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

1. Salt and Sodium

Salt is an ionic compound made up of cation and anion. Edible salt consists of 40% sodium and 60% chloride by weight. Salt was historically used as a preservative since bacteria cannot flourish in the presence of high salt concentrations. Human cells require approximately 0.5 g/day of sodium to maintain vital functions. Most food preservatives have high sodium content and are major causes of increased dietary intake of sodium. The average sodium intake in most Americans is 3.4 g/day or 1.5 teaspoons of salt, which is greater than the physiological requirement for the human body. High sodium or salt intake can lead to chronic comorbidities including hypertension, heart failure (HF), chronic kidney disease, stroke, cardiovascular diseases, and increase mortality. Hence, current guidelines recommend restricting sodium consumption to 2–3 g/day [1].

HF ,(Heart failure) is a major burden of morbidity and mortality on the health care system and is classified into two major groups, heart failure with reduced ejection fraction (HFrEF)

and heart failure with preserved ejection fraction (HFpEF). Treatment of HFrEF involves both pharmacologic and non-pharmacologic strategies, 

while mainly heart rate and blood pressure control strategies are used in HFpEF since multiple clinical trials have not shown significant benefits of pharmacologic therapy [2].

 Sodium restriction has historically been taught in textbooks as a cornerstone of the management of HF patients. 

However, data on this management strategy are controversial. In addition, the adherence to following a low sodium diet is challenging, especially after a recent hospitalisation as shown by Riegel et al. [3]. 

Before we vigorously start educating HF patients to limit sodium intake in their diet, we need to understand the evidence 

behind such recommendations. In this paper, we review evidence relating sodium to HF, pathophysiological mechanisms of increased sodium intake, and the relation of sodium intake to HF outcomes.

Ref

. 2020 Dec 13;21(24):9474. doi: 10.3390/ijms21249474

Sodium Intake and Heart Failure

Yash Patel ¹, Jacob Joseph ^2,3,*