New data question guideline recommendations regarding sodium restriction in heart failure patients
Impact of Dietary Sodium Restriction on Heart Failure Outcomes
Doukky R, Avery E, Mangla A, et al.
J Am Coll Cardiol HF 2016;4:24–35
BackgroundThe restriction of dietary sodium intake has long been central to the nonpharmacological treatment of heart failure patients, although the relevant data are controversial [1-5]. Some investigators came to the conclusion that if sodium intake is limited to less than 3 g/day, heart failure symptoms and signs can be improved , and that individualised salt and fluid restriction improves heart failure signs and symptoms without negative effects on thirst, appetite or quality of life . Others generated data suggesting that 3 g/day dietary sodium restriction may be most appropriate only for heart failure at stage NYHA III-IV , normal-sodium diet improves outcomes in heart failure patients, but low sodium intake has negative renal and neurohormonal effects , moderate sodium diet restriction determines long-term benefit in heart failure patients with NYHA class III .
This controversy has been reflected in guidelines for the management of heart failure, in which sodium restriction was downgraded from Class I to Class IIa (Level of Evidence C) [6,7].
In this study, the impact of sodium restriction on heart failure outcomes in patients enrolled in the Heart Failure Adherence and Retention Trial (HART) was investigated . Data from 902 patients with heart failure NYHA II/III were analysed. These patients were classified into sodium restricted (<2,500 mg/d) and unrestricted (≥2,500 mg/d) groups, and were followed up for a median of 36 months. The primary outcome was the composite of death or hospitalisation for heart failure.
- Sodium-restricted patients were more frequently women, more likely to have chronic kidney disease or prior stroke, more likely to receive bèta-blockers, and higher doses of loop diuretics.
- Sodium restriction was associated with significantly higher risk of death or heart failure hospitalisation (42.3% vs. 26.2%; HR: 1.85; 95% CI: 1.21 - 2.84; P = 0.004), driven by:
- a non-significant increase in the rate of cardiac death (HR: 1.62; 95% CI: 0.70 - 3.73; P = 0.257) and all-cause mortality (p = 0.074).
- Exploratory subgroup analyses suggested that sodium restriction was associated with increased risk of death or heart failure hospitalisation in patients not receiving angiotensin-converting enzyme inhibitor or angiotensin receptor blocker (HR: 5.78; 95% CI: 1.93 - 17.27; P = 0.002). This suggests that renin-angiotensin-aldosterone system blockade may mitigate the neurohormonal effects of sodium restriction.
- There was a trend toward a significant interaction between sodium restriction and NYHA class (interaction p = 0.138): sodium restriction was associated with a significantly higher risk of adverse outcomes in patients with NYHA class II.
ConclusionSodium restriction may influence negatively the clinical outcomes in symptomatic patients with chronic heart failure. Although a causal effect of sodium restriction on rehospitalisations due to heart failure worsening cannot be established, these findings challenge the systematic sodium restriction strategy for heart failure patients and calls for a multicenter trial to address this issue.
Editorial comments [9,10]Although the findings of this study are contradictory to traditional management of heart failure, they are supported by several pieces of evidence. Sodium restriction may increase sympathetic and renal-angiotensin-aldosterone system activation by contributing to intravascular volume depletion. This is particularly true in the setting of fluid restriction and diuretic therapy. According to Hummel and Konerman, ‘’the results of this study highlight the need for further research investigating the effect of sodium restriction on heart failure physiology and outcomes. It is notable that only 145 of the 902 study patients were restricting their sodium intake to <2,500 mg/d. Considering the challenge this restriction poses for patients, it is even more important to clarify whether sodium restriction is beneficial at all. Furthermore, studies need to determine if variables such as heart failure subtype and severity, comorbidities, medical therapies, or “salt sensitivity” (a specific vulnerability to adverse effects during high-sodium diet) should affect a patient’s recommended daily sodium intake. Ongoing randomized trials in outpatients with stable heart failure (NCT02012179) and patients with heart failure after their hospital discharge (NCT02148679 and NCT02467296) may provide some answers. Until more data are available, however, guidelines regarding sodium intake in patients with heart failure should be taken with a grain of salt.’’ 
According to basic pathophysiology, sodium restriction in heart failure leads to control of excess volume, avoidance of congestion, and prevention of recurrent decompensations. According to Yancy, ‘’the traditional logic has been so clear that to call for proof seemed heretical. Yet, an exhaustive search of available literature does not provide evidence supporting a threshold sodium intake, or the appropriate context for sodium restriction, that is, for prevention, at the time of hospitalisation, and/or for advanced disease. There may even be a signal of harm. Thus, the more fundamental question becomes the very premise for sodium restriction. Does it exist?’’
Given the high health care costs needed to cover heart failure hospitalisations, the simple question of the right dietary recommendations for the right patients cannot remain unanswered. ‘’In our exuberance over new drugs and devices that may lead to modest improvements in HF outcomes, perhaps our greater opportunity is to revisit our core recommendations to patients. Those admonitions should be unwaveringly correct. That is not the case at present for sodium restriction. The advice many of us consistently give to our patients and their families may not be correct. We can do better than this. The time has come for a well-designed, appropriately powered dietary intervention trial. How can we not proceed?‘‘ 
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