Reduced salt intake for heart failure
- ️Wed Dec 08 2021
Abstract
This is a protocol for a Cochrane Review (Intervention). The objectives are as follows:
To review RCTs examining the effects of reduced dietary salt intake in individuals with heart failure.
Background
Despite advancements in diagnosis and management the prevalence of heart failure is increasing (Al‐Mohammad 2011). A recent epidemiological analysis found that in 2010 more than 41 million people were living with heart failure globally (Forouzanfar 2013). The majority of heart failure cases were attributable to ischaemic heart disease (Forouzanfar 2013; Mosterd 2007). UK estimates suggest that 13% of males and 12% of females aged over 75 years have heart failure (BHF 2012). The increasing burden of disease management is predicted to affect both primary and secondary care, with the majority of costs being attributable to the hospitalization of individuals with heart failure (Stewart 2002; Stewart 2003).
While pharmacological management is widely accepted as the mainstay of treatment, several international guidelines emphasize the importance of lifestyle changes as an adjunct to pharmaceutical therapies (BHF 2012; Canada 2012; Dickstein 2008; SIGN 2007; HFSA 2010). For example, the UK National Institute for Health and Care Excellence (NICE) advises beneficial changes relating to diet, physical activity, weight loss, smoking, alcohol consumption and annual vaccinations (NICE 2010).
Several guidelines worldwide also advocate the importance of dietary advice in individuals with heart failure, specifically advice to reduce sodium intake both in the hospital and community (outpatient) setting (Gupta 2012). The rationale for such advice is described below.
Description of the condition
Heart failure is characterized by the impairment of the heart to maintain an adequate circulation of blood throughout the rest of the body. Broadly speaking it can be divided into two types: 1) heart failure with reduced ejection fraction; and 2) heart failure with preserved ejection fraction. Both types result in similar clinical symptoms, such as breathlessness and fatigue, and signs of fluid retention (e.g. oedema) (NICE 2010). The onset of symptoms can be acute, although more often this is seen on a background of chronic long‐term symptoms.
The American College of Cardiology Foundation (ACCF)/American Heart Association (AHA) describe four stages of heart failure, a system that complements the New York Heart Association (NYHA) functional classification of heart failure (Table 1 and Table 2) (Yancy 2013). The emphasis of the ACCF/AHA system is on the presence of structural disease and symptoms, whereas the NYHA functional classification emphasizes the impact on physical activity and symptoms.
Table 1.
ACCF/AHA stages of heart failure
Stage | Description |
A | At high risk for HF but without structural heart disease or symptoms of HF |
B | Structural heart disease but without signs or symptoms of HF |
C | Structural heart disease with prior or current symptoms of HF |
D | Refractory HF requiring specialized interventions |
Table 2.
New York Heart Association functional classification of heart failure
Class | New York Heart Association functional classification |
I | No limitation of physical activity Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea or anginal pain |
II | Slight limitation of physical activity They are comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnea or anginal pain |
III | Marked limitation of physical activity They are comfortable at rest. Less than ordinary activity causes fatigue, palpitation, dyspnea or anginal pain |
IV | Inability to carry out any physical activity without discomfort Symptoms of heart failure or the anginal syndrome may be present even at rest. If any physical activity is undertaken, discomfort increases |
There are several causes of heart failure of which ischaemic heart disease and hypertension are the most common (Dickstein 2008). Other causes include cardiac arrhythmias and myopathies, certain drugs and toxins, and endocrine and connective tissue disorders (NICE 2010). The classification of severity is commonly based on the NHYA system, which ranges from class I (asymptomatic with no limitations on daily living) to class IV (severe symptoms persistent at rest). Greater severity of symptoms is associated with poorer prognosis, and most individuals with heart failure experience morbidity and eventually mortality. Estimates suggest that nearly half of those diagnosed with heart failure die within four years, and those with a higher number of hospital admissions having a particularly poor prognosis. (Dickstein 2008).
Description of the intervention
The mainstay for the management of individuals with heart failure is largely pharmacologic through combinations of drugs such as diuretics, beta‐blockers and angiotensin‐converting enzyme (ACE) inhibitors (NICE 2010). However, like many chronic diseases, pharmacological management is underpinned by self‐care and lifestyle advice, such as recognizing the worsening of symptoms, monitoring weight (as a marker of fluid overload), maintaining physical activity levels where possible, minimizing alcohol intake, stopping smoking and reducing the intake of dietary salt (Dickstein 2008; NICE 2010).
Such is the drive to reduce the dietary salt intake of the overall population that the World Health Organization (WHO) member states have agreed to target a 30% relative reduction in mean population salt intake by 2025 (WHO 2010; WHO 2013). Recent guidance has advocated that adults should consume less than 5 g of salt per day (WHO 2013). In the UK, the Department of Health has taken this further by setting a target limit of 3 g per day for adults by 2025 (NICE 2013).
For the purpose of this review we are using the term 'salt' to refer to sodium chloride, where 1 g of standard sodium chloride contains 0.38 g of sodium (SACN 2003).
How the intervention might work
The rationale for advocating reduced salt intake in individuals with heart failure is not fully understood but is based on several possible mechanisms. One mechanism is that reduced dietary salt has a positive impact on sodium‐fluid homeostasis, thus preventing fluid overload (He 2010). Low‐salt diets have also been shown to lower blood pressure in individuals with hypertension, which may also have benefit in those with heart failure (He 2013a). There is also evidence that salt depletion can directly lead to a reduction in left ventricular mass (Ferrara 1984).
Why it is important to do this review
Existing Cochrane reviews have looked at the effect of reduced dietary salt on blood pressure, concluding that even modest reductions can reduce blood pressure in both normotensive and hypertensive individuals (He 2013a; He 2013b). Broader Cochrane reviews have examined the effect of reduced dietary salt on preventing cardiovascular disease (Hooper 2004; Taylor 2013). However, neither review could draw any conclusions regarding the impact of low‐salt diets in individuals with heart failure. Our review is therefore important as we will include only trials of participants with existing heart failure that have examined the impact of low‐salt diets on participant health.
Despite the rationale for advocating low‐salt diets in individuals with heart failure, the evidence base is weak. A recent review highlighted a lack of clarity on this management option despite widespread advocacy (Gupta 2012). The narrative review went on to highlight variations in results between observational and randomized controlled trials (RCTs) while also pointing out areas in which there is little evidence at all (e.g. reduced dietary salt in individuals with heart failure with preserved ejection fraction). A recent systematic review and meta‐analysis included six RCTs examining the role of dietary salt restriction in individuals with heart failure. All six trials showed that a low‐salt diet, compared with a normal‐salt diet, significantly increased morbidity and mortality in individuals with heart failure (DiNicolantonio 2013a). Such a conclusion goes against current consensus (Gupta 2012), and led to a growing call for a re‐evaluation of guidelines and current practice (Jun 2013; Lucan 2013). However, the review was retracted in its entirety after concerns were expressed over the integrity of the data (Dinicolantonio 2013b). Our preliminary searches have identified at least two further RCTs showing a beneficial role of dietary salt restriction in individuals with heart failure that were not included in the above systematic review (Colin 2004; Colin 2010). The lack of evidence in this area has been reflected in a recent executive summary from the US National Heart, Lung, and Blood Institute and the National Institutes of Health Office of Dietary Supplements calling for better‐quality evidence for diet‐related therapies in heart failure (Van Horn 2013). Hence, a systematic review examining the role of reduced dietary salt in individuals with heart failure is needed.
Objectives
To review RCTs examining the effects of reduced dietary salt intake in individuals with heart failure.
Methods
Criteria for considering studies for this review
Types of studies
We will consider all RCTs (including cluster RCTs and cross‐over studies) that compare a low‐salt diet with standard‐salt diet. We will not restrict our inclusion criteria as to study duration. We will include studies reported as full text, those published in abstract form only and unpublished data.
Types of participants
Adults (≥18 years old) with heart failure of either ischemic or non‐ischemic etiology, and with any combination of history and clinical findings, for whom Doppler echocardiography and serum natriuretic peptide data are available. We will therefore not specifically exclude studies that include participants with heart failure and preserved ejection fraction, nor restrict inclusion to a specific NYHA class. However, where possible, we will carry out subgroup analyses on any relevant included studies based on the starting heart failure participant population (e.g. left ventricular systolic dysfunction versus preserved ejection fraction). We will include studies in individuals with chronic stable heart failure who are managed in the community or outpatient settings, as well as those who have been admitted to hospital with acutely decompensated heart failure and whose management includes dietary salt restriction (versus controls) in that setting. We will carry out a subgroup analysis for each setting.
Types of interventions
We will include RCTs that use strategies intended to reduce dietary sodium intake compared with usual care or placebo. We will not stipulate a specific value for what constitutes a reduction in dietary salt intake, but will consider a study for inclusion where an attempt has been made to test the effect of a reduced salt diet in a controlled trial setting. We anticipate that the likely strategies will include reduced intake through dietary advice, sodium substitutes (e.g. potassium chloride) or food restriction methods. We will record the details of the intervention and create a table to compare and contrast them. However, we will not include studies in which the dietary intervention is administered via enteral or parenteral feeding. For included studies, we will record the target value for salt restriction that the authors aimed for (e.g. < 5 g/day) in 'Characteristics of included studies' tables. A secondary endpoint will be to compare and contrast this desired level of salt intake to actual values achieved (as confirmed by sodium measurement), as a measure of adherence to the intervention.
Types of outcome measures
Primary outcomes
Cardiovascular‐related mortality
All‐cause mortality.
Adverse events (e.g. stroke, myocardial infarction, hypo‐ and hypernatremia, changes in serum lipids or renal function)
Secondary outcomes
Hospitalizations (in outpatient‐based sample populations)
Length of inpatient stay (in hospital settings)
Change in NYHA functional class
Adherence to a low‐salt diet, as confirmed by sodium measurement (e.g. 24‐hour urinary collections); comparing and contrasting actual to desired levels, as per the protocol
Changes in blood pressure (systolic and diastolic)
Search methods for identification of studies
Electronic searches
We will identify trials through systematic searches of the following bibliographic databases:
Cochrane Central Register of Controlled Trials (CENTRAL), part of The Cochrane Library;
Database of Abstracts of Reviews of Effects (DARE), part of The Cochrane Library;
MEDLINE (OvidSP);
EMBASE (OvidSP);
CINAHL (EBSCOhost);
Science Citation Index Expanded (SCI‐EXPANDED) on Thomson Reuters' Web of Science;
Conference Proceedings Citation Index‐Science (CPCI‐S) on Thomson Reuters' Web of Science.
Two authors (NR and KRM) will devise a search strategy, which will be used to search the above databases from inception. We will apply the Cochrane sensitivity‐precision maximizing RCT filter to MEDLINE and adaptations of it to the other databases, with the exception of CENTRAL (Lefebvre 2011). We will also search for ongoing studies on:
Clinicaltrials.gov (http://clinicaltrials.gov);
WHO International Clinical Trials Registry Platform (http://www.who.int/ictrp/en/);
Current Controlled Trials (http://www.controlled‐trials.com/).
We will apply no language restrictions to the searches. We will contact authors of included studies for missing data and other unpublished or ongoing studies. We show a preliminary search strategy in Appendix 1.
Searching other resources
We will check the reference lists of all included studies and review articles for additional references.
Data collection and analysis
Selection of studies
Two review authors (KRM, DN) will independently screen the titles and abstracts of all the potential studies we identify as a result of the search for inclusion and code them as 'retrieve' (eligible or potentially eligible/unclear) or 'do not retrieve'. If there are any disagreements, we will ask a third author to arbitrate (CJH). We will retrieve the full‐text study reports/publications; two review authors (KRM, DN) will independently screen the full text and identify studies for inclusion, and identify and record reasons for exclusion of the ineligible studies. We will resolve any disagreement through discussion or, if required, we will consult a third author (CJH). We will identify and exclude duplicates and collate multiple reports of the same study so that each study rather than each report is the unit of interest in the review. We will record the selection process in sufficient detail to complete a PRISMA (Preferred Reporting Items for Systematic Reviews andMeta‐Analyses) flow diagram (Moher 2009), and 'Characteristics of included studies' and 'Characteristics of excluded studies' tables.
Data extraction and management
We will use a data collection form that has been piloted on at least one study in the review to record study characteristics and outcome data. Two review authors (KRM, DN) will extract the following study characteristics from included studies.
Methods: study design, total duration of study, details of any 'run‐in' period, number of study centers and location, study setting, withdrawals and date of study
Participants: numbers, mean age, age range, gender, severity of condition, diagnostic criteria, inclusion criteria and exclusion criteria
Interventions: intervention, comparison, concomitant medications and excluded medications
Outcomes: primary and secondary outcomes specified and collected, and time points reported
Notes: funding for trial, and notable conflicts of interest of trial authors
Risk of bias
Two review authors (KRM, DN) will independently extract outcome data from included studies. We will resolve disagreements by consensus or by involving a third author (CJH). One review author (KRM) will transfer data into Review Manager (RevMan 2012). We will double‐check that data are entered correctly by comparing the data presented in the systematic review with those in the study reports. A second review author (DN) will spot‐check study characteristics for accuracy against the trial reports.
Assessment of risk of bias in included studies
Two review authors (KRM, DN) will independently assess risk of bias for each study using the criteria outlined in the Cochrane Handbook for Systematic Reviews of Interventions (Higgins 2011). We will resolve any disagreements by discussion or by involving another author (CJH). We will assess the risk of bias according to the following domains:
random sequence generation;
allocation concealment;
blinding of participants and personnel;
blinding of outcome assessment;
incomplete outcome data;
other bias (e.g. industry funding, conflicts of interest).
We will grade each potential source of bias as high, low or unclear, and provide a quote from the study report together with a justification for our judgment in the 'Risk of bias' table. We will summarize the 'Risk of bias' judgments across different studies for each of the domains listed. Where information on risk of bias relates to unpublished data or to correspondence with a trialist, we will note this in the 'Risk of bias' table.
When considering treatment effects, we will take into account the risk of bias for the studies that contributed to that outcome.
Assessment of bias in conducting the systematic review
We will conduct the review according to this published protocol and report any deviations from it in the 'Differences between protocol and review' section of the systematic review.
Measures of treatment effect
We will analyze dichotomous data (such as number of deaths, hospitalizations) as odds ratios or risk ratios with 95% confidence intervals, and continuous data (e.g. blood pressure, 24‐hour urinary collection) as mean differences or standardized mean differences with 95% confidence intervals. We will enter data presented as a scale with a consistent direction of effect.
Where data appears skewed we will report the median and Interquartile ranges (Higgins 2011).
Unit of analysis issues
We anticipate that the majority of included studies will be of a parallel‐study design. We will therefore record, or where necessary calculate, the treatment effect as the difference in values at the end of the study minus those at the start. Where a cross‐over study has been included we will calculate the effect at the end of one period compared to the start of that period and compare this to the effect at the end of the cross‐over period compared to that at the start of the cross‐over period. We will refer to the Cochrane Handbook for Systematic Reviews of Interventions for guidance (Higgins 2011).
Dealing with missing data
We will contact investigators or study sponsors in order to verify key study characteristics and obtain missing numerical outcome data where possible (e.g. when a study is identified in abstract form only). Where this is not possible, and the missing data are thought to introduce serious bias, we will explore the impact of including such studies in the overall assessment of results by a sensitivity analysis.
Assessment of heterogeneity
We will use the I² statistic to measure heterogeneity among the trials in each analysis. We will refer to the Cochrane Handbook for Systematic Reviews of Interventions for guidance (Higgins 2011).
Assessment of reporting biases
If we are able to pool more than 10 trials, we will create and examine a funnel plot to explore possible small study biases for the primary outcomes.
Data synthesis
We will analyze our results using both fixed‐effect and random‐effects models and report any differences in the effect size for each model. If heterogeneity exists (I2 = 50% to 75%), a random‐effects model will be employed. If a high degree of heterogeneity (I2 > 75%) is detected we will not pool data for meta‐analysis. Clinical heterogeneity will be assessed through the description of the participants, setting and the intervention used in each study. This will be reported in narrative.
Subgroup analysis and investigation of heterogeneity
We plan to carry out the following subgroup analyses:
starting sample population: community (outpatient) versus hospital (inpatient) setting;
type of heart failure: left ventricular systolic dysfunction versus preserved ejection fraction;
white versus non‐white populations;
age;
gender;
severity of heart failure (based on the NYHA classification).
Sensitivity analysis
We plan to carry out the following sensitivity analyses:
including only studies with a low risk of bias
Reaching conclusions
We will base our conclusions only on the findings from the quantitative or narrative synthesis of the studies included in this review. We will use the results of our review to make recommendations for practice and our implications for research will suggest priorities for future research and outline any remaining uncertainties.
Acknowledgements
KRM is funded through an National Institute for Health Research (NIHR) Academic Clinical Lectureship in General Practice.
Appendices
Appendix 1. MEDLINE search strategy
1 exp Heart Failure/
2 exp Ventricular Dysfunction/
3 Cardiomyopathy/
4 (heart failure or chf).ti,ab.
5 ((cardia* or myocardial) adj (failure or insufficienc*)).ti,ab.
6 ((heart or cardia* or myocardial) adj5 (systolic failure or diastolic failure)).ti,ab.
7 (decompensat* adj2 (heart* or cardia*)).ti,ab.
8 ((left ventric* adj2 (failure or dysfunction or function)) or lvf or lvd).ti,ab.
9 cardiomyopath*.ti,ab.
10 1 or 2 or 3 or 4 or 5 or 6 or 7 or 8 or 9
11 Diet, Sodium‐Restricted/
12 exp Sodium, Dietary/
13 (Sodium Chloride/ or Sodium/) and (low* or high* or normal* or reduc* or restrict* or chang* or decreas* or intake or consum* or diet*).ti,ab.
14 ((salt or sodium) adj5 (low* or high* or normal* or reduc* or restrict* or chang* or decreas* or intake or consum*)).ti,ab.
15 (sodium adj3 (urin* or excret*)).ti,ab.
16 ((salt or sodium) and diet*).ti,ab.
17 (hyposodic or normosodic or hypersodic).ti,ab.
18 11 or 12 or 13 or 14 or 15 or 16 or 17
19 randomized controlled trial.pt.
20 controlled clinical trial.pt.
21 randomized.ab.
22 placebo.ab.
23 drug therapy.fs.
24 randomly.ab.
25 trial.ab.
26 groups.ab.
27 19 or 20 or 21 or 22 or 23 or 24 or 25 or 26
28 exp animals/ not humans.sh.
29 27 not 28
30 10 and 18 and 29
What's new
Date | Event | Description |
---|---|---|
22 February 2018 | Amended | This protocol has been withdrawn as the author team is unable to progress to the final review stage. |
Contributions of authors
KRM was responsible for registering the title with the Cochrane Heart Group and preparing the first draft of this protocol. All remaining authors contributed to the editing of this draft prior to submission.
Sources of support
Internal sources
-
National Institute for Health Research (NIHR) School for Primary Care Research (SPCR), UK.
A proportion of this project is funded by the National Institute for Health Research (NIHR) School for Primary Care Research (SPCR).
Disclaimer:
This article presents independent research part‐funded by the National Institute for Health Research (NIHR). The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR or the Department of Health.
External sources
-
Royal College of General Practicioners, UK.
This research was part‐funded by the Scientific Foundation board of the Royal College of General Practitioners (Grant number SFB 2013‐14)
Declarations of interest
None declared.
Notes
This protocol has been withdrawn as the author team is unable to progress to the final review stage.
Withdrawn from publication for reasons stated in the review
References
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