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CHAPTER 26 Saumitra Ray, Arghya Chattopadhyay • SodiumRestriction in Heart Failure: What Should We Recommend?

Saumitra Ray, Arghya Chattopadhyay

SodiumRestriction in Heart Failure:

What Should We Recommend?


Dietary sodium restriction is viewed as a potentially modifiable precipitant of heart failure related admissions. 1-5 Restriction of sodium is considered the most frequent home care management recommended to patients with HF 6 and its recommendations are a mandated component of discharge instructions of heart failure patients. 7,8 Although current guidelines vary widely in their recommended degree of sodium restriction, on an average daily consumption of sodium varies between 3,400 mg/day and 3,700 mg/day of sodium. 9 Based primarily on data from cohort studies in hypertensives without HF, a recent American Heart Association task force called for a sodium restriction of <1500 mg of sodium per day. 10 The 2013 American Heart Association/ American College of Cardiology guidelines suggest 3 grams or less per day in symptomatic HF patients. 11 The Heart Failure Society of America recommends 2–3 g/day in all HF patients and for moderate-to-severe HF further restriction to less than 2 g/day. 12 The 2012 European Society of Cardiology HF Guidelines omit completely any recommendations regarding sodium intake for the management of chronic HF. 13 The variability in these guidelines is not surprising, as much of the rationale for sodium restriction stems from studies in hypertension, a major HF risk factor, but it is unclear how these lessons translate to patients with prevalent HF. Most observational studies support the concept that low sodium intake improves HF outcomes. On the other hand, few resent controlled trials that have been suggested that strict sodium restriction can be

harmful in some HF patients. In light of this apparent contradiction, it is worthwhile to review the evidence arguing for and against sodium restriction in HF.


Activation of the sympathetic nervous system and the renin angiotensin aldosterone system, in heart failure may be due to diminished renal perfusion as result of reduced cardiac output, elevated systemic venous pressures, or shunting of blood away from the kidney 14 and creating a vicious cycle of sodium and water retention despite fluid overload. 15 Moreover, considering the hypo-osmolar, volume-overloaded state, inappropriate physiological vasopressin levels are seen in HF. The natriuretic peptide system in HF is inadequate to counteract this dynamic because of decreased efficacy and inadequate cleaving of natriuretic peptides, 16,17 downregulation of renal natriuretic peptide receptors, 18 and degradation of natriuretic peptides by endopeptidases in the renal tubule. Therefore, despite the need for sodium and water excretion, sodium-retaining factors prevail. 19 Further, dietary sodium restriction is associated with neurohormonal activation. In animal studies, a sodium- restricted diet leads to increased vascular resistance and a decrease in cardiac output owing to activation of renin angiotensin aldosterone system. 20 Also, although blocking renin angiotensin aldosterone system does provide an improvement in renal blood flow but when accompanied by a low-sodium diet it is not associated with an increase in glomerular filtration rate or natriuresis. Recently, the


Section 4: Heart Failure

Valsartan in Heart Failure Trial investigators reported that higher plasma renin activity (PRA) is a strong and independent predictor of mortality regardless of angiotensin-converting enzyme inhibitor or β-blocker treatment. 21


Over 40% of the population-attributable risk for HF contributed by systemic hypertension, and precedes

the development of HF in up to 91% of cases. 22 Systemic hypertension doubles the lifetime risk for HF with blood pressure ≥160/100 versus <140/90 mm Hg, 23 and there is

a marked reduction of incidence of HF on treatment of

systolic hypertension. 24 High sodium consumption has long been considered one of the main modifiable factors promoting hypertension within populations. 25 Several observational studies have demonstrated associations between improved HF status with lower dietary sodium intake. In a prospective study, Son et al. found that patients with a 24-hour urine sodium excretion of >3 g exhibited a greater symptom burden and shorter cardiac event-free interval over a 12 months period. 26 Arcand and colleagues also found that sodium intake was associated with increased episodes of decompensated HF, increased HF hospitalizations, and increased mortality. 27 Frequent intake of salty foods has been associated with the need for high urgency transplantation. 28 The arguments against sodium restriction comes when low dietary sodium has been identified as an independent risk factor for HF admission, 29 and conflicting data exist regarding the benefit of dietary education on HF outcomes. In the Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients With Heart Failure (OPTIMIZE-HF), Fonarow et al. noted no impact of discharge instructions of dietary sodium restriction on 60– 90 days hospitalization or mortality rates in HF patients. 7 In a 2008 study of 232 outpatients with stable heart failure who had been discharged from the hospital after an exacerbation of heart failure and who were in stable

condition at the time of their one-month follow-up visit, 30 were randomized at the one-month visit to consume

a low-sodium diet (an average of 1,840 mg/day) or a

normal-sodium diet (approximately 2,800 mg/day). Both groups received high-dose diuretic therapy and were

advised to limit fluid intake to 1 L/day. Six months later, the group consuming a low-sodium diet had experienced

a higher rate of readmission (26.3% vs 7.6%) and deaths.

Explanation suggested for these differences is that sodium restriction combined with diuretic therapy leads to higher levels of aldosterone and renin secretion, and this may adversely affect cardiac function. The sodium-restricted

may adversely affect cardiac function. The sodium-restricted Fig. 1 J-shaped curve for sodium consumption. On the

Fig. 1 J-shaped curve for sodium consumption. On the J-shaped curve, reduction of sodium consumption below the optimal level appears to increase the risk of adverse outcomes for patients with heart failure, including higher rates of hospital readmission and higher rates of death. But, sodium consumption above the optimal level increases the risk of adverse outcomes to a far greater degree

group also had lower serum sodium levels and higher creatinine levels (2.1 mg/dL [186 μmol/L] vs 1.5 mg/dL [133 μmol/L]), which could be further indication of the deleterious effects of sodium restriction; however, these differences may simply have been the result of fluid restriction and high-dose diuretic therapy rather than sodium restriction. In another study with hospitalized patients having decompensated heart failure, were randomized to a diet with fluid and sodium restriction (800 mg/day) or to a standard hospital diet. Follow-up results showed no advantage to sodium restriction, no difference in weight loss and no difference in clinical improvement scores or 30-day readmission rates. 31 Given this controversy, current thinking is that the effects of sodium restriction in patients with established cardiovascular disorders, including heart failure, likely follow a J-shaped curve (Fig. 1), in which reducing sodium intake below the high levels is beneficial, but marked sodium restriction is not beneficial and carries risk. Although the optimal level of dietary sodium is unclear, analyses by the Institute of Medicine and others suggest that a sodium intake less than 2,300–2,500 mg/day may be undesirable for patients with established cardiovascular disease because it has no clear benefit and may carry risk. 32,33 Therefore, based on current evidence and until further studies are completed, patients with heart failure should probably be discouraged from reducing their sodium consumption to less than 2,300 mg/day. 34


Mechanistic studies focusing on effect of sodium restriction on the myocyte (both at the level of cellular signaling and

Chapter 26: Sodium Restriction in Heart Failure: What Should We Recommend?


also at the organ level), vasculature, renal function, and neurohormonal activation cloud be the future direction of research to look for sodium effect, however, these 4 physiological domains are directly affected by, or the effect of sodium on them can be modified by, baseline medical therapy. It is also possible that the effect of sodium intake varies considerably among different individuals. Some ways to personalize sodium intake recommendations that could be assessed include studies based on genomic factors, body size, renal function, comorbidity burden, symptoms status, etc. Behavioral research is also important beyond the mechanistic and clinical outcomes studies, as heart failure patients, like the population at large, despite medical advice, continue to consume large quantities of sodium daily. Further research investigating reliable means of longer-term sodium intake assessment over time is important, because current means are either prone to recall bias (e.g. food frequency questionnaires) or are episodic and reveal the status for the past 24 hours, which may not be reflective of the overall sodium intake pattern. How to best implement sodium intake recommendations so that the adherence rates improve, and how much that will involve advocacy versus behavior change interventions, needs further exploration. The possibility that aggressive sodium restriction may lead to unfavorable outcomes in patients with heart failure should not, however, be misconstrued as meaning that we should lose our focus on reducing sodium intake in the general population. The average American adult consumes 3,000–5,000 mg of sodium per day, 34 which is on the far right-hand upslope of the J-shaped curve in. Because such high sodium intake is strongly associated with development of cardiovascular disorders, there is still an urgent need for Americans to reduce their sodium consumption. 35,36


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