Hyponatraemia in heart failure: time for new solutions?

Hyponatraemia is very common in heart failure (HF), especially in decompensated patients. It is associated with increased mortality and morbidity and considered a marker of advanced disease. Recognition of hyponatraemia and its causes may help guide treatment strategy. Historically, therapy has primarily focused on water restriction, decongestion with loop diuretics in case of volume overload (dilutional hyponatraemia) and sodium repletion in case of depletion. In this review, we summarise the potential benefits of established and emerging HF therapies on sodium homeostasis, with a focus on dual vasopressin antagonists, angiotensin receptor-neprilysin inhibitors, sodium-glucose cotransporter 2 inhibitors and hypertonic saline, and propose a potential therapeutic approach for hyponatraemia in HF.

Should ß-blockers be used in patients with heart failure and atrial fibrillation?

PURPOSE: There is overwhelming evidence that ß-blockers reduce cardiovascular hospitalizations and mortality in patients with heart failure and a reduced left ventricular ejection fraction provide they are in sinus rhythm. However, a recent meta-analysis of individual patient data provides compelling evidence that ß-blockers are not effective in patients with heart failure and atrial fibrillation, although neither did they increase risk. The purpose of this article is to review the evidence, seek possible explanations for this observation, and make recommendations based on the limited evidence available. METHODS: Review and critical analysis of recent publications and meta-analyses on the use of ß-blockers and other heart rate-slowing medicines in heart failure. FINDINGS: The reasons for the lack of effect of ß-blockers in patients with heart failure are uncertain. There is a substantial body of evidence to suggest that patients with heart failure and atrial fibrillation who have less stringent ventricular rate control have a better outcome. The most plausible explanation for these findings, in our view, is that ß-blockers exert similar benefits through similar mechanisms regardless of intrinsic heart rhythm but that the benefits of ß-blockers are neutralized in patients with atrial fibrillation due to the induction of pauses that may impair cardiac function leading to worsening heart failure or cause arrhythmias resulting in death. IMPLICATIONS: Smaller doses of ß-blockers and other rate lowering agents to achieve a resting clinic heart rate in the range of 75-89beats/min might improve outcome. Preventing pauses by pacing or pulmonary vein ablation of atrial fibrillation are strategies that should be researched.