Targeting Sodium in Heart Failure.

A dominant event determining the course of heart failure (HF) includes the disruption of the delicate sodium (Na⁺) and water balance leading to (Na⁺) and water retention and edema formation. Although incomplete decongestion adversely affects outcomes, it is unknown whether interventions directly targeting (Na⁺), such as strict dietary (Na⁺) restriction, intravenous hypertonic saline, and diuretics, reverse this effect. As a result, it is imperative to implement (Na⁺)-targeting interventions in selected HF patients with established congestion on top of quadruple therapy with angiotensin receptor neprilysin inhibitor, β-adrenergic receptor blocker, mineralocorticoid receptor antagonist, and sodium glucose cotransporter 2 inhibitor, which dramatically improves outcomes. The limited effectiveness of (Na⁺)-targeting treatments may be partly due to the fact that the current metrics of HF severity have a limited capacity of foreseeing and averting episodes of congestion and guiding (Na⁺)-targeting treatments, which often leads to dysnatremias, adversely affecting outcomes. Recent evidence suggests that spot urinary sodium measurements may be used as a guide to monitor (Na⁺)-targeting interventions both in chronic and acute HF. Further, the classical (2)-compartment model of (Na⁺) storage has been displaced by the (3)-compartment model emphasizing the non-osmotic accumulation of (Na⁺), chiefly in the skin. 23(Na⁺) magnetic resonance imaging (MRI) enables the accurate and reliable quantification of tissue (Na⁺). Another promising approach enabling tissue (Na⁺) monitoring is based on wearable devices employing ion-selective electrodes for electrolyte detection, including (Na⁺) and (Cl^-). Undoubtably, further studies using 23(Na⁺)-MRI technology and wearable sensors are required to learn more about the clinical significance of tissue (Na⁺) storage and (Na⁺)-related mechanisms of morbidity and mortality in HF.