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

The clinical efficacy and safety of enalapril were evaluated in dogs with moderate or severe heart failure. This study was conducted at 19 centers and included 211 client-owned dogs with heart failure caused by mitral regurgitation (MR) due to acquired valvular disease or dilated cardiomyopathy (DCM). Dogs of various breeds, ages, and weights were included in the study. Replicates of 2 dogs each were formed, using separate allocation schedules for dogs with MR or DCM. One dog within each replicate received placebo tablets (vehicle tablets without enalapril) PO sid or bid, and the other dog received enalapril tablets at approximately 0.5 mg/kg sid or bid, based on individual need. In addition to the experimental drug, all dogs, except 1 in the placebo group, received furosemide; 73.3% of the dogs in the placebo group and 78.3% of those in the enalapril group received digoxin. Doses of enalapril or placebo were administered for approximately 28 days. In the placebo group, 68.6% of the dogs completed the study compared with 84.9% in the enalapril group; the difference between groups was significant (P < .01). Significantly (P < .01) more dogs in the placebo group compared with the enalapril group died or were removed from the study because of progression of heart failure. On day 28, all 14 clinical variables measured improved significantly (P < .01) in the enalapril group compared with the placebo group. Five dogs (3 from the placebo group and 2 from the enalapril group) had to be removed from the study as a result of azotemia.
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PMID:Controlled clinical evaluation of enalapril in dogs with heart failure: results of the Cooperative Veterinary Enalapril Study Group. The COVE Study Group. 852 21

Despite advances in the pharmacological management of cardiac failure, some patients remain refractory to this therapy. However, improved understanding of the physiology and technique of peritoneal dialysis has recently allowed ambulatory peritoneal ultrafiltration to be applied to the treatment of patients with intractable heart failure. We report the management of three such patients with New York Heart Association (NYHA) class IV cardiac failure, each with a left ventricular ejection fraction < 20%. They had become unresponsive to maximum pharmacological management with inotropes, diuretics and ACE inhibitors. All patients had biochemical evidence of pre-renal azotemia. Initially, patients received aggressive ultrafiltration by continuous veno-venous haemofiltration (CVVH) or one- to two-hourly peritoneal dialysis exchanges until they achieved an optimal dry body weight. Once stabilized, they were converted to an intermittent ambulatory peritoneal ultrafiltration (IAPU) regimen of one to three exchanges per 24 h according to their individual needs. During an 18 +/- 10-month follow-up, their duration of hospital confinement was reduced by 85% and all three patients improved from class IV to class II cardiac failure. IAPU may have a useful role in the long-term management of intractable heart failure in a selected group of patients.
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PMID:Long-term successful management of refractory congestive cardiac failure by intermittent ambulatory peritoneal ultrafiltration. 891 42

Author investigated the safety of combined ACE inhibitor (captopril) and spironolacton therapy on 237 pts with severe heart failure (NYHA III-IV.) treated with digitalis and loop diuretic during on average 65.4 months follow-up period. Incidence of clinically significant increase in serum urea, creatinine and potassium level was evaluated and compared with those of in group treated 47 pts with the same standard therapy captopril, digitalis, furosemide, without spironolacton. There was no significant difference between the incidence of azotemia and hyperkalemia in the two groups. The author emphasizes on the base of their results the safety of combined captopril and low dose spironolactone therapy in heart failure.
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PMID:[Effect of combined captopril-spironolactone therapy of cardiac insufficiency on kidney function and serum electrolyte values]. 945 4

Diuretic therapy decreases capillary wedge pressure and improves New York Heart Association (NYHA) functional class both in acute and chronic heart failure. In advanced symptomatic heart failure, loop diuretics are generally necessary to improve symptoms of congestion. Diuretic resistance in the edematous patient has been defined as a clinical state in which diuretic response is diminished or lost before the therapeutic goal of relief from edema has been reached. The major causes of diuretic resistance are functional renal failure (prerenal azotemia), hyponatremia, altered diuretic pharmacokinetics, and sodium retention caused by counterregulatory mechanisms intended to reestablish the effective arterial blood volume. Therapeutic approaches to combat diuretic resistance include restriction of fluid and sodium intake, use of angiotensin-converting-enzyme (ACE) inhibitors, changes in route (oral, intravenous) and timing (single dose, multiple doses, continuous infusion) of diuretic therapy, and use of diuretic combinations.
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PMID:Diuretic treatment and diuretic resistance in heart failure. 1032 Jan 23

Acute glomerulonephritis (AGN) manifests with abrupt onset of hematuria, facial edema, hypertension and impairment of renal function. The commonest form of AGN in developing countries is that following a beta hemolytic streptococcal infection where the glomerular injury is mediated by deposition of immune complexes. In the usual patient with moderately severe poststreptococcal AGN (PSAGN) the above-mentioned features are present However, gross or microscopic hematuria may be the only abnormality. A similar picture may occasionally be produced by a variety of infections (when GN is referred to as post-infectious and the mechanism of glomerular damage and the renal histology are similar to that in PSAGN), primary renal glomerular disorders (e.g. membranoproliferative GN, IgA nephropathy), collagen vascular diseases (systemic lupus erythematosus), systemic vasculitis (Henoch Schonlein purpura) and hereditary nephritis and some nonglomerular conditions. PSAGN may also present with one or more of its complications such as profound volume expansion with heart failure and hypertensive encephalopathy. PSAGN resolves rapidly and has an excellent prognosis. Patients with severe renal involvement and life threatening complications need expert supportive management. AGN with associated systemic features or very pronounced azotemia, nonstreptococcal AGN and unresolving GN need prompt, appropriate evaluation that often includes a renal biopsy. If extensive crescentic changes are found (crescentic GN), aggressive immunosuppression will be necessary.
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PMID:Acute glomerulonephritis. 1079 62

In renal failure, blood urea nitrogen and serum creatinine usually rise in tandem; the normal BUN: Cr ratio is 10-15: 1. Disproportionate rises in BUN: Cr (> 20: 1) often imply pre-renal azotemia but may be caused by increased protein catabolism or an excessive protein load. In this study we looked at intensive care patients who acutely developed markedly increased BUN (> or = 100 mg/dL) with only modest elevation of Cr (< or = 5 mg/dL) for possible causes of the disproportionate azotemia. There were 19 such cases collected over 6 months, nine women and ten men, with mean age 69.2 +/- 4.4 years (13/19 > 75 years). Peak BUN was 156 +/- 11 mg/dL; peak Cr 4.3 +/- 0.5 mg/dL. Eleven patients expired. Mean serum albumin at the time of consultation was 2.7 +/- 0.2 g/dL; mean total lymphocyte count 1.0 +/- 0.1/mm3. Of possible factors causing the azotemia, nine patients had documented hypovolemia; eight had congestive heart failure; six were in septic or hypovolemic shock, and two received high-dose steroids. As contributing factors, eight patients had Salb < 2.5 g/dL; eight were given a high protein intake > 100 g/d; two had HIV, and two others had gastrointestinal bleeding. Infection was present in 14 patients; seven had sepsis (bacteremia with hypotension). All patients had at least one of these factors present and 16/19 had two or more. Fractional Na excretion was < 1% (consistent with pre-renal azotemia) in only four of the 11 patients in whom it was measured. We conclude that severely disproportionate BUN : Cr is frequently multifactorial and is most common in the elderly, perhaps due to their lower muscle mass, and in ICU patients given a high protein intake. It is often not indicative of uncomplicated renal hypoperfusion, although low renal perfusion (hypovolemia, shock, or heart failure) is common. Mortality is high due to the severe illnesses, especially infection, worsened by decreased renal function and hypercatabolic state.
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PMID:Massive and disproportionate elevation of blood urea nitrogen in acute azotemia. 1254 57

Endotoxemia induces a hemodynamic form of acute renal failure (ARF; renal vasoconstriction +/- reduced glomerular ultrafiltration coefficient, K(f); minimal/no histological damage). We tested whether levosimendan (LS), an ATP-sensitive K+ (K(ATP)) channel opener with cardiac ionotropic and possible anti-inflammatory properties, might have utility in combating this form of ARF. CD-1 mice were injected with LPS +/- LS. LS effects on LPS-induced systemic inflammation (plasma TNF-alpha/MCP-1; cardiorenal mRNAs), plasma NO levels, and azotemia were assessed. Because K(ATP) channel opening has been reported to mediate hypoxic tubular injury, possible adverse LS effects on ischemic ARF and ATP depletion injury were sought. Effects of diazoxide (another K(ATP) channel agonist) and glibenclamide (a channel antagonist) on hypoxic tubular injury also were assessed. Finally, the ability of LS to alter rat mesangial cell (MC) contraction in response to ANG II (elevated in sepsis) was tested. LS conferred almost complete protection against LPS-induced ARF, without any apparent reduction in the LPS-induced inflammatory response. Neither LS nor diazoxide altered ATP depletion-mediated tubule injury (in vivo or in vitro). Conversely, glibenclamide induced a marked and direct cytotoxic effect. LS completely blocked ANG II-induced MC contraction, an action likely to increase K(f). We concluded that 1) LS can confer marked protection against LPS-induced ARF; 2) this likely stems from vasoactive properties, rather than reductions in LPS-induced inflammation; and 3) K(ATP) channel agonists (but not antagonists) appear to be devoid of toxic proximal tubular cell effects. This suggests that LS, and other K(ATP) channel agonists, have a margin of safety if employed in situations (sepsis syndrome, heart failure) in which severe renal vasoconstriction might lead to ischemic ARF.
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PMID:Levosimendan protects against experimental endotoxemic acute renal failure. 1641

Over the past few years, acute worsening of renal function has emerged as a powerful and independent predictor of adverse cardiac outcomes among patients hospitalized with acute heart failure exacerbation. This phenomenon has been recently termed acute cardio-renal syndrome. Acute cardio-renal syndrome is not uncommon, affecting roughly one third of acute decompensated heart failure patients. The mechanism of acute cardio-renal syndrome is poorly understood and difficult to elucidate in light of the complex and multifactorial comorbidities associated with acute heart failure syndrome. Acute cardio-renal syndrome is commonly explained by hypoperfusion of the kidney with intravascular volume depletion, hypotension and low flow state ("pre-renal syndrome"). This perception, however, is challenged by the actual hemodynamics present during acute cardio-renal syndrome characterized by hypervolemia, normal cardiac output, and elevated filling pressures of the systemic and venous circulation. This review discusses the long-standing and unnoticed evidence in support of the notion that right-sided failure with raised filling pressure of the renal vein by itself can indeed lead to acute worsening renal function with oliguria, azotemia, and reduced glomerular filtration rate.
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PMID:Acute cardio-renal syndrome: progression from congestive heart failure to congestive kidney failure. 1788 88

Heart failure is a major and growing health problem. Major advances leading to newer therapies are being made in understanding the pathophysiology of heart failure as a chronic progressive disorder. Whatever the cause, all heart failure patients eventually progress to a refractory stage characterized by worsening renal function and resistance to diuretic therapy with attending severe edema. A logical treatment for this "cardiorenal syndrome" is the use of dialysis, which is efficient in treating both the hypervolemia and azotemia of refractory heart failure. Although all modalities of dialysis have been tried, peritoneal dialysis (PD) is the simplest choice and offers several advantages. It is an already-established long-term home-based therapy and does not require complex machinery or hospital resources. It is associated with preservation of residual renal function, gentle continuous ultrafiltration, hemodynamic stability, better middle-molecule clearance, sodium sieving with maintenance of normonatremia and perhaps less inflammation than hemodialysis is, especially with newer PD solutions. In the present paper, we discuss the potential advantages of PD in the treatment of heart failure, review the available literature, and lay some foundations for future research.
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PMID:Peritoneal dialysis in congestive heart failure. 1788 9

A mainstay of therapy for congestive heart failure has been the use of potent diuretic agents, such as furosemide, that target the kidney to enhance sodium and water excretion. Although furosemide is widely used to treat the symptoms of acute decompensated heart failure (ADHF), the consequent activation of the renin-angiotensin-aldosterone system may limit the natriuretic response by reducing the glomerular filtration rate. In addition, excessive diuresis may reduce cardiac preload and result in systemic hypotension, which reduces renal perfusion pressure and prerenal azotemia and raises levels of blood urea nitrogen. In order to preserve and/or enhance renal function in ADHF, especially with agents such as conventional diuretics and vasodilators, an understanding of intrarenal factors that may protect the kidney may provide a direction for optimal use of current therapies and also lead to newer therapeutic strategies. Vasodilators, especially those that are linked to cGMP activation, may provide an alternative approach.
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PMID:Targeting the kidney in acute decompensated heart failure: conventional diuretics and renal-acting vasodilators. 1841 8


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