Background-Worsening renal function (WRF), traditionally defined as an increase in serum creatinine levels Ն0.3 mg/dL, is a frequent finding in patients with acute heart failure (AHF) and has been associated with poorer outcomes in some but not all studies. We hypothesized that these discrepancies may be caused by the interaction between WRF and congestion in AHF patients. Methods and Results-We measured serum creatinine levels on a daily basis during the hospitalization and assessed the persistence of signs of congestion at discharge in 599 consecutive patients admitted at our institute for AHF. They had a postdischarge mortality and mortality or AHF readmission rates of 13% and 43%, respectively, after 1 year. Patients were subdivided into 4 groups according to the development or not of WRF and the persistence of Ն1 sign of congestion at discharge. Patients with WRF and no congestion had similar outcomes compared with those with no WRF and no congestion, whereas the risk of death or of death or AHF readmission was increased in the patients with persistent congestion alone and in those with both WRF and congestion (hazard ratio, 5.35; 95% confidence interval, 3.0 -9.55 at univariable analysis; hazard ratio, 2.44; 95% confidence interval, 1.24 -4.18 at multivariable analysis for mortality; hazard ratio, 2.14; 95% confidence interval, 1.39 -3.3 at univariable analysis; and hazard ratio, 1.39; 95% confidence interval, 0.88 -2.2 at multivariable analysis for mortality and rehospitalizations). Conclusions-WRF alone, when detected using serial serum creatinine measurements, is not an independent determinant of outcomes in patients with AHF. It has an additive prognostic value when it occurs in patients with persistent signs of congestion. (Circ Heart Fail. 2012;5:54-62.)

The prevalence of heart failure (HF) increases with age. While clinical trials suggest that contemporary evidence-based HF therapies have reduced morbidity and mortality, these trials largely excluded the elderly. Questions remain regarding the clinical characteristics of elderly HF patients and the impact of contemporary therapies on their outcomes. This review presents the epidemiology of HF in the elderly and summarizes the data on the pathophysiology of the ageing heart. The clinical characteristics, treatment patterns, and outcomes of elderly HF patients are explored. Finally, the main gaps regarding HF therapies in the elderly and the opportunities for future trials are highlighted.Heart failure † Heart failure with preserved ejection fraction † Elderly † Outcomes † Therapy Heart failure (HF) is a major and growing public health problem worldwide, with high morbidity, mortality, and cost. 1 Despite recent improvements in the outcomes of patients with chronic HF through contemporary therapies, 2 concerns exist as to whether the subjects included in major HF clinical trials were representative of real-world patients. In particular, the elderly are under-represented in clinical trials and may be at an increased risk for worse outcomes.A consensus definition of elderly does not exist. Traditionally, 65 years have been considered the conventional threshold for older age, since this age cut-off has historically represented a common age for retirement in many cultures. 3 However, increased life expectancy may make this age cut-off inappropriately low. Recent HF studies classified 'elderly' patients heterogeneously, as those older than 70 4 to 80 years, 5 -7 while patients older than 85 years were often classified as 'very elderly'. 8 This latter cut-off has been proposed as potentially a more appropriate threshold for old age. 3 Regardless of the specific definition for elderly, it is clear that HF is primarily a condition of the older population in developed countries. Elderly HF patients demonstrate distinctive pathophysiological features, complex co-morbidity profiles, and unique issues of medication tolerance. Our understanding of proper patient management of the elderly is limited by their frequent referral to general practitioners (GPs) or geriatricians rather than cardiologists, as well as by their under-representation in major HF trials. In this review, we summarize the current data on HF in the elderly, focusing on the pathophysiology of the ageing heart, and the clinical characteristics and outcomes. The differential response to HF therapies in the elderly and the opportunities for future investigation are also highlighted.

In patients hospitalised for ADHF, the addition of the discharge NT-proBNP values as well as the change in NT-proBNP to known risk markers, generates a relatively simple yet robust discharge risk score that importantly improves the prediction of adverse events.

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Aims Previous heart failure (HF) trials suggested that age influences patient characteristics and outcome; however, under‐representation of elderly patients has limited characterization of this cohort. Whether standard prognostic variables have differential utility in various age groups is unclear. Methods and results The PROTECT trial investigated 2033 patients (median age 72 years) with acute HF randomized to rolofylline or placebo. Patients were divided into five groups based on the quintiles of age: ≤59, 60–68, 69–74, 75–79, and ≥80 years. Baseline characteristics, medications, and outcomes (30‐day death or cardiovascular/renal hospitalization, and death at 30 and 180 days) were explored. The prognostic utility of baseline characteristics for outcomes was investigated in the different groups and in those aged <80 years vs. ≥80 years. With increasing age, patients were more likely to be women with hypertension, AF, and higher EF. Increased age was associated with increased risk of 30‐ and 180‐day outcomes, which persisted after multivariable adjustment (hazard ratio for 180‐day death = 1.17; 95% confidence interval 1.11–1.24 for each 5‐year increase). The prognostic utility of baseline characteristics such as previous HF hospitalization and serum sodium, systolic blood pressure, and NYHA class was attenuated in the elderly for the endpoint of 180‐day mortality. An increase in albumin was associated with a greater reduction in risk in patients aged ≥80 years vs. <80 years. Conclusions In a large trial of acute HF, there were differences in baseline characteristics and outcomes amongst patients of different ages. Standard prognostic variables exhibit different utility in elderly patients.

Amino acids (AAs) availability is reduced in patients with heart failure (HF) leading to abnormalities in cardiac and skeletal muscle metabolism, and eventually to a reduction in functional capacity and quality of life. In this study, we investigate the effects of oral supplementation with essential and semi-essential AAs for three months in patients with stable chronic HF. The primary endpoints were the effects of AA’s supplementation on exercise tolerance (evaluated by cardiopulmonary stress test and six minutes walking test (6MWT)), whether the secondary endpoints were change in quality of life (evaluated by Minnesota Living with Heart Failure Questionnaire—MLHFQ) and N-terminal pro-brain natriuretic peptide (NT-proBNP) levels. We enrolled 13 patients with chronic stable HF on optimal therapy, symptomatic in New York Heart Association (NYHA) class II/III, with an ejection fraction (EF) <45%. The mean age was 59 ± 14 years, and 11 (84.6%) patients were male. After three months, peak VO2 (baseline 14.8 ± 3.9 mL/minute/kg vs follow-up 16.8 ± 5.1 mL/minute/kg; P = 0.008) and VO2 at anaerobic threshold improved significantly (baseline 9.0 ± 3.8 mL/minute/kg vs follow-up 12.4 ± 3.9 mL/minute/kg; P = 0.002), as the 6MWT distance (baseline 439.1 ± 64.3 m vs follow-up 474.2 ± 89.0 m; P = 0.006). However, the quality of life did not change significantly (baseline 21 ± 14 vs follow-up 25 ± 13; P = 0.321). A non-significant trend in the reduction of NT-proBNP levels was observed (baseline 1502 ± 1900 ng/L vs follow-up 1040 ± 1345 ng/L; P = 0.052). AAs treatment resulted safe and was well tolerated by all patients. In our study, AAs supplementation in patients with chronic HF improved exercise tolerance but did not change quality of life.

Renal dysfunction is often present and/or worsens in patients with heart failure and this is associated with increased costs of care, complications and mortality. The cardiorenal syndrome can be defined as the presence or development of renal dysfunction in patients with heart failure. Its mechanisms are likely related to low cardiac output, increased venous congestion and renal venous pressure, neurohormonal and inflammatory activation and local changes, such as adenosine release. Many drugs, including loop diuretics, may contribute to worsening renal function through the activation of some of these mechanisms. Renal damage is conventionally defined by the increase in creatinine and blood urea nitrogen blood levels. However, these changes may be not related with renal injury or prognosis. New biomarkers of renal injury seem promising but still need to be validated. Thus, despite the epidemiological evidence, we are still lacking of satisfactory tools to assess renal injury and function and its prognostic significance.