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.