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.

Highlights

  • Salt is an ionic compound made up of cation and anion

  • HF 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)

  • A randomized clinical trial to see the effect of a diet with sodium and fluid restriction compared to an unrestricted diet in patients admitted with acute decompensated HFpEF showed that aggressive sodium and fluid restriction does not decrease readmission and mortality rate, and that it impairs the patient’s food intake without any significant neurohormonal effect [37]

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Summary

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. 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. Sodium restriction has historically been taught in textbooks as a cornerstone of the management of HF patients. Data on this management strategy are controversial. Before we vigorously start educating HF patients to limit sodium intake in their diet, we need to understand the evidence behind such recommendations. We review evidence relating sodium to HF, pathophysiological mechanisms of increased sodium intake, and the relation of sodium intake to HF outcomes

Guideline Recommendations for Sodium Intake
Evidence in Favor of Low Sodium Intake in Prevention or Management of HF
Low Sodium Intake and Worsening of HF
Potential Mechanism for Adverse Impact of Low Sodium Intake in HF
Potential Molecular Mechanism of Salt Diet and Heart Failure
Sodium Intake and Ambulatory Heart Failure
Sodium Intake in Selected Patient Populations
Serum Sodium Values and HF
Future Directions
10. Our Recommendations
Findings
11. Conclusions
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