CHAPTER 26
Saumitra Ray, Arghya Chattopadhyay
Sodium Restriction in Heart Failure:
What Should We Recommend?
INTRODUCTION
Dietary sodium restriction is viewed as a potentially
modifi able precipitant of heart failure related
admissions.1-5 Restriction of sodium is considered the
most frequent home care management recommended
to patients with HF6 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 23 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.
PATHOPHYSIOLOGY OF HEART FAILURE
AND ROLE OF SODIUM
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 kidney14 and creating a
vicious cycle of sodium and water retention despite fluid
overload.15 Moreover, considering the hypo-osmolar,
volume-over loaded 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
174 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 -blocker
treatment.21
STANDARD RECOMMENDATION
AND NEWER CONTROVERSY
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
Fig. 1J-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 mol/L] vs 1.5 mg/dL
[133 mol/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 2,3002,500 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
CONCLUSION
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 3,0005,000 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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