR for each electrolyte. The ratios of HCTZ-induced excretion of the different electrolytes were constant and independent of the GFR. After HCTZ, there was a double peak of Na+ excretion related to the abrupt reduction in GFR and Na+ excretion when the latter exceeded 40 mmol/h in normal subjects and 15 mmol/h in patients with advanced renal failure. The dose-response curves for HCTZ and FU were both relatively flat: doubling the dose of each produced statistically insignificant increases in sodium excretion. In contrast, when the lower doses of each were coadministered, there was a substantial and statistically significant increase in Na+ excretion. The clinical implication of these findings is that a combination of low doses of diuretics acting at different functional sites of electrolyte reabsorption in the nephron is superior in saluretic potency to increasing the dose of either diuretic alone.

Adult↗
PubMed1998

K-ATP-blocking diuretic PNU-37883A reduces plasma renin activity in dogs.

We determined the effects of the K-adenosine triphosphate (ATP)-blocking diuretic PNU-37883A on plasma renin activity (PRA) in conscious and anesthetized dogs. In conscious dogs, oral PNU-37883A (6-60 mg/kg) was less potent than hydrochlorothiazide (0.15-1.5 mg/kg) and furosemide (FURO; 0.3-3.0 mg/kg) but exhibited high natriuretic efficacy with little kaliuresis. Unlike the standard diuretics, PNU-37883A reduced PRA by 46-76%, and its high dose minimally affected 24-h urinary aldosterone excretion. PNU-37883A, 1 mg/kg i.v., also blunted the hyperreninemia induced by 1 mg/kg i.v. FURO. In cannulated dogs, 10 mg/kg i.v. PNU-37883A maximally increased fractional Na+ clearance 140% and reduced PRA 76%, but these effects were accompanied by a mean 13 mm Hg pressor effect. In anesthetized dogs, renal artery-infused PNU-37883A (3 mg/kg/h i.r.a.) increased Na+ excretion and reduced renal venous PRA independent of hemodynamics, whereas half this dosage selectively reduced renal venous PRA and renin release, independent of hemodynamics and natriuresis. These data demonstrate that the K-ATP blocker diuretic PNU-37883A reduces PRA in dogs after oral, i.v., and i.r.a. administration and could be a useful pharmacologic agent for exploring the role of K-ATP channels in regulating renin release.

Adamantane↗
PubMed1994

Regulation of tissue-type plasminogen activator-mediated fibrinolysis by plasminogen activator inhibitor type-1 in patients with ischaemic heart disease: possible unfavourable effect of diuretics.

BACKGROUND: Impaired endogenous tissue-type plasminogen activator (t-PA)-mediated fibrinolysis may be involved in the evolution of myocardial infarction. t-PA-mediated fibrinolysis is believed to depend on the amount of active t-PA present in the circulation. Accordingly, we investigated the possible mechanisms responsible for impaired t-PA-mediated fibrinolysis in patients with ischaemic heart disease. METHODS: Forty-five survivors of acute myocardial infarction were examined 8 weeks after discharge from hospital. Intravenous infusion of 1-desamino-8-D-arginine vasopressin (DDAVP; 0.4 micrograms/kg bodyweight) was used to stimulate the endogenous fibrinolytic system, and blood samples were collected before and after infusion. We compared the response of the t-PA-plasminogen activator inhibitor type-1 (PAI-1) fibrinolytic system in patients with preinfusion levels of active t-PA below or at the detection limit of the assay with that in patients with higher preinfusion levels of active t-PA. RESULTS: All patients responded to DDAVP infusion with an increase in plasma concentration of t-PA antigen. This response did not differ between the two groups. In contrast, the preinfusion levels of PAI activity were significantly higher in patients with undetectable plasma levels of active t-PA compared with patients with higher levels of active t-PA (22.3 versus 12.8 IU/ml; P < 0.01). Subgroup analyses demonstrated that patients treated with diuretics had significantly higher plasma concentrations of PAI-1 antigen (28.5 versus 17.9 ng/ml; P < 0.03) and a trend towards higher PAI activity (24.0 versus 14.6 IU/ml; P = 0.07) compared with patients not receiving diuretics. CONCLUSION: Our study strongly suggests that a high plasma level of PAI-1, the main inhibitor of t-PA, is responsible for impaired t-PA-mediated fibrinolysis in patients with ischaemic heart disease, and that treatment with diuretics may be associated with an unfavourable effect on the fibrinolytic system.

Aged↗
PubMed2004

Low-salt diet and diuretic effect on blood pressure and organ damage.

This review focuses on some aspects of the complex relationship among dietary salt intake, BP, organ complication, and genetic factors. First, the reason regarding the debate in the effect of a low-salt diet on BP and organ damage is discussed. Certainly, the lack of controlled long-term studies, taken together with the opposite effect of a low-salt diet on cardiovascular risk factors, justifies the contrasting opinions about the opportunity to reduce the sodium (Na) content in the diet of the general population. Second, the contribution that the genetic polymorphisms may furnish to explain the BP response in studies that apply either a moderate or a brisk reduction of salt intake is considered. Finally, the long-term effects of diuretics that produce a decrease in body Na similar to that achieved by moderate long-term dietary salt reduction are examined. Diuretics are able to reduce organ complications in the general population. However, these beneficial effects may be the net results of opposite effects in a subset of patients. Recently, the results of an observational study on hypertensive patients who were treated with a variety of antihypertensive drugs have been published. These results show that in carriers of the 460Trp ADD1 allele (38% of the population), the administration of diuretics halves the incidence of myocardial infarction and stroke when compared with other antihypertensive treatments that produce similar reduction of BP. These data support the notion that matching of the genetic mechanism with the drug mechanisms of action produces a clear therapeutic benefit.

Blood Pressure↗
PubMed2006

Potent potentiating diuretic effects of prednisone in congestive heart failure.

UNLABELLED: Animal studies showed glucocorticoids could specifically dilate renal vasculature, regulate synthesis and release of atrial natriuretic peptide (ANP), upregulate ANP receptors on vascular endothelial cells, and thus have potent potentiating diuresis and natriuresis effects in animal studies; however, their diuretic efficacy in humans is yet to be known. Therefore, we designed this randomized, double- blind, placebo-controlled, clinical study to determine the diuretic efficacy of prednisone, a glucocorticoid, in patients with congestive heart failure (CHF). METHODS: Twenty clinically stable patients with CHF without overt fluid retention were randomized to a prednisone group or placebo group. Prednisone (1 mg/kg/day with a maximum dose of 60 mg/day) was added to standard care for 7 days, leaving other medications unchanged. Variables included urine volume and electrolytes, serum electrolytes, and change from baseline in serum creatinine. RESULTS: Adding prednisone resulted in striking diuresis and natriuresis with time. As compared with the placebo group, the maximum of mean daily urine volume was 810.5 mL larger than those in the placebo group (95% confidence intervals [CI] 276.25 to 1344.86, P < 0.05). The maximum mean daily sodium excretion was 123.8 mmol higher than those patients given placebo (95% CI 11.4 to 236.2, P < 0.05). The placebo-corrected effect on change from baseline in serum creatinine was -19.5 mumol/L (95% CI -7.4 to -31.6, P < 0.01), favoring prednisone. CONCLUSIONS: This pilot study showed that prednisone had potent potentiating diuretic effects in patients with heart failure and might improve renal function in the same time. Further prospective randomized clinical studies are warranted to determine the preferable dose and its efficacy in decompensated congestive heart failure.

Adult↗
PubMed2005

Comparison of antihypertensive effects of an angiotensin-converting enzyme inhibitor, a calcium antagonist and a diuretic in patients with hypertension not controlled by angiotensin receptor blocker monotherapy.

OBJECTIVE: To compare the additional antihypertensive effects of an angiotensin-converting enzyme inhibitor (ACEI), a dihydropyridine calcium antagonist and a diuretic in patients whose hypertension is not controlled by full-dose angiotensin receptor blocker (ARB) monotherapy. DESIGN AND METHODS: Individuals with an ambulatory blood pressure (ABP) that was not controlled by valsartan 160 mg once daily were allocated randomly to two groups: those in group A (n = 35) were assigned randomly to treatment with benazepril 20 mg once daily or chlorthalidone 12.5 mg once daily, whereas patients in group B (n = 29) were assigned randomly to benazepril 20 mg once daily or amlodipine 5 mg once daily. All individuals continued to receive background valsartan 160 mg once daily. After 5 weeks, patients crossed over to the alternative valsartan-based combination treatment of each group for a second 5-week period. Twenty-four-hour ABP monitoring was performed before the random allocation to groups and at the end of each randomized combination pharmacotherapy period. RESULTS: Sixty-four individuals completed the study: 32 men and 32 women (mean +/- SD age 48.2 +/- 7.9 years, average 24-h ABP on valsartan monotherapy 143.4 +/- 12.6/87.7 +/- 7.8 mmHg). Significant additional antihypertensive effects on the average 24-h ABP were obtained with benazepril (8.6 +/- 8.8/6.3 +/- 6.7 mmHg), amlodipine (15.2 +/- 12.9/9.9 +/- 6.8 mmHg) and chlorthalidone (13.5 +/- 11.6/9.5 +/- 7.7 mmHg) (P < 0.001 for all additional antihypertensive effects). The additional effects of amlodipine and chlorthalidone added to valsartan were approximately 6/3.5 mmHg (P < 0.05) greater than that of benazepril. CONCLUSIONS: In patients in whom hypertension was not controlled by full-dose ARB monotherapy, a diuretic, a calcium antagonist or an ACE inhibitor provided significant additional antihypertensive effect. The antihypertensive effects of the ARB-diuretic and the ARB-calcium antagonist combinations were superior to that of the ARB-ACE inhibitor combination.

Adolescent↗
PubMed1985

Renal excretion of electrolytes in patients on long-term diuretic therapy for arterial hypertension and/or congestive heart failure.

Renal excretion, skeletal muscle content and plasma concentration of electrolytes were studied in 108 patients on long-term diuretic therapy for congestive heart failure and/or arterial hypertension. As reference populations served a group of 16 healthy volunteers and a group of 22 patients with liver cirrhosis, but not on diuretic therapy. Diuretic therapy was found to deprive the patients of their ability to conserve potassium and magnesium when there was a simultaneous cellular depletion of these ions. Magnesium excretion was found to be correlated to the skeletal muscle magnesium content. An inverted Na/K ratio in urine and a low magnesium excretion were fair indicators of cellular magnesium depletion.

Aged↗
PubMed1986

Potassium-sparing diuretics.

The hemodynamic and the endocrine disturbances in congestive heart failure (CHF) impose major changes in electrolyte balance with a retention of sodium and concomitant losses of potassium and magnesium from the body. These changes are of great importance for the development of cardiac dysrhythmias, a diminished glucose tolerance and for the well-being of the patient. The use of conventional diuretics imposes further burdens on the already deranged electrolyte balance. On long-term therapy with conventional diuretics in CHF we observed that approximately 50% of the 297 patients studied had potassium and magnesium deficiencies and an increased sodium content as judged by skeletal muscle biopsies. The magnesium deficiency is especially dangerous since it prevents the cells from keeping their high intracellular potassium concentration unchanged. Potassium substitution is without effect in a magnesium deficiency since magnesium is necessary for the transportation of potassium over the cell membrane against the concentration gradient. In case of magnesium depletion, potassium substitution may even have negative effects on the body potassium content. The reason for this is probably the increase of p-potassium concentration induced by the substitution, leading to an increase of aldosterone secretion. An increase of p-potassium levels by 0.2-0.4 mmol/l may thus result in a 50-100% rise in p-aldosterone concentration. These changes promote further urinary losses of potassium and magnesium. Several studies have demonstrated the positive effects of the potassium-sparing diuretics amiloride, spironolactone and triamterene on p-potassium concentration, but also on the body potassium content.(ABSTRACT TRUNCATED AT 250 WORDS)

Amiloride↗
PubMed1981

Influence of previous diuretic intake on the humoral and hormonal profile of idiopathic oedema.

Three groups of women underwent water loading tests: normal subjects, idiopathic oedema patients who had taken no medication for at least 3 months, and a second oedema group with recent diuretic intake. Idiopathic oedema in drug-free patients was characterized by an abnormal capillary permeability, lower basal protein values, a dramatic drop in urinary output in the upright position due to reduced glomerular filtration, enhanced reabsorption of sodium and water and stimulation of aldosterone and antidiuretic hormone (AVP) secretions. In these idiopathic oedema cases, osmolar AVP regulation was disrupted but AVP control by plasma volume was maintained. In the basal state, patients with recent diuretic intake were characterized by a gain in body weight and by depletion of plasma volume and plasma potassium. In these subjects, urinary output in the upright posture was as insufficient as in drug-free patients but was due to higher sodium reabsorption. Renal insensitivity to AVP action was also observed. Osmolar regulation and volume regulation of AVP were both disrupted in these cases with recent diuretic intake.

Adult↗
PubMed1994

Continuous infusion of furosemide in the treatment of patients with congestive heart failure and diuretic resistance.

OBJECTIVES: To assess the value of treatment with continuous intravenous infusion of furosemide (F) in patients with refractory congestive heart failure. DESIGN: Open uncontrolled dose-response study. SUBJECTS: Patients with congestive heart failure (those with New York Heart Association (NYHA) classes III and IV with an assessed amount of oedema of more than 5 kg and diuretic resistance were included [n = 10]). Diuretic resistance was defined as: failure to lose weight and/or inappropriate urinary sodium excretion (50 mmol 24 h-1) despite bed rest for a period of 2-3 days, salt and water restriction, orally and intravenously administered furosemide in a dose of 250 mg day-1, digoxin, and when possible an ACE inhibitor. Included patients were treated with continuous F infusion at a delivery rate of 20 mg-1 over 24 h. The infusion rate was gradually heightened up to a maximum dose of 160 mg h-1. MAIN OUTCOME MEASURES: Daily physical examination, history of side-effects, determination of serum electrolytes and 24-h electrolyte excretion during treatment with furosemide. RESULTS: Weight loss (mean +/- SD; 12.5 +/- 5 kg) and relief of symptoms was achieved in all patients. Mean (+/- SD) 24-h sodium output rose from 19 +/- 16 mmol 24 h-1 (n = 10) on oral therapy with 250 mg F to 137 +/- 85 mmol 24 h-1 (n = 8) during 80 mg h-1 and to 268 +/- 124 mmol 24 h-1 (n = 3) on the maximal dose of 160 mg h-1. CONCLUSION: Continuous infusion of F under careful monitoring of the patient is a safe, controllable and efficient treatment in patients with severe congestive heart failure and diuretic resistance.

Aged↗