Iron deficiency defined as depleted iron stores accompanied by unmet cellular iron requirements identifies patients at the highest risk of death after an episode of acute heart failure.

AIM: Acute heart failure (AHF) critically deranges haemodynamic and metabolic homoeostasis. Iron is a key micronutrient for homoeostasis maintenance. We hypothesized that iron deficiency (ID) defined as depleted iron stores accompanied by unmet cellular iron requirements would in this setting predict the poor outcome. METHODS AND RESULTS: Among 165 AHF patients (age 65 ± 12 years, 81% men, 31% de novo HF), for ID diagnosis we prospectively applied: low serum hepcidin reflecting depleted iron stores (<14.5 ng/mL, the 5th percentile in healthy peers), and high-serum soluble transferrin receptor (sTfR) reflecting unmet cellular iron requirements (≥1.59 mg/L, the 95th percentile in healthy peers). Concomitance of low hepcidin and high sTfR (the most profound ID) was found in 37%, isolated either high sTfR or low hepcidin was found in 29 and 9% of patients, and 25% of subjects demonstrated preserved iron status. Patients with low hepcidin and high sTfR had peripheral oedema, high NT-proBNP, high uric acid, low haemoglobin (P < 0.05), and 5% in-hospital mortality (0% in remaining patients). During the 12-month follow-up, 33 (20%) patients died. Those with low hepcidin and high sTfR had the highest 12-month mortality [(41% (95% CI: 29-53%)] when compared with those with isolated high sTfR [15% (5-25%)], isolated low hepcidin [7% (0-19%)] and preserved iron status (0%) (P < 0.001). Analogous mortality patterns were seen separately in anaemics and non-anaemics. CONCLUSION: Iron deficiency defined as depleted body iron stores and unmet cellular iron requirements is common in AHF, and identifies those with the poor outcome. Its correction may be an attractive therapeutic approach.

Liver function tests in patients with acute heart failure.

INTRODUCTION: Acute heart failure (AHF) is associated with multiorgan dysfunction, which may unfavorably affect prognosis. OBJECTIVES: We investigated the prevalence, clinical determinants, and prognostic consequences of abnormal liver function tests (LFTs) in population with AHF. PATIENTS AND METHODS: We conducted a retrospective analysis of patients with AHF, in whom the following LFTs were performed on admission: serum bilirubin, aspartate transaminase (AST), alanine transaminase (ALT), and albumin. Abnormal LFTs were defined as the elevation above the upper normal limit of bilirubin, AST, and ALT, or reduction below the lower normal limit of albumin. RESULTS: The study involved 189 patients (age, 68 ±11 years; men, 68%; de novo AHF, 25%). On admission, abnormal LFTs were observed in 46% of the patients for AST, 31% for ALT, 33% for bilirubin, and 44% for albumin. Only 29% of the patients had all LFTs within the normal ranges. The following variables were independently related to abnormal LFTs: high hemoglobin and N­terminal pro­B­type natriuretic peptide (NT­proBNP) levels for AST; high hemoglobin, bilirubin, and NT­proBNP levels for ALT; high hemoglobin, low sodium levels, and dilated right ventricle for bilirubin; and high NT­proBNP levels for albumin (all P <0.05). In 21 patients, hemodynamic monitoring was performed, which revealed that among LFTs only elevated bilirubin independently correlated with higher right atrial pressure (P <0.005). In a univariate Cox model, among LFTs, low albumin and markedly elevated AST and ALT (>3 times above the upper normal limit) were associated with increased mortality during 180­day follow­up. CONCLUSIONS: Abnormal LFTs are common in patients with AHF and may have prognostic relevance. Among them, only elevated bilirubin was correlated with impaired hemodynamic parameters.