Sodium Intake and Heart Failure

Abstract

Sodium is an essential mineral and nutrient used in dietary practices across the world and is important to maintain proper blood volume and blood pressure. A high sodium diet is associated with increased expression of β-myosin heavy chain, decreased expression of α/β-myosin heavy chain, increased myocyte enhancer factor 2/nuclear factor of activated T cell transcriptional activity, and increased salt-inducible kinase 1 expression, which leads to alteration in myocardial mechanical performance. A high sodium diet is also associated with alterations in various proteins responsible for calcium homeostasis and myocardial contractility. Excessive sodium intake is associated with the development of a variety of comorbidities including hypertension, chronic kidney disease, stroke, and cardiovascular diseases. While the American College of Cardiology/American Heart Association/Heart Failure Society of America guidelines recommend limiting sodium intake to both prevent and manage heart failure, the evidence behind such recommendations is unclear. Our review article highlights evidence and underlying mechanisms favoring and contradicting limiting sodium intake in heart failure.

Keywords: ambulatory heart failure; epidemiological studies; heart failure; salt; sodium.

Figure 1

Potential mechanisms linking dietary sodium restriction to better heart failure outcomes DBP—diastolic blood pressure, PCWP—pulmonary capillary wedge pressure, SBP—systolic blood pressure. Abbreviations: DBP, diastolic blood pressure; SBP, systolic blood pressure; PCWP, pulmonary capillary wedge pressure.

Figure 2

Potential mechanisms whereby dietary sodium restriction may worsen heart failure. Abbreviations: Na, sodium; RAAS, renin–angiotensin–aldosterone system.