1,720,966 research outputs found

    Loop Diuretics Strategies in Acute Heart Failure: From Clinical Trials to Practical Application

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    Although loop diuretics are the most commonly used drugs for the treatment of acute heart failure (AHF), their short and long-term effects are relatively unknown. The use of loop diuretics is essential in the management of HF, particularly during episodes of acute decompensation, therefore more than 90% of patients admitted with HF receive this drug. The administration of intravenous loop diuretics to patients with heart failure and congestion typically results in the improvement of dyspnea, pulmonary congestion and in the reduction of Left Ventricular (LV) filling pressures. However, little is known about its appropriate dose, timing and modality administration in patients with AHF: several side effects may result from the administration of high diuretics dose, including worsening kidney function, diuretic resistance and sympathetic overdrive. Furthermore, there is no specific strategy that shows a clear benefit in HF outcome in relation to continuous versus intermittent administration modalities. Current data based on small and heterogeneous studies did not demonstrate a clear risk benefit ratio and larger prospective trials need to be completed in order to be able to provide definitive recommendations in the future. Since every patient represents a single entity and may have different responses to the same treatment, the best clinical approach should take into account physical examination, neuro-hormonal overdrive and kidney functional status. Due to these reasons, treatment with loop diuretics should be specifically customized for each patient, until multicenter blinded trials will provide satisfactory answers regarding optimal dosing, modality administration and precise targets

    Different diuretic dose and response in acute decompensated heart failure: Clinical characteristics and prognostic significance

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    Background The question regarding the correct balance between optimal loop diuretic dose administration and best modality is under debate as well as the exact relation existing between congestion and renal dysfunction. We sought to evaluate the effects of different diuretic modalities (low [LD] versus high dose [HD]) and dose administration on decongestion, Worsening renal function (WRF) and outcome. Methods We retrospectively analyzed data of DIUR-HF study matching for LD vs HD (cut off 125 mg/day), and diuretic efficiency (DE) (weight loss/40 mg daily of furosemide). We also evaluated WRF rate (creatinine increase during hospitalization ≥ 0.3 mg/dl or estimated glomerular filtration rate (eGFR) reduction ≥ 25%) together with decongestion. Results HD patients (n.55) were older, more frequently affected by diabetes and chronic kidney disease (CKD) and demonstrated higher rate of inhospital WRF (65% vs 29% p = 0.001) and 180-days adverse events (70% vs 23% p < 0.001) respect to LD patients (n.41). Patients with low DE showed a higher 180 days adverse events rate than higher DE patients (p = 0.02). Univariate and multivariable analysis suggests a significant relationship between adverse events and low DE (patients with DE under median value) (U-HR = 2.59 [1.44–4.64]; p = 0.001. M-HR = 3.16 [1.55–6.46]; p = 0.002); continuous administration (HR = 3.12 [1.65–5.91]; p < 0.001) and WRF (HR = 5.30 [2.79–10.09]; p < 0.001) were also related with adverse events. Conclusions HD and poor DE are two conditions associated with adverse outcome. Both situations are the consequence of previous detrimental clinical status and they appear strictly related to WRF occurrence

    The prognostic combined role of B-type natriuretic peptide, blood urea nitrogen and congestion signs persistence in patients with acute heart failure

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    AIMS: B-type natriuretic peptide (BNP) decrease during hospitalization has been related to reduced risk of readmission and death in patients with acute heart failure (AHF). Conversely, the exact role of blood urea nitrogen (BUN) is still debated. Currently, no data have been published regarding the relation between these two biomarkers and the relation between them and clinical signs of congestion. METHODS: We consecutively studied 107 patients with diagnosis of AHF and systolic dysfunction. All patients were observed during a 6-month follow-up period. BUN and BNP were measured according to the decrease of BNP levels at discharge of greater than 30% with respect to basal values; the persistence of congestion signs at discharge and BUN increase at discharge to more than 20% with respect to baseline. RESULTS: In all patients mean BNP was 1014?±?767?pg/ml; in patients with severe systolic dysfunction BNP was higher (1382?±?1025 vs. 848?±?549; P?=?0.002). Mean BUN in all patients was 93?±?42?mg/dl; BUN was higher in patients affected by chronic kidney disease compared with patients with preserved renal function (114?±?45 vs. 68?±?21?mg/dl; P?<?0.001). Cox regression analysis demonstrated that BNP decrease of at least 30% together with congestion signs resolution was related to outcome improvement (univariate hazard ratio: 0.45 [0.19–0.97], P?=?0.05; multivariate hazard ratio: 0.44 [0.20–0.98], P?=?0.05). BUN increase of greater than 20% at discharge was associated with poor outcome independent of persistence of congestion signs (univariate hazard ratio: 2.72 [1.03–7.28], P?=?0.04; multivariate hazard ratio: 3.00 [1.12–8.06], P?=?0.03). Changes (Δ) of both BNP (univariate hazard ratio: 1.30 [1.04–1.61], P?=?0.01) and BUN (univariate hazard ratio: 5.24 [1.72–15.95], P?=?0.003) were associated with mortality, independently of congestion. CONCLUSIONS: In patients with AHF, BNP reduction of greater than 30% during hospitalization is associated with outcome improvement only if it occurs together with congestion resolution. Conversely, BUN increase of more than 20% was associated with poor outcome, independently of the persistence of congestion signs

    Chronic kidney disease and worsening renal function in acute heart failure: different phenotypes with similar prognostic impact?

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    Nearly a third of patients with acute heart failure experience concomitant renal dysfunction. This condition is often associated with increased costs of care, length of hospitalisation and high mortality. Although the clinical impact of chronic kidney disease (CKD) has been well established, the exact clinical significance of worsening renal function (WRF) during the acute and post-hospitalisation phases is not completely understood. Therefore, it is still unclear which of the common laboratory markers are able to identify WRF at an early stage. Recent studies comparing CKD with WRF showed contradictory results; this could depend on a different WRF definition, clinical characteristics, haemodynamic disorders and the presence of prior renal dysfunction in the population enrolled. The current definition of acute cardiorenal syndrome focuses on both the heart and kidney but it lacks precise laboratory marker cut-offs and a specific diagnostic approach. WRF and CKD could represent different pathophysiological mechanisms in the setting of acute heart failure; the traditional view includes reduced cardiac output with systemic and renal vasoconstriction. Nevertheless, it has become a mixed model that encompasses both forward and backward haemodynamic dysfunction. Increased central venous pressure, renal congestion with tubular obliteration, tubulo-glomerular feedback and increased abdominal pressure are all potential additional contributors. The impact of WRF on patients who experience preserved renal function and individuals affected with CKD is currently unknown. Therefore it is extremely important to understand the origins, the clinical significance and the prognostic impact of WRF on CKD

    Diagnostic utility of contemporary echo and BNP assessment in patients with acute heart failure during early hospitalization

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    Background The use of B-type natriuretic peptide (BNP) and echocardiography in acute heart failure (AHF) diagnosis is poorly employed in the Emergency Department. The aim of the present study is to evaluate relation among BNP levels systolic and diastolic dysfunction during early phases of AHF hospitalization. Methods We performed contemporary echocardiographic and BNP assessment in 310 patients with AHF within 12 h since hospital admission. We studied the correlation among BNP and degree of diastolic dysfunction evaluated by pulsed Doppler transmitral flow and Tissue Doppler flow. Finally we investigated the relation among BNP and the right systolic longitudinal ventricular function (TAPSE) and the systolic pulmonary arterial pressure (PAPs). Results BNP levels were 1417 ± 1126, 1081 ± 955, 894 ± 901 pg/mL, for patients with EF ≤ 25%, EF 25-40% and EF 40-50% (p = 0.005), respectively. BNP levels linearly correlate with the degree of diastolic dysfunction: 582 ± 406 pg/mL in altered relaxation pattern, 712 ± 557 pg/mL in pseudonormal pattern and 1694 ± 805 in restrictive filling pattern (p < 0.001 for all patterns). BNP levels were significantly increased in patients with right systolic ventricular dysfunction (TAPSE < 18 mm; p = 0.006) and in patients with PAPs ≥ 40 mmHg (p = 0.001). ROC curve and logistic regression analysis highlighted the power of BNP to detect severe systolic dysfunction, right ventricular (RV) overload and dysfunction and diastolic dysfunction patterns. Conclusions BNP levels correlate linearly with LV systolic dysfunction as well as with impaired degree of diastolic dysfunction. Significant PAP increase is a further factor influencing BNP elevation in patients with AHF during early hospitalization phase

    Pulmonary hypertension: a correct diagnosis for a suitable therapy in scleroderma patients

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    Systemic sclerosis (SSc) is a heterogeneous disorder characterised by dysfunction of the endothelium and dysregulation of fibroblasts, resulting in excessive production of collagen, and abnormalities of the immune system. Progressive fibrosis of the skin and internal organs is a pathologic hallmark of the disease, resulting in major organ damage and failure. Pulmonary hypertension (PH) is frequent in patients with SSc and, pulmonary arterial hypertension (PAH) represents one of the main causes of death. PH is not a specific disease, but a haemodynamic condition characterized by a mean pulmonary pressure ≥25mmHg. In SSc, because of the great variability in clinical manifestation, it is possible to identify pulmonary hypertension due to left heart disease, PH due to respiratory disease or pulmonary arterial hypertension. The knowledge of PH and the right diagnosis are crucial to assess the most appropriate therapeutic strategy. In this article, the new classification criteria of PH have been examined taking into account the SSc clinical evolution and focusing on the different underlying pathogenetic mechanisms

    Prognostic significance of hyperuricemia in patients with acute heart failure

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    Serum uric acid (UA) is associated with death and hospitalization in chronic heart failure (HF). However, UA in acute HF has not been well studied with respect to its relation to renal dysfunction and vascular congestion. We measured admission serum UA along with baseline variables in 281 patients with acute HF screened from the Loop Diuretics Administration and Acute Heart Failure (Diur-HF) trial. Hyperuricemia was defined as serum UA &gt;7 mg/dl in men and &gt;6 mg/dl in women. Chronic kidney disease (CKD) was defined as an estimated glomerular filtration rate &lt;60 ml/min/1.73 m2 before hospital admission. Death or HF hospitalization at 6 months was the primary outcome. The mean UA concentration was 6.4 ± 2.5 mg/dl, and 121 patients (43.1%) were classified as hyperuricemic. UA values were significantly increased in patients with CKD compared to patients without CKD (6.8 ± 2.7 vs 6.1 ± 2.1 mg/dl; p = 0.02); however, UA was not associated with the development of acute kidney injury. Patients with hyperuricemia had greater degrees of pulmonary and systemic congestion than normouricemic patients (congestion score 3.5 vs 2.1, p &lt;0.01). Hyperuricemia was associated with higher risk of death or HF rehospitalization (univariate hazard ratio 1.46 [1.02 to 2.10]; p = 0.04, multivariate hazard ratio 1.69 [1.16 to 2.45]; p = 0.005). In conclusion, hospitalized patients with acute HF, elevated UA levels were associated with both CKD and pulmonary congestion. After controlling for potential confounders, hyperuricemia was associated with rehospitalization and death at 6 months

    Comparison of neutrophil gelatinase-associated lipocalin versus B-type natriuretic peptide and cystatin C to predict early acute kidney injury and outcome in patients with acute heart failure

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    Neutrophil gelatinase-associated lipocalin (NGAL) has been described in chronic heart failure (HF) as marker of tubular damage and renal dysfunction; however, less data are available in patients with acute HF. Because of high rate of acute kidney injury (AKI) development, we aimed to investigate the role of NGAL in predicting early AKI development; second, we compared NGAL with respect to cystatin C, B-type natriuretic peptide (BNP), renal function, and blood urea nitrogen (BUN) for outcome prediction. We measured admission serum NGAL, cystatin C, and BNP in 231 patients affected to acute HF; all patients were submitted to daily creatinine, estimated glomerular filtration rate, and measurement to identify inhospital AKI defined by Risk, Injury, Failure, Loss, End-Stage Kidney Disease and Acute Kidney Injury Network criteria. We also measured admission and discharge estimated glomerular filtration rate, creatinine, and BUN to evaluate their prognostic role during a 6-month follow-up period; 78 patients developed AKI during hospitalization. In these subjects, NGAL levels were significantly increased respect to patients without AKI (295 ± 228 vs 129 ± 108 ng/ml, p <0.001). A cutoff of 134 ng/ml has been related to AKI with good sensibility and specificity (85% and 80%, respectively; area under the curve 0.81, p <0.001). BNP was also mildly increased (1,000 ± 906 vs 746 ± 580 pg/ml, p = 0.03) but not cystatin C. Patients with chronic kidney disease demonstrated higher NGAL levels compared with subjects with preserved renal function (258 ± 249 and 120 ± 77 ng/ml, p <0.001). The receiver-operating characteristic curve analysis demonstrated that increased NGAL values were associated with increased mortality (cutoff 170 ng/ml, sensibility 60%, specificity 82%, accuracy 71%, area under the curve 0.77, p <0.001). The same significant correlation was also found for BUN at discharge (cutoff 100 mg/dl, sensibility 65%, specificity 85%, accuracy 71%, area under the curve 0.77, p <0.001). Multivariable Cox regression analysis showed that cutoff 170 ng/ml was related with adverse outcome (hazard ratio 1.77, confidence interval 1.24 to 2.83, p = 0.01). In conclusion, NGAL measurement is a sensible tool to predict AKI during hospitalization. Elevated NGAL levels appear to be related to BUN increase and post-discharge outcome. This suggests a prognostic role of tubular damage beyond renal dysfunction
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