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PubMed1993

Mechanism of death in heart failure. The Vasodilator-Heart Failure Trials. The V-HeFT VA Cooperative Studies Group.

BACKGROUND: The Vasodilator-Heart Failure Trial (V-HeFT) data base provides information on the mechanism of death of male veterans entered into two trials that evaluated the effect of vasodilator therapy on survival in heart failure. METHODS AND RESULTS: Men aged 18-75 years with heart failure were recruited at 13 Department of Veterans Affairs Medical Centers. In V-HeFT I, 283 of 642 patients (44%) died during follow-up (average, 2.3 years), and in V-HeFT II, 285 of 804 randomized patients (35.5%) died during follow-up (average, 2.5 years). Mechanism of death was established centrally using a standardized classification. In V-HeFT I, 124 of the 283 deaths (43.8%) were sudden with no worsening of symptoms; in V-HeFT II, 104 of the 285 deaths (36.5%) were sudden. An average of 31.5% of the deaths (31.4% and 31.6%, respectively) in the two trials was due to pump failure. The proportion of sudden deaths that occurred without worsening of symptoms was similar in patients with and without ischemic heart failure. Sudden deaths tended to occur earlier and pump failure deaths later in both V-HeFT studies. There was a trend for a lower percentage of cardiac deaths from pump failure and a higher percentage from sudden death in subgroups with higher peak exercise oxygen consumption (VO2), higher ejection fraction, and lower plasma norepinephrine levels. The proportion of deaths that occurred suddenly was similar in placebo, prazosin, and hydralazine plus isosorbide dinitrate treatment groups but was significantly lower in the enalapril treatment group. In V-HeFT I, measures of cardiac function and VO2 predicted pump failure death and sudden death. In V-HeFT II, VO2 and cardiothoracic ratio were independent predictors of all-cause deaths and pump failure deaths; only ejection fraction was an independent predictor of both pump failure and sudden death. CONCLUSION: Although mechanistically distinct terminal events can be identified in patients with heart failure and physiological measurements can provide some insight into the risk of these disparate events, sudden death and pump failure death both appear largely to be linked to the severity of cardiac dysfunction and symptoms. Strategies to identify individuals for selective preventive therapy are not yet practical.

Cause of Death↗
PubMed1996

Prognostic factors in acute renal failure due to sepsis. Results of a prospective multicentre study. The French Study Group on Acute Renal Failure.

BACKGROUND: Sepsis is a major cause of acute renal failure in hospital patients, but its incidence and the associated prognostic factors have rarely been assessed prospectively by multivariate analysis. METHODS: We conducted a prospective 6-month study in 20 multidisciplinary intensive care units to assess the prognosis of patients hospitalized with acute renal failure due to sepsis. Sepsis syndrome and septic shock were defined according to the criteria of the Society of Critical Care Medicine Consensus Conference. Severity scoring indexes (SAPS, APACHE II, and organ system failure (OSF)) were measured on ICU admission and on inclusion. The end-point was hospital mortality. RESULTS: Acute renal failure had a septic origin in 157 patients (Group 1), comprising 68 with septic shock and 89 with sepsis syndrome, and did not result from infection in 188 patients (Group 2). Patients with septic acute renal failure were older (mean age: 62.2 versus 57.9 years, P<0.02) and had on inclusion a higher SAPS (19.3 versus 16.1, P<0.001), APACHE II (29.6 versus 24.3, P<0.001), and OSF (2.07 versus 1.52, P<0.001) than patients with non-septic acute renal failure. They had a higher need for mechanical ventilation (69.1% versus 47.3%, P<0.001), and acute renal failure was more often delayed during the ICU stay than was present on admission (47.7% versus 32.4% respectively, P<0.005). Hospital mortality was higher in patients with septic acute renal failure (74.5%) than in those whose renal failure did not result from sepsis (45.2%, P<0.001). Mortality was influenced by the presence of a septic shock (79.4%) or of a sepsis syndrome on inclusion (70.8%). Using a stepwise logistic regression model, sepsis was an independent predictor of hospital mortality (OR, 2.51; 95% CI, 1.44-4.39) as well as a delayed occurrence of acute renal failure, oliguria, an altered previous health status hospitalization prior to ICU, need for mechanical ventilation, age and severity scoring indexes on inclusion. In total patients, mortality was higher in dialyzed than in non-dialyzed patients (P<0.001), and in those treated by continuous compared to intermittent techniques (P<0.01). Patients dialyzed with biocompatible membranes had a lower mortality than those treated with cellulose membranes (P<0.005). CONCLUSIONS: Patients with acute renal failure due to sepsis have a worse prognosis than those with non-septic acute renal failure. Sepsis and the above-defined predictive factors are to be considered in studies on prognosis of ARF patients. Our results suggest that the use of biocompatible membranes may reduce significantly mortality in these patients.

Acute Kidney Injury↗
PubMed2002

Association of nonsteroidal anti-inflammatory drugs with first occurrence of heart failure and with relapsing heart failure: the Rotterdam Study.

BACKGROUND: Nonsteroidal anti-inflammatory drugs (NSAIDs) have been associated with first hospitalization for congestive heart failure (CHF). It is likely, however, that NSAIDs precipitate a relapse but are less likely to induce a first occurrence of (incident) heart failure. METHODS: A total of 7277 participants in the Rotterdam Study were followed up from the interview date until the first of the following events: a diagnosis of incident heart failure, death, removal, or end of the follow-up period. Excluded from the study population were all participants with prevalent heart failure at baseline. Exposure to NSAIDs and other medication was calculated on the basis of automated data on filled drug prescriptions in the pharmacies within the study area. In a second analysis, we followed up all participants with incident heart failure until the first relapse or the end of follow-up. RESULTS: Incident heart failure was encountered in 345 participants during follow-up. Current use of NSAIDs was associated with a relative risk of incident heart failure of 1.1 (95% confidence interval [CI], 0.7-1.7), after adjustment for age, sex, and concomitant medication. In patients with prevalent heart failure who filled at least 1 NSAID prescription since diagnosis of heart failure, the univariate and adjusted relative risks of a relapse were 3.8 (95% CI, 1.1-12.7) and 9.9 (95% CI, 1.7-57.0), respectively. CONCLUSIONS: The use of NSAIDs is not associated with an increased risk of incident heart failure. In patients with prevalent heart failure, current use of NSAIDs is associated with a substantially increased risk of a relapse.

Aged↗
PubMed2004

Interleukin-6 and B-type natriuretic peptide are independent predictors for worsening of heart failure in patients with progressive congestive heart failure.

BACKGROUND: Neurohormones and cytokines have been associated with poor prognosis in patients with congestive heart failure. However, direct comparisons between them are rare and the best predictor for worsening of heart failure remains to be elucidated. The aim of the study was to identify independent predictors for worsening of heart failure. METHODS: We studied 100 patients with congestive heart failure (LVEF <or=25%). Serum levels of interleukin-6 (IL-6), tumor necrosis factor (TNF)-alpha, aminoterminal atrial natriuretic peptide (N-ANP), B-type natriuretic peptide (BNP), aminoterminal B-type natriuretic peptide (N-BNP), norepinephrine (NE) and big endothelin (big ET) were measured at entry into the study. Univariate and stepwise multivariate regression analyses were performed to compare variables and clinical parameters. The end-point was defined as worsening of heart failure. RESULTS: During follow-up (mean 378 days), 30 patients reached the defined end-point. Univariate risk factors of worsening of heart failure were IL-6 (p = 0.0001), log BNP (p = 0.0001), log N-ANP (p = 0.0259), big ET (p = 0.0032), log N-BNP (p = 0.0495), NE (p = 0.0013) and LVEF (p = 0.0498). Multivariate regression analysis identified IL-6 as the strongest independent predictive value for worsening of heart failure (p = 0.0001), followed by log BNP (p = 0.0002). Mean IL-6 levels were 1.76 +/- 1.73 in stable patients and 4.62 +/- 7.98 pg/ml in patients who developed worsening of heart failure. Using a cut-off value of 1.66 pg/ml for IL-6 Kaplan-Meier freedom from worsening, heart failure was significantly higher in patients below this cut-off point compared with those above (p = 0.0002). CONCLUSIONS: IL-6 and BNP independently predict worsening of heart failure. A single measurement could help to identify patients at high risk for worsening of heart failure and these individuals should be monitored more closely.

Angiotensin-Converting Enzyme Inhibitors↗
PubMedDate not supplied

Treatment of chronic heart failure in long-term care facilities: implications of recent heart failure guidelines recommendations.

Use of angiotensin-converting enzyme inhibitor in heart failure with left ventricular systolic dysfunction has revolutionized management of heart failure and resulted in several national heart failure guidelines. However, studies have documented underutilization of these life saving drugs. Subsequently, results of other randomized clinical trials revealed the beneficial effects of angiotensin receptor blockers, beta-blockers, and spironolactone in heart failure with systolic dysfunction, which prompted several other guidelines. However, all these guidelines were primarily restricted to systolic dysfunction. Heart failure is as much a geriatric syndrome as it is a cardiac. Most heart failure patients are older adults. About half of the heart failure in older adults is not associated with left ventricular systolic dysfunction. Two recent heart failure guidelines, from the European Society of Cardiology and the American College of Cardiology/American Heart Association, published respectively in September and December 2001 included recommendations for patients with preserved left ventricular systolic function and other special populations, including older adults and those at end of life. The purpose of this article is to review the relevance of these two guidelines to heart failure patients living in long-term care facilities. As our population is aging, more heart failure patients are expected to live in long-term care facilities. Appropriate evaluation and management of these patients are essential to improve quality of heart failure care in the coming decades.

Aged↗
PubMed1996

Acute renal failure in intensive care units--causes, outcome, and prognostic factors of hospital mortality; a prospective, multicenter study. French Study Group on Acute Renal Failure.

OBJECTIVE: To assess the causes, the prognostic factors, and the outcome of patients with severe acute renal failure. DESIGN: Prospective, multicenter study. SETTING: Twenty French multidisciplinary intensive care units (ICUs). PATIENTS: All patients with severe acute renal failure were prospectively enrolled in the study for a 6-month period. Severe acute renal failure was defined by the following criteria: a) a serum creatinine concentration of > or = 3.5 mg/dL ( > or = 310 mumol/L) and/or a blood urea nitrogen concentration of > or = 100 mg/dL ( > or = 36 mmol/L); or b) an increase in blood urea nitrogen or serum creatinine concentration, such that the concentration is 100% above the baseline value in patients with previous chronic renal insufficiency (serum creatinine concentration of > 1.8 mg/dL [ > 150 mumol/L]), excluding those patients with a basal serum creatinine concentration of > 3.4 mg/dL ( > 300 mumol/L). INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Age, sex, previous health status and preexisting organ dysfunction, and type and origin of acute renal failure were recorded. The Simplified Acute Physiology Score, the Acute Physiology and Chronic Health Evaluation (APACHE II) score, and the number of Organ System Failures were calculated on ICU day 1 and at the time of inclusion in the study. Prognostic factors were determined by univariate methods and stepwise logistic regression analysis. There were 360 patients in the study; 217 patients were admitted to the study at the time of ICU admission and 143 patients were admitted to the study after ICU admission. Only 41% of these patients were in good health 3 months before ICU entry. The reason for admission was medical in 78% of cases. The type of acute renal failure was prerenal (n = 16), renal (n = 282), or postrenal (n = 17). Renal replacement therapy was used in 174 patients. Two hundred ten (58%) patients died during the hospital stay. Using stepwide logistic regression, seven variables were predictive of death. These variables were advanced age, altered previous health status, hospitalization before ICU admission, delayed occurrence of acute renal failure, sepsis, oliguria, and severity of illness as assessed at the time of study inclusion by Simplified Acute Physiology Score, APACHE II, or Organ System Failure. CONCLUSIONS: The hospital mortality rate of patients with severe acute renal failure in patients requiring intensive care remains high. In order to compare patient groups in further trials concerning acute renal failure, recorded characteristics of the population should include age, previous health status, disease characteristics (initial or delayed acute renal failure, oliguria, sepsis), and the severity of the illness as assessed by physiologic scoring systems recorded at the time of study inclusion.

APACHE↗
PubMed1981

Renal failure in fulminant hepatic failure and terminal cirrhosis: a comparison between incidence, types, and prognosis.

Forty patients with terminal cirrhosis and 40 patients with fulminant hepatic failure-all consecutively admitted-were studied with regard to incidence, types, and prognosis of complicating renal insufficiency. Renal failure was considered present when the serum creatinine was greater than 0.20 mmol/l. Of the patients with cirrhosis 26 (65%) developed renal failure. In 15 the type was functional, in three due to acute tubular necrosis, and in eight indeterminable. Of the patients with fulminant hepatic failure 22 (55%) had renal insufficiency; of these 13 had functional renal failure, five acute tubular necrosis, and in four the type was indeterminable. In both categories of patients, renal failure was equally frequent among patients with or without gastrointestinal bleeding and with or without ascites or diuretic therapy. The biochemical tests of liver function were similar in patients with or without renal failure in both categories. The mean renal blood flow in seven unselected patients with fulminant hepatic failure was reduced in the same order as previously observed in patients with cirrhosis. In terminal cirrhosis the mortality rate was 88% in the presence of renal failure, 71% in its absence (p greater than 0.05), while the same figures in fulminant hepatic failure were 100% and 67% (p less than 0.05). The incidence, relative frequency, and prognosis of renal failure were not different in the two conditions, indicating identical pathophysiological circumstances.

Acute Kidney Injury↗
PubMed1996

Carvedilol inhibits clinical progression in patients with mild symptoms of heart failure. US Carvedilol Heart Failure Study Group.

BACKGROUND: We tested the hypothesis that carvedilol inhibits clinical progression in patients with mildly symptomatic heart failure due to left ventricular (LV) systolic dysfunction. METHODS AND RESULTS: Patients (n = 366) who had mildly symptomatic heart failure with an LV ejection fraction (LVEF) < or = 0.35, had minimal functional impairment (defined as the ability to walk 450 to 550 m on a 6-minute walk test), and were receiving optimal standard therapy, including ACE inhibitors, were randomized double-blind to carvedilol (n = 232) or placebo (n = 134) and followed up for 12 months. The primary end point was clinical progression, defined as death due to heart failure, hospitalization for heart failure, or a sustained increase in heart failure medications. Clinical progression of heart failure occurred in 21% of placebo patients and 11% of carvedilol patients, reflecting a 48% (P = .008) reduction in the primary end point of heart failure progression (relative risk, 0.52; CI, 0.32 to 0.85). This effect of carvedilol was not influenced by sex, age, race, cause of heart failure, or baseline LVEF. Carvedilol also significantly improved several secondary end points, including LVEF, heart failure score, NYHA functional class, and the physician and patient global assessments. Carvedilol reduced all-cause mortality but had no effects on the Minnesota Living With Heart Failure scale, the distance walked in 9 minutes on a self-powered treadmill, or cardiothoracic index. The drug was well tolerated. CONCLUSIONS: Carvedilol, when added to standard therapy, including an ACE inhibitor, reduces clinical progression in patients who are only mildly symptomatic with well-compensated heart failure.

Adolescent↗
PubMed2000

Management of heart failure: evidence versus practice. Does current prescribing provide optimal treatment for heart failure patients?

Heart failure is an increasingly common and costly chronic disorder, with a rising prevalence of at least 2% in populations over the age of 45 years, mortality rates that are as poor as common solid cancers, and very high health care utilisation costs. Despite increased evidence supporting a range of effective interventions, predominantly therapeutic, there remain significant degrees of physician underperformance in terms of heart failure diagnosis and management. Until the early 1990s, the management of heart failure was largely confined to the symptomatic relief of patients with well established heart failure in fluid overload. The introduction of angiotensin-converting enzyme (ACE) inhibitors provided the first treatments that beneficially altered the prognosis of patients with the most common expression of heart failure, namely established systolic dysfunction, whether symptomatic or asymptomatic. Evidence has now extended these benefits to delaying progression of heart failure and reducing hospitalisation. Much of our understanding of the pathophysiology of heart failure stems from these studies. More recent data has clarified the limited role of digoxin, the important benefits of beta-blockade and aldosterone blockers as adjuvants to ACE inhibition, and the emerging evidence on angiotensin II antagonists. There are, in contrast to these positive findings, reliable data from Europe and North America revealing significant underperformance of primary care and hospital physicians in heart failure diagnosis and management, with evidence of underuse and underdosing of evidence-based therapies. Limited qualitative data suggest the reasons for this underperformance are complex and relate to lack of access to objective testing of ventricular function and exaggerated concerns over treatment risks and side-effects. Heart failure represents a complex cluster of aetiologies and risks that are not easy to correctly identify, even in specialist settings. Since there is now powerful evidence on how heart failure can be modified and improved, explicit guidance is needed for which suspected patients should be referred, for confirmation of diagnosis and advice on appropriate treatment regimes, and for which patients can be handled mainly within primary care but with enhanced access to objective non-invasive tests to improve diagnostic reliability and to stratify patients to evidence-based therapies. Current evidence suggests that in North America and Europe today primary care physicians do underperform in their management of patients with heart failure, often owing to factors outside of their immediate control.

Adrenergic beta-Antagonists↗
PubMed2002

Cumulative failure rate of ileal pouch-anal anastomosis and quality of life after failure.

PURPOSE: The aim of the study was to calculate the cumulative occurrence of pouch failure among 486 patients who had undergone proctocolectomy and ileoanal anastomosis for ulcerative colitis or familial adenomatous polyposis. The other goal was to compare the quality of life in the failure group of 21 patients, the successful group, and the healthy population. METHODS: Data were collected from patient histories, with the probability of pouch failure being calculated by the Kaplan-Meier method. Patients with pouch failure and controls were sent a Short-Form 36-item quality-of-life questionnaire, and data were analyzed with paired -test. RESULTS: The overall failure rate was 5.3 percent (26), including 24 pouch excisions and 2 early deaths (0.4 percent). Cumulative probabilities of pouch failure were 1, 5, and 7 percent at 1, 5, and 10 years, respectively. Neither pouchitis, gender, nor diagnosis correlated with pouch failure, but fistula formation ( p< 0.001) did. Patients with failure had lower quality-of-life scores for physical function (p < 0.02), social function ( p< 0.04), energy ( p< 0.02), and physical role function ( < 0.03) than the healthy population. Scores for physical function ( p< 0.01), energy ( p< 0.01), and physical role function ( p< 0.05) were also lower than those of control patients. CONCLUSIONS: The most common cause of pouch failure is fistula, whereas pouch excision is rarely caused by pouchitis. The impaired quality of life of patients in the failure group was caused by impairment of physical function and restrictions in social life.

Adenomatous Polyposis Coli↗
PubMed2006

Impact of the history of congestive heart failure on the utility of B-type natriuretic peptide in the emergency diagnosis of heart failure: results from the Breathing Not Properly Multinational Study.

PURPOSE: B-type natriuretic peptide is known to correlate with hemodynamic state, presence and severity of congestive heart failure, and prognosis. Although low-range B-type natriuretic peptide less than 100 pg/mL has a high negative predictive value (90%), and high-range B-type natriuretic peptide greater than 500 pg/mL has a high positive predictive value (87%), there remains some ambiguity in the interpretation of results in the medium range (100-500 pg/mL). We hypothesized that taking into account the history of congestive heart failure along with other clinical variables would be helpful in this range of B-type natriuretic peptide levels. METHOD: The Breathing Not Properly Multicenter Study was an international, 7-center, prospective study including 1475 patients with a mean age of 63 years (57% were male, and 54% were female); 35% of patients with a history of congestive heart failure were enrolled, and a final diagnosis of congestive heart failure was made in 46%. The index criteria was defined as positive if any 2 index findings (ie, history of coronary artery disease, lower extremity edema, pulmonary edema, cephalization of the pulmonary arteries, and cardiomegaly) were present. RESULTS: The interval likelihood ratios (LR) for low, medium, and high B-type natriuretic peptide ranges are 0.13, 1.85, and 8.1, respectively. For medium B-type natriuretic peptide levels a positive history of congestive heart failure makes the diagnosis of congestive heart failure more probable with a cumulative LR of 4.3. Also in this range a positive index criterion was strongly indicative of congestive heart failure even in the absence of a history of congestive heart failure (LR 3.3). Where there are both a positive history of congestive heart failure and a positive index criteria for the medium B-type natriuretic peptide group, the cumulative LR (10.2) is similar to that of a high B-type natriuretic peptide level (8.1). CONCLUSION: Even in the medium range (100-500 pg/mL), when using the history of congestive heart failure and index criteria, B-type natriuretic peptide can be a powerful diagnostic tool in the hands of clinicians in the emergency department.

Aged↗
PubMed2002

Metoprolol CR/XL in female patients with heart failure: analysis of the experience in Metoprolol Extended-Release Randomized Intervention Trial in Heart Failure (MERIT-HF).

BACKGROUND: Underrepresentation of women in heart failure clinical trials has limited conclusions regarding the effect of various management strategies on survival in women with heart failure and decreased left ventricular ejection fraction (LVEF). METHODS AND RESULTS: MERIT-HF (Metoprolol Extended-Release Randomized Intervention Trial in Heart Failure) was a randomized, placebo-controlled study, the purpose of which was to evaluate the effect of metoprolol controlled-release/extended-release (CR/XL) in 3991 patients with New York Heart Association class II to IV heart failure and LVEF < or =0.40. We performed a post hoc analysis to evaluate the effect of metoprolol CR/XL on outcome in women (n=898), including the outcome in 183 women with severe heart failure (New York Heart Association class III/IV and LVEF < 0.25). Treatment with metoprolol CR/XL in women resulted in a 21% reduction in the primary combined end point of all-cause mortality/all-cause hospitalizations (164 versus 137 patients; P=0.044). The number of cardiovascular hospitalizations was reduced by 29% (164 versus 120; P=0.013), and hospitalization for worsening heart failure was reduced by 42% (95 versus 56; P=0.021). Similar results were noted in the subgroup of women with severe heart failure, with a 57% reduction in cardiovascular hospitalizations (63 versus 30; P=0.005) and a 72% reduction in hospitalization due to worsening heart failure (46 versus 14; P=0.0004). A pooling of mortality results from MERIT-HF, the Cardiac Insufficiency Bisoprolol Study (CIBIS II), and the Carvedilol Prospective Randomized Cumulative Survival Study (COPERNICUS) showed very similar survival benefits in women and men. CONCLUSIONS: The beneficial effects of metoprolol CR/XL extend to women with heart failure, including women with clinically stable severe heart failure.

Adrenergic beta-Antagonists↗
PubMed2002

[Adaptation of guidelines for the treatment of chronic heart failure in a specialized heart failure clinic].

BACKGROUND: Chronic heart failure is associated with high mortality and morbidity. In spite of a number of trials showing significant improvement in survival and reduction in hospitalization for patients who received ACE inhibitors/AT1 receptor antagonists (ACEI/ARB), beta-blockers and spironolactone, and notwithstanding the recommendations of national and international guidelines for the management of heart failure, substantial proportions of patients are not receiving this treatment. The aim of our study was to analyse 1. the efficiency of a specialized heart failure clinic in translating guidelines into clinical practice, and 2. the effect of optimized neurohormonal therapy on patient outcome. METHODS AND RESULTS: The data of patients with systolic heart failure and an ejection fraction < or = 35% referred to the Innsbruck Heart Failure and Transplantation Program between February 2000 and October 2001 were analysed. The number of patients treated with ACEI/ARB, beta-blocker and spironolactone increased significantly in the investigation period (p < 0.05). Equivalent dose for captopril and bisoprolol per patient developed from 66.4 +/- 42.8 to 96.5 +/- 41.9 mg (p < 0.001) and from 2.0 +/- 2.9 to 6.3 +/- 4.0 mg (p < 0.001), respectively. Optimization of neurohormonal therapy was associated with a significant improvement in NYHA class (2.5 +/- 0.8 vs. 1.9 +/- 0.8; p < 0.001). No relevant changes were noticed for blood pressure, serum creatinine, serum sodium, and serum potassium, whereas heart rate dropped significantly. Kaplan-Meier curves examining the time to first event of the combined end point of mortality and hospitalisation for worsening heart failure revealed a clear benefit for patients on combined neurohormonal therapy (ACEI/ARB and beta-blocker, n = 86) when compared with patients on neurohormonal monotherapy (ACEI/ARB or beta-blocker, n = 35), (p < or = 0.001). Differences remained significant (p = 0.022) after adjusting for NYHA class at referral, age, gender, etiology of the underlying cardiomyopathy, ejection fraction, and atrial fibrillation in Cox regression analysis. CONCLUSION: Guidelines for the management of chronic heart failure patients can be translated efficiently into clinical practice by a specialized heart failure clinic. Optimization of therapy is associated with an improvement in functional status and a decrease in mortality or hospitalization for worsening heart failure. Therefore the nationwide installation of specialized heart failure clinics is required.

Adrenergic beta-Antagonists↗
PubMed1986

Renal failure in children with hepatic failure undergoing liver transplantation.

Over a 3 1/2 year period, 133 children with hepatic failure underwent orthotopic liver transplantation (OLT) at our center. Renal failure (creatinine clearance less than 20 ml/min/1.73 m2) was present in 19 (14.3%) of these children. In seven of the 19 children, renal failure was present before OLT, and in the other 12 after OLT. The causes of renal failure included hepatorenal syndrome in seven, postischemic acute tubular necrosis in five, severe prerenal azotemia in five, and cyclosporine nephrotoxicity in two. Eight other patients died of renal failure while awaiting emergency transplantation. Of the total of 31 deaths among 133 children who underwent OLT, nine occurred in the 19 patients with renal failure. Thus patients with OLT and renal failure had a significantly higher mortality than other patients with transplants (P less than 0.025). Dialysis was not associated with improved survival. The majority of deaths in patients with renal failure were related to severe hemorrhage, thromboembolic events, and systemic fungal infections. Our experience suggests that renal failure is common in children with hepatic failure and is associated with reduced patient survival after OLT.

Acute Kidney Injury↗
PubMed2005

Immunological aspects of the statins' function in patients with heart failure: a report from the Annual Conference of ESC - Heart Failure 2005.

The annual meeting of the Heart Failure Association of ESC in Lisbon, in June 2005, was exceptionally successful. There were many very interesting presentations and workshops with the unique title: Statins in heart failure- Cholesterol-lowering is not the only goal. Heart failure (HF) is a progressive disease with coronary artery disease (CAD) as the most often underlying etiology. Treatment to prevent progression of heart failure has been targeted to reverse the consequences of HF and to a less extent the cause - the atherosclerotic plaque itself. On the average 50% of patients with heart failure are treated with lipid intervention. Lipid-lowering treatment with statins clearly reduces morbidity and mortality of patients with documented CAD. Since the prevalent etiology of heart failure is CAD, its prevention may reduce heart failure progression. However, recent studies suggest that pleiotropic effects of statins are more important than the influence related to their cholesterol lowering mechanism. Furthermore it is suggested that low levels of circulating lipoproteins and cholesterol may be independent predictors of impaired outcome in patients with heart failure. There are some possible explanations for this finding. High levels of cholesterol can be beneficial to heart failure patients; cholesterol-rich serum lipoproteins are able to modulate inflammatory immune function because they bind and detoxify bacterial lipopolysaccharide, a very strong stimulator of the release of proinflammatory cytokines that promote heart failure progression and death. So current recommendations strongly emphasize that the aim of treatment of HF is not to lower cholesterol.

Disease Progression↗
PubMed1986

Renal failure and dialysis therapy in children with hepatic failure in the perioperative period of orthotopic liver transplantation.

Severe renal failure (GFR less than or equal to 20 ml/min/1.73 m2) complicated the clinical course in 27 of 146 children (18.5%) admitted for orthotopic liver transplantation (OLT). Hepatorenal syndrome (HRS) was the cause of renal failure in 12 of 15 patients in whom renal failure preceded OLT while acute tubular necrosis, pre-renal factors and cyclosporine nephrotoxicity were the major causes of renal failure post-OLT. Eight patients died from hemorrhage, infection or other complications of hepatic failure before OLT could be performed. Survival in the remaining 19 patients undergoing OLT was significantly lower compared to 114 patients with OLT and no renal failure (53% vs 81%, p less than 0.025). Dialysis therapy in 13 of the 27 patients with renal failure (10 hemodialysis and 3 peritoneal dialysis) was frequently complicated by severe gastrointestinal hemorrhage and hypotension, and directly contributed to the death of two patients prior to OLT. Among the 19 patients with renal failure who were actually transplanted, the survival rate was similar whether dialysis was used or not (5/10 vs 5/9) even though the mean GFR was significantly lower in dialyzed patients (p less than 0.05). However, although small patient numbers precluded meaningful statistical analysis, dialysis appeared to be beneficial for the subgroup of 12 patients with HRS, 4 of whom had complete recovery of renal function after successful OLT. We conclude that, renal failure is common in children with advanced liver failure; dialysis in such patients may increase morbidity and does not improve overall mortality; and dialysis support may improve survival in the subgroup of patients with HRS.

Acute Kidney Injury↗
PubMed2000

Low protein diets delay end-stage renal disease in non diabetic adults with chronic renal failure.

BACKGROUND: Since more than fifty years, low protein diets are proposed to patients with kidney failure. However, the effects of these diets in preventing severe renal failure and the need for maintenance dialysis is still controversial. OBJECTIVES: To determine the efficacy of low protein diets in delaying the need to start maintenance dialysis. SEARCH STRATEGY: Medline and Embase search from January 1966 through June 1999. Congress abstracts (American Society of Nephrology since 1990, European Dialysis Transplant Association since1985, International Society of Nephrology since 1987). Direct contacts with investigators. SELECTION CRITERIA: Randomised trials comparing two different levels of protein intake in adult patients suffering from moderate to severe renal failure, followed for at least one year. Exclusion of patients with diabetic nephropathy. DATA COLLECTION AND ANALYSIS: Seven trials selected over 40 studies since 1975. A total of 1494 patients analysed, 753 receiving a reduced protein intake and 741 a larger protein intake. Collection of the number of "renal death" being the need for starting dialysis, the death of a patient or the transplantation of a kidney during the trials. MAIN RESULTS: 242 renal deaths were recorded, 101 in the low protein diet and 141 in the larger protein diet group, giving an odds ratio of low protein to control of 0.62 with a 95% confidence interval of 0.46 to 0.83 (p<0.001, Peto odds ratio). To spare one extra renal death, 17 patients need to be treated (NNT) with a low protein diet for approximately two years. REVIEWER'S CONCLUSIONS: Reducing protein intake in patients with chronic renal failure do reduce the occurence of renal death by about 40% as compared with larger or unrestricted protein intake and therefore should be warmly recommended to patients. The optimal level of protein intake cannot be deduced from the present work. However, based on other nutritional studies perfomed in patients having chronic renal failure, we recommend a protein intake of 0.6 g/kg/day and an energy intake no less than 35 kcal/kg/day. Skilled dietitian survey should be offered to closely monitor these values and the patient's nutritional status.

Adult↗
PubMedDate not supplied

Management of heart failure. IV. Anticoagulation for patients with heart failure due to left ventricular systolic dysfunction.

OBJECTIVE: This article reviews the incidence of arterial thromboembolism in patients with heart failure who are not receiving anticoagulants. We also examine whether more severe ventricular dysfunction increases this incidence and the efficacy and risks of anticoagulation for patients in sinus rhythm. DATA SOURCES: English-language studies referenced in MEDLINE or EMBASE (January 1966 to September 1993) were reviewed. We used the search terms heart failure, congestive; congestive heart failure; heart failure; cardiac failure; and dilated cardiomyopathy in conjunction with the terms anticoagulation, cerebrovascular disorders, stroke, and thromboembolism. STUDY SELECTION: All studies with separate data for patients with chronic heart failure not receiving anticoagulants were included. Articles addressing valvular heart disease or heart failure secondary to acute myocardial infarction or Chagas' disease were excluded. Studies of the occurrence of left ventricular mural thrombi were also reviewed. DATA EXTRACTION AND SYNTHESIS: Inclusion and exclusion criteria, prevalence of atrial fibrillation, mean follow-up, and the occurrence of arterial thromboembolic events were extracted. If the incidence was not given, this was estimated using the proportion of patients with events divided by the mean follow-up. CONCLUSION: The incidence of arterial thromboembolism ranged from 0.9 to 5.5 events per 100 patient-years, with the largest studies reporting incidence of 2.0% and 2.4%. Findings regarding the relationship between ventricular function and thromboembolic events are contradictory. No controlled trial has assessed the efficacy or risks of anticoagulation for patients with heart failure and sinus rhythm, and reported efficacy in case series ranged from 0% to 100%. Until adequate studies are performed, anticoagulation should be discouraged for patients with heart failure who are in sinus rhythm.

Anticoagulants↗