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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 74 year old man was admitted to the hospital for purpura. The history revealed coronary heart disease. Bypass surgery had been performed 18 months ago. Furosemide had recently been prescribed for cardiac insufficiency and the patient had taken the drug intermittently over two weeks. Laboratory analysis showed severe thrombocytopenia. Despite immediate treatment with intravenous prednisolone and platelet transfusions the patient succumbed to cerebral hemorrhage. Autopsy confirmed a diffuse hemorrhagic diathesis and a cellular response of the bone marrow typical for an acute immune reaction. The start of the purpura nine to ten days after the first dose of furosemide, the exclusion of other possible causes for purpura and the focal proliferation of T-lymphocytes in the bone marrow render it highly probable, that furosemide was responsible for the fatal thrombocytopenia. Furosemide is discussed to have a potential for autoimmunological untoward effects due to its sulfonamide structure. Few case reports describe vasculitic and allergic phenomena. The generation of antibodies against thrombocytes and the depression of megakaryocytic function are thought to be involved. Our patient had been treated with furosemide during the bypass surgery 18 months before the development of purpura. A sensitization to furosemide probably took place at that time.
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PMID:[Fatal untoward effect of furosemide: immunocytopenic purpura and cerebral hemorrhage]. 1546 82

Diuretics, which are primarily used to modify the volume and the composition of body fluids, are widely used to treat hypertension. The diuretics include a) the thiazides and thiazide-like agents, which are the most common drugs used to treat high blood pressure (these drugs inhibit sodium reabsorption in the early distal convoluted tubule); b) loop diuretics, such as furosemide, block chloride and sodium reabsorption by inhibition of the Na/K/2Cl cotransport system in the thick ascending limb of the loop of Henle; and c) potassium-sparing (retaining) diuretics, including aldosterone receptor blockers (such as spironolactone and eplerenone) and epithelial sodium channel blockers (such as amiloride and triamterene, which interfere with the reabsorption of sodium and excretion of potassium and hydrogen that takes place in the late distal tubule, the connecting tubule, and the cortical collecting duct). Hydrochlorothiazide 12.5 mg once daily or equivalent low dosages of other similar agents reduce blood pressure in approximately one-half to two-thirds of patients who are responsive to this class of drugs; higher doses add little to the effect on blood pressure and also increase side effects. Some combinations of very small doses of thiazide diuretics - for example, 6.25 mg hydrochlorothiazide or 0.625 mg indapamide, with a low dose of an antihypertensive drug of a different class - have average antihypertensive efficacy when used once daily. Furosemide is used in patients with renal failure or severe heart failure and is best given by continuous intravenous infusion. The potassium-sparing diuretics are generally used in combination with thiazide diuretics to treat hypertension. Side effects occur at about the same frequency and severity with equipotent doses of all diuretics. The incidence of side effects is dose-dependent and also increases as a function of the duration of the renal excretory and antihypertensive actions. However, longer-acting diuretics provide better 24-hour control of blood pressure and increase compliance and adherence to the treatment regimen.
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PMID:Update of diuretics in the treatment of hypertension. 1741 83

Diuretics are frequently required to treat fluid retention in patients with chronic heart failure (CHF). Unfortunately, they can lead to a decline in renal function, electrolyte depletion, and neurohormonal activation. Arginine vasopressin (AVP) promotes renal water reabsorption via the V(2) receptor (V(2)R) and its levels are increased in CHF. This study was conducted to characterize the diuretic effect of tolvaptan, a non-peptide AVP V(2)R antagonist, and furosemide, a loop diuretic in a rat model of CHF after experimental autoimmune myocarditis. CHF was elicited in Lewis rats by immunization with porcine cardiac myosin, and 28 days after immunization rats were treated for 28 days with oral tolvaptan, and furosemide. CHF was characterized by left ventricular remodeling and impaired systolic and diastolic function. Tolvaptan produces a diuresis comparable to furosemide. Unlike tolvaptan, furosemide significantly increased urinary sodium and potassium excretion. Tolvaptan markedly elevated electrolyte-free water clearance (E-CH(2)O) or aquaresis to a positive value and increased urinary AVP excretion. In contrast to tolvaptan, furosemide elevated only electrolyte clearance (E-Cosm) but not E-CH(2)O. The differences in diuretic profile reflected the changes in plasma sodium and hormone levels. Tolvaptan dose dependently elevated plasma sodium concentration, but furosemide tended to decrease it. Furosemide significantly elevated plasma renin activity and aldosterone concentration. On the other hand, tolvaptan did not affect these parameters. Our results suggest that, tolvaptan have a potential medical benefit for the treatment of edematous conditions in CHF by removing excess water from the body without activating the RAAS or causing serum electrolyte imbalances.
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PMID:Effects of V2-receptor antagonist tolvaptan and the loop diuretic furosemide in rats with heart failure. 1817 82

Furosemide (FUR), a drug that promotes urine excretion, is used in the pharmacotherapy of various diseases and is considered as a doping agent in sports. FUR is a powerful diuretic (water pill). This medicine is used to treat excessive fluid accumulation and swelling (edema) of the body caused by heart failure, cirrhosis, chronic kidney failure, and nephrotic syndrome. Owing to its extensive use as a powerful diuretic, FUR has long attracted the attention of many analysts. A variety of analytical methods have been proposed for the determination of FUR in biological fluids and pharmaceutical samples. The revision includes the most relevant analytical methodologies used in its determination from the nineties decade at present.
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PMID:Recent developments in analytical determination of furosemide. 1870 Dec 32

Recent studies have shown that patients with heart failure over-express pro-inflammatory cytokines which enhance natural killer (NK) activity and negatively influence contractility and contribute to the remodeling of myocardium. The question is that how cardiovascular drugs influence on the cytokines of Peripheral Blood Mononuclear Cells (PBMCs) in Chronic Heart Failure (CHF). To study the effect of cardiovascular drugs on PBMCs-cytokines and NK activity of CHF patients. PBMCs of CHF patients/normal controls collected by Ficoll-paque density centrifugation. NK activity against K562 target cell was measured with MTT colorimetric assay. PBMCs were cultivated in RPMI/FCS, stimulated with phytohaemaglutinin (PHA). Tumor necrosis factor (TNF)-alpha interleukin (IL)-6, IL-2 and IL-1beta of culture supernatants after 24 h incubation with/without furosemide, captopril and digoxin were measured with sandwitch ELISA. Patients had higher NK activity than controls (56.9% +/- 1.6 vs 50.9% +/- 1.2, p < 0.05). NK activity of patients who already consumed Captopril/Furosemide didn't show difference with controls. Captopril (3, 1, 0.3 microg mL(-1)) and Furosemide (5, 2.5, 1.25 microg mL(-1)) caused a dose dependent inhibition in TNF-alpha compared with control (329 +/- 23, 427 +/- 15, 519 +/- 19 and 343 +/- 19, 430 +/- 14, respectively vs. 562 +/- 24 pg mL(-1) p < 0.05). Furosemide caused a dose dependent decrease in IL-6 (421 +/- 31, 534 +/- 33 vs. 662 +/- 41 pg mL(-1) p < 0.05). Captopril and Furosemide didn't show any significant effect on IL-1beta/IL-2. Digoxin had no significant effect on PBMCs-cytokines. These data suggest that the immunomodulatory effects of Captopril and Furosemide may contribute to their beneficial and no long-term adverse effects on PBMCs.
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PMID:The effect of cardiovascular drugs on pro-inflammatory cytokine secretion and natural killer activity of peripheral blood mononuclear cells of patients with chronic heart failure in vitro. 1908 2

One million patients are hospitalized each year with acute decompensated heart failure, and up to 20% of these patients are rehospitalized within a month after the acute presentation. Acute heart failure (AHF) accounts for 50,000 deaths annually and is the most frequent reason for hospital admissions in the United States. This article reviews the therapeutic options and the results of recent clinical trials in the treatment of AHF. Most patients can be effectively managed by use of diuretic agents or diuretics in combinations with nitrates, IV nitroglycerin, IV nitroprusside, and possibly IV nesiritide. Ultrafiltration is a promising technique that can be very helpful in the resistant patient. However, given the ease of initiation of diuretic therapy, it is unlikely that ultrafiltration would supplant diuretic use in acutely symptomatic patients. Patients in acute distress with AHF almost invariably respond to diuretics or a vasodilator combined with diuretic therapy. The loop diuretics are the most effective diuretics and thus most frequently used agents in treating AHF. Currently, there are 4 loop diuretics in the US market: furosemide, bumetanide, torsemide, and ethacrynic acid. IV furosemide and ethacrynic acid have a prompt venous dilatory effect, consequently decrease left ventricular filling pressure and immediately relieve symptoms of pulmonary congestion, before a diuresis can occur. Furosemide is more often used than ethacrynic acid due to its reduced ototoxic potential. However, ethacrynic acid should be used in sulfa-sensitive patients because ethacrynic acid is the only loop diuretic, which does not contain a sulfa moiety.
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PMID:The management of acute heart failure and diuretic therapy. 1914 55

Acute cardiogenic pulmonary edema (CPE) is a pathology frequently seen in patients presenting to emergency departments (EDs) and can usually be attributed to preexisting cardiovascular disease. Heart failure alone accounts for more than 1 million hospital admissions annually and has one of the highest ED morbidity and mortality to date (). Historically, CPE has been managed by the treating clinician in a manner that is based largely on anecdotal evidence. Furosemide (Lasix), morphine, and nitroglycerin have historically been the baseline standard for drug therapy in CPE management. A lack of drastic improvement in the patient's condition over the course of the ED visit may reflect a management style that results in higher morbidity and mortality for CPE patients. Several recent articles provide evidence-based outcomes that suggest changing standard therapy along with the adjunctive use of other medications. These articles also describe treatment modalities that result in a marked improvement in the management of patients with CPE along with decreases in adverse outcomes and hospital length of stay. The goal of this article is to present a summary of the evidence regarding the management of CPE and discuss the implications for current practice.
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PMID:Management of acute cardiogenic pulmonary edema: a literature review. 2011 52

Chronic heart failure (CHF) is the cause of significant morbimortality all over the world and its incidence and prevalence are increasing. Fluid retention and volume overload are responsible of large part of morbility related to heart failure. There are a variety of therapy options for CHF, but loop diuretics play an essential role. Furosemide is the most commonly used loop diuretic. Torasemide is a loop diuretic belonging to the pyridine sulfonylurea class. It is a high-ceiling diuretic that has a longer half-life, longer duration of action and higher bioavailability compared to furosemide. It has additional actions such as antialdosterone and vasodilatation effects. It is the only loop diuretic for which it has been shown to effectively lower high blood pressure even with low doses. Thus, torasemide is recommended for CHF treatment instead of furosemide. Clinical trials have indicated that torasemide improves left ventricular function, reduces mortality as well as the frequency and duration of heart failure-related hospitalization. It also increases exercise tolerance, improves New York Heart Association functional classification and quality of life in patients with CHF. In addition, torasemide is a very safe drug. In a postmarketing surveillance study (TORIC) of 1,377 patients with CHF, torasemide significantly reduced cardiovascular mortality in comparison to furosemide. Torasemide reversed myocardial fibrosis and reduced collagen type I synthesis, improving cardiac remodeling in patients with CHF. Torasemide prolonged-release (PR) is a new formulation that, compared with torasemide immediate-release, has a similar systemic exposure but significantly slower rates of absorption and lower fluctuations in plasma concentrations. Its natriuretic efficiency is higher and diuresis is more constant, with a better tolerability.
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PMID:[Update: prolonged-release torasemide]. 2088 98

The role of repeated infusions of Levosimendan (LEVO) in patients with chronic advanced heart failure is still unclear. Thirty-three patients with chronic heart failure presenting clinical deterioration were randomized 2:1 to receive monthly infusions of LEVO (n = 22) or Furosemide (Controls, n = 11). At the first drug's administration, noninvasive hemodynamic evaluation was performed; before and after each infusion, we assessed NYHA class, systolic and diastolic function, functional mitral regurgitation, and brain natriuretic peptide (BNP) levels. Noninvasive hemodynamic in the LEVO group showed vasodilation and decrease in thoracic conductance (index of pulmonary congestion), whereas in Controls, only a reduced thoracic conductance was observed. In the LEVO group, systolic and diastolic function, ventricular volumes, severity of mitral regurgitation, and BNP levels improved over time from baseline and persisted 4 weeks after the last infusion (P < 0.01). In Controls, no change developed over time in cardiac function and BNP levels. In LEVO-treated patients, 1-year mortality tended to be lower than in those treated with Furosemide. In conclusion, serial LEVO infusions in advanced heart failure improved ventricular performance and favorably modulated neurohormonal activation. Multicenter randomized studies are warranted to test the effect of LEVO on long-term outcome.
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PMID:Intermittent levosimendan infusions in advanced heart failure: favourable effects on left ventricular function, neurohormonal balance, and one-year survival. 2293 5

Furosemide is the most widely prescribed loop diuretic in the setting of systolic heart failure (HF), yet torsemide has been shown to have less inter- and intra-individual variation in bioavailability and a longer duration of action compared with furosemide. Thus, a systematic review and meta-analysis of randomized controlled trials comparing torsemide versus furosemide in patients with systolic HF using OVID MEDLINE, Excerpta Medica (Embase), Web of Science, PubMed and Google Scholar was performed. Extracted data included study design, sample characteristics, intervention, outcomes and control for potential confounding factors. A DerSimonian and Laird random-effects model was used to compute summary risk ratios for HF and cardiovascular (CV) readmission outcomes. Two randomized trials comparing furosemide with torsemide in 471 patients with systolic HF were identified. Compared to furosemide, torsemide significantly reduced total HF readmissions (relative risk [RR]: 0.41, 95% CI: 0.28-0.61, p < 0.0001) and HF readmissions (RR: 0.53, 95% CI: 0.33-0.84, p = 0.008) as well as CV readmissions (RR: 0.77, 95% CI: 0.60-0.98, p = 0.03) in patients with "at least 1 readmission." Moreover, compared with furosemide, torsemide caused a 14% reduction in all-cause mortality (RR: 0.86 [0.53-1.39], p = 0.54). Compared with furosemide, torsemide significantly reduces HF and CV-related hospital readmissions in systolic HF. Furthermore, torsemide is associated with a trend in reducing all-cause mortality.
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PMID:Should torsemide be the loop diuretic of choice in systolic heart failure? 2301 24


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