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. Author manuscript; available in PMC: 2023 Apr 26.
Published in final edited form as: J Am Coll Cardiol. 2022 Apr 26;79(16):1623–1635. doi: 10.1016/j.jacc.2022.02.025

Nutrition Assessment and Dietary Interventions in Heart Failure

JACC Review Topic of the Week

Elissa Driggin a, Laura P Cohen a, Dympna Gallagher b, Wahida Karmally c, Thomas Maddox d, Scott L Hummel e, Salvatore Carbone f,g, Mathew S Maurer a
PMCID: PMC9388228  NIHMSID: NIHMS1826805  PMID: 35450580

Abstract

Despite the high prevalence of nutrition disorders in patients with heart failure (HF), major HF guidelines lack specific nutrition recommendations. Because of the lack of standardized definitions and assessment tools to quantify nutritional status, nutrition disorders are often missed in patients with HF. Additionally, a wide range of dietary interventions and overall dietary patterns have been studied in this population. The resulting evidence of benefit is, however, conflicting, making it challenging to determine which strategies are the most beneficial. In this document, we review the available nutritional status assessment tools for patients with HF. In addition, we appraise the current evidence for dietary interventions in HF, including sodium restriction, obesity, malnutrition, dietary patterns, and specific macronutrient and micronutrient supplementation. Furthermore, we discuss the feasibility and challenges associated with the implementation of multimodal nutrition interventions and delineate potential solutions to facilitate addressing nutrition in patients with HF.

Keywords: diet, heart failure, nutrition


As the prevalence of heart failure (HF) rises with time, a multidisciplinary approach to treatment is paramount. Nutrition disorders, including abnormalities in body composition such as obesity and malnutrition and/or macronutrient and micronutrient deficiencies, are highly prevalent in HF, with the potential to affect the disease trajectory.1,2 Despite this, major HF guidelines have very limited recommendations on nutrition disorders because of a lack of consensus on how to effectively treat them.36 Accordingly, we reviewed the available published reports related to nutrition and HF using an online search strategy outlined in the Supplemental Appendix. In this review, we discuss the major assessment tools and focus areas for nutrition in HF. Furthermore, we describe the challenges associated with implementing nutrition interventions and offer potential solutions to mitigate these challenges so that nutrition becomes a focus area of future attention and research as a treatment target in HF (Central Illustration).

CENTRAL ILLUSTRATION. Major Heart Failure Nutrition Domains and Challenges to Implementation.

CENTRAL ILLUSTRATION

Schematic representing the major nutrition-related research focus areas in the context of potential challenges to the implementation of nutrition interventions in heart failure.

QUANTIFYING NUTRITIONAL STATUS IN HF

The prevalence of malnutrition in HF is estimated at 15% to 90%, depending on the assessment method and, when present, is associated with more than double the risk for mortality.3,7 Given the heterogeneity of nutrition disorders and limited comprehensive head-to-head studies comparing assessment tools, there is no gold standard for assessing malnutrition in HF.8 In this section, we will outline and appraise common assessment methods (Table 1).

TABLE 1.

Nutritional Status Assessment Methods in Heart Failure

Method Measures Advantages Disadvantages

BMI Weight indexed to height squared (kg/m2) Easy to calculate
Routinely measured High clinical awareness
High clinical awareness
Does not differentiate lean vs fat vs fluid mass
Does not reflect distribution of adiposity
Body composition analysis • DXA
• MRI
• CT
• Quantitative MRI
• BIA
Differentiates lean vs fat vs fluid mass Certain measures inaccurate with excess body water (ie, DXA, BIA)
Certain methods expensive and/or impractical (ie, MRI)
No established cutoffs for nutritional disorders
Biomarkers Albumin
Prealbumin
Lymphocyte count
Total cholesterol
Biomarkers of cardiac cachexia:
• Ghrelin
• Adiponectin C-terminal agrin fragment Growth differentiation factor 15
• Atrial natriuretic peptide
• N-terminal propeptide of type III procollagen
• Type VI collagen N-terminal globular, domain epitope
• Myostatin
• Me-3-His
Easy to measure Confounded by comorbidity, hepatopathy, medication, and inflammation
Multidimensional assessment tools • CONUT
• GLIM
• GNRI
• NRI
• NRS
• MNA
• MSRA
• NUTRIC
• PNI
• SARC-F
Easy to measure
Incorporate multiple domains of nutrition status assessment (ie, anthropometrics, biomarkers, intake patterns, and so on)
Low clinical awareness
Reflects severity of underlying illness rather than malnutrition directly (ie, nonspecific)

BIA = bioelectrical impedance analysis; CONUT = Controlling Nutritional Status score; DXA = dual-energy X-ray absorptiometry; GLIM = Global Leadership Initiative on Malnutrition; GNRI = Geriatric Nutritional Risk Index; MNA = Mini Nutritional Assessment; MRI = magnetic resonance imaging; MSRA = Mini Sarcopenia Risk Assessment; NRI = Nutritional Risk Index; NRS = Nutritional Risk Screening; NUTRIC =Nutrition Risk in the Critically Ill; PNI = Prognostic Nutritional Index; SARC-F = Strength, Assistance With Walking, Rising From a Chair, Climbing Stairs, and Falls.

BODY MASS INDEX.

The most common tool to approximate nutritional status is body mass index (BMI). Although easy to measure in routine clinical practice, BMI does not distinguish weight attributable to excess fluid vs lean and/or fat mass.9 In this context, patients with HF who are volume overloaded may be classified according to the World Health Organization criteria as having falsely normal or high BMI yet still have low lean body mass and/or malnutrition.9 Additionally, a significant proportion of patients with HF and obesity are malnourished or at risk of malnutrition, estimated at 10% to 50%, depending on the population and screening instrument.10 Furthermore, among patients with excess fat mass, BMI does not reflect adipose distribution (ie, visceral vs subcutaneous), which may have prognostic implications in HF.11 A reliance on BMI alone as a measure of nutritional status clearly misses patients at risk for poor outcomes.

BODY COMPOSITION.

Body composition analysis is an important assessment tool in HF that informs the proportion of body mass that is fat mass vs fat-free mass (FFM). However, HF-related increases in body water and reductions in muscle mass violate the underlying assumptions for many body composition assessment techniques, rendering them inaccurate.9,12 Dual-energy X-ray absorptiometry, though an efficient and highly accurate technique to assess bone, lean, and fat mass, assumes minimal effects of hydration on FFM, which is inaccurate in HF.12 Although magnetic resonance imaging and computed tomography are ideal to quantify muscle and fat mass, their clinical use is limited by impracticality and cost as well as contraindications to magnetic resonance imaging such as claustrophobia and/or incompatible pacemakers or defibrillators. Quantitative magnetic resonance techniques with short scan times developed for the purpose of body composition analysis may be accurate in HF, although they are not yet widely available.12 Despite the potentially high discriminatory ability of these modalities, the lack of diagnostic criteria for nutrition disorders based on fat and FFM mass quantification limits their clinical utility to date.

BIOMARKERS.

There are multiple candidate biomarkers as surrogates for nutritional status in HF (Table 1). Serum albumin is a hepatic protein affected by nutrition that has been studied extensively regarding HF prognosis. In large HF cohort studies, hypoalbuminemia (ie, serum albumin of <3.4 g/dL) was an independent predictor of all-cause mortality.13 Similarly, low prealbumin level, lymphopenia, and low serum cholesterol level have all been implicated as poor nutrition-related prognostic indicators in HF.1416 Despite these associations, these biomarkers are affected by comorbidities, medications, volume status, and inflammation, and they are difficult to interpret in isolation. Importantly, there are several candidate biomarkers specific to cardiac cachexia, such as ghrelin, adiponectin, and myostatin, that are the subject of future research and may aid in the diagnosis of this high-risk condition in advanced HF.17 In addition, metabolomics, including amino acid profiling, have identified elevated 3-methylhistidine (3-Me-His), a histidine derivative, as a marker of cardiac cachexia that predicts poor prognosis in patients with HF.18

MULTIDIMENSIONAL ASSESSMENT TOOLS.

There are numerous multidimensional tools to diagnose malnutrition in HF (Table 1).8,10 These assessment methods incorporate several parameters related to nutrition and often use a scoring system to categorize the severity of malnutrition. Given the potential confounding clinical factors in HF associated with any individual measurement, these assessment tools are potentially useful because they take into account variable combinations of anthropometrics, biomarkers, and appetite assessments.8 Although there are limited head-to-head studies that have compared these assessment methods directly, the Geriatric Nutritional Risk Index, which assesses current body weight indexed to ideal body weight and serum albumin level, and the Mini Nutritional Assessment, which assesses dietary intake, mobility, and BMI, have shown the strongest association with mortality risk in HF cohort studies.8,10 The Subjective Global Assessment, which incorporates physical examination findings such as muscle wasting and loss of subcutaneous fat, has also been identified as one of the most specific malnutrition assessments in HF.19 Notably, there is no accepted gold standard instrument, and although these scores are often quick to calculate, their results may reflect the severity of the patient’s underlying illness rather than malnutrition directly.

CURRENT FOCUS AREAS IN NUTRITION AND HF

To date, there are several nutrition disorders known to affect HF incidence, progression, and prognosis.1,3 Although the evidence to support interventions for some nutrition disorders is robust, in others it is lacking, resulting in limited nutrition-related recommendations in the HF guidelines. In this section, we summarize the evidence for and controversies related to the major nutrition focus areas in HF (Table 2).2043

TABLE 2.

Nutrition Domains in Heart Failure: Societal Recommendations, Considerations for Intervention, and Key Areas for Future Research

Nutrition Domain Sodium Restriction Obesity Malnutrition Dietary Patterns Macronutrient and Micronutrient Supplements

Society recommendations
HFSA, 2010 Restrict sodium to 2–3 g, consider <2g in moderate to severe HF 3MI of <30 kg/m2 to prevent HF; treat “severe obesity” in established HF Caloric supplementation for cardiac cachexia None Consider n-3 PUFA in NYHA class II-IV HFrEF
ACC/AHA, 2013 Reasonable if symptomatic Weight loss to prevent HF; unknown efficacy for treatment in established HF None None Intravenous iron in NYHA class II-IV HF with iron deficiency
n-3 PUFA reasonable in NYHA class II-IV HF
ESC, 2021 None Same as ACC/AHA 2013 None None Consider intravenous iron in HFrEF with symptoms or recent hospitalization and iron deficiency
Considerations with intervention
Potential benefits Improve symptoms20 Reduce incidence of HF with weight loss27 Potential mortality benefit with malnutrition interventions3234 Reduce incidence of HF with plant-based diet35 Potential mortality benefit in women with DASH diet36 Improved exercise capacity with intravenous iron38
Lower diuretic doses mprove CRF with weight loss 28 Fewer HF hospitalizations with malnutrition interventions32,34 mprove symptoms with DASH diet Improved quality of life with intravenous iron38
Potential mortality benefit in NYHA classes III-IV21 Improved functional capacity and quality of life with malnutrition
interventions33,34
Improve quality of life with DASH diet37 Improved quality of life with n-3 PUFA39 Lower HF hospitalization with n-3 PUFA40
Potential mortality benefit with n-3 PUFA40
Improved exercise capacity with UFA41
Potential mortality benefit with coenzyme Q42
Potential harms Neurohormonal
activation2224
Potential for increased mortality in established HF, ie, the obesity paradox2931 Potential for gastrointestinal side effects with supplements to treat malnutrition33 Potential for malnutrition attributable to lower overall intake with plant- based diet26 Potential for
gastrointestinal side effects with oral iron and n-3 PUFA
Potential increase in HF hospitalizations22,23,25 Lean mass loss with caloric restriction Higher infection risk with intravenous iron administration
Potential increased mortality, especially in NYHA class I-II HF21 Long-term weight regain after weight loss Increased incidence of atrial fibrillation with n-3 PUFA supplementation43
Malnutrition attributable to lower overall intake with sodium restriction26
Future research Patient-level factors that influence sodium restriction recommendations nfluence of body composition on the obesity paradox Ideal method to quantify malnutrition in HF Impact of the Mediterranean diet in HF Need for micronutrient supplementation in context of well-rounded whole-food diet
Specific strategies for HFpEF vs HFrEF Specific strategies for HFpEF vs HFrEF Effective and practical malnutrition intervention strategies in HF Role for other diets (ie, ketogenic) in HF

ACC = American College of Cardiology; AHA = American Heart Association; BMI = body mass index; CRF = cardiorespiratory fitness; DASH = Dietary Approaches to Stop Hypertension; ESC = European Society ofCardiology; HF = heart failure; HFpEF = heart failure preserved ejection fraction; HFrEF = heart failure reduced ejection fraction; HFSA = Heart Failure Society ofAmerica; n-3 PUFA =omega-3 polyunsaturated fatty acids; NYHA = New York Heart Association; UFA = unsaturated fatty acids.

SODIUM RESTRICTION.

The most common dietary recommendation in HF is sodium restriction. However, recent data are conflicting, leading to the downgrading of this recommendation in the major HF guidelines.44,45 The data on sodium restriction in HF is largely observational in nature and varies widely in study design, patient population, and sodium and/or fluid restriction strategy, making the results difficult to interpret in aggregate.44 Some studies to date have shown potential benefits to reduce congestive symptoms, improve functional class, and reduce diuretic dose.20,46 Contrastingly, other studies have reported neurohormonal activation in response to sodium restriction in HF, demonstrating higher levels of hormones associated with renin-angiotensin-aldosterone system activation and worse renal function compared to those with more liberalized sodium intake.22,47 Potential mechanisms include intravascular volume depletion, decreased renal perfusion, and lower sodium delivery to nephrons; however, confounding by medication use cannot be excluded.44 Regarding hard outcomes, sodium restriction has been associated with increased hospitalizations and mortality, which may be confounded by the lower intake of calorie and micronutrients associated with the prescription of low-sodium diets.25,26 SODIUM-HF (Study of Dietary Intervention Under 100 mmol in Heart Failure) is an ongoing multicenter trial in ambulatory patients with chronic HF that will study the impact of a low-sodium diet on a composite of all-cause mortality, HF hospitalization, and/or HF emergency department visits (NCT02012179).

OBESITY.

Obesity, or excess body fat, is an independent risk factor for cardiovascular diseases such as hypertension, diabetes, and coronary artery disease that, in turn, promote the development of HF. Maintaining a healthy weight across the lifespan substantially decreases the risk of developing HF and among patients with obesity, weight loss through bariatric surgery reduces incident HF by 35%.27 As such, major HF guidelines recommend intentional weight reduction to reduce adiposity to lower the risk of incident HF.46 In addition, obesity is thought to play a pathogenic role in heart failure with preserved ejection fraction (HFpEF) specifically and is associated with distinct echocardiographic, hemodynamic, and cardiorespiratory fitness (CRF)-related attributes that differ from other HFpEF phenotypes.48 In a randomized trial of 100 patients with HFpEF and obesity, caloric restriction and/or aerobic exercise led to significant improvement in CRF with loss of body weight.28 However, in this study, patients had low severity of illness and impressive adherence to the intervention because meals were provided by the research team, which may not be generalizable. Whether these benefits can be achieved with real-world caloric restriction-induced weight loss without bariatric surgery remains unclear.

Despite the association between obesity and incident HF, numerous studies show a protective effect of class I or II obesity on survival in established HF, termed the obesity paradox.29 Whether measured by BMI, percent body fat, or waist circumference, overweight and obesity are consistently associated with improved short-term prognosis compared to normal or underweight. Even in those patients with HFpEF for which obesity may be pathogenic, overweight and obesity (classes I-III) were associated with improved survival in 2,501 ambulatory patients.30 Potential mechanisms include higher metabolic reserve, increased muscle mass, and improved CRF in those meeting BMI criteria for overweight or obesity.31 Of note, despite the potential benefit for survival, obesity is still associated with a greater risk for HF hospitalizations, which is counterintuitive given the association of HF hospitalizations with survival.49 Clearly, further studies are needed to elucidate these mechanisms.

MALNUTRITION: CARDIAC CACHEXIA AND SARCOPENIA.

In a recent meta-analysis including 12,537 patients, malnutrition, diagnosed using a variety of multidimensional assessment tools, more than doubled the risk for all-cause mortality in patients with HF (HR: 2.15; 95% CI: 1.89–2.45).7 Cardiac cachexia, or the unintentional loss of >5% of edema-free body weight over 6 to 12 months, is associated with a particularly poor prognosis in HF.50 Sarcopenia, or loss of muscle strength, quantity, and/or physical performance, is estimated at up to 20% prevalence in patients with HF and is associated with worse functional class, CRF, and quality of life.9 Given that sarcopenia may occur with excess fat mass, termed sarcopenic obesity, this consequence of malnutrition is highly likely to be missed.9 Proposed pathophysiologic mechanisms linking HF with the development of malnutrition and wasting are depicted in Figure 1.50

FIGURE 1. Pathophysiologic Mechanisms for Malnutrition and Wasting in Heart Failure.

FIGURE 1

Schematic representing of the pathophysiologic mechanisms involved in the development and progression of malnutrition and wasting in patients with HF, including inflammation, neurohormonal activation, and reduced intake and/or physical activity. CAF = C-terminal agrin fragment; GDF = growth differentiation factor; IL = interleukin; P3NP = N-terminal propeptide of type III procollagen; TNF = tumor necrosis factor.

Several dietary interventions have been trialed in patients with HF and malnutrition. The PICNIC (Programa de IntervenCión Nutricional en pacientes hospitalizados por Insuficiencia Cardiaca desnutrido) trial randomized 120 patients to a 6-month intervention involving diet optimization and/or nutrition supplement prescriptions, which resulted in a significant reduction in all-cause death or readmission for HF (HR: 0.45; 95% CI: 0.19–0.62).32 The NOURISH (Nutrition effect On Unplanned ReadmIssions and Survival in Hospitalized patients) trial randomized 652 malnourished hospitalized patients $65 years of age, 25% of whom had HF, to a protein supplement or placebo for 90 days.33 Although there was no difference in the primary endpoint of death or readmission, 90-day mortality was significantly lower in the supplement group (RR: 0.49; 95% CI: 0.27–0.90). Most recently, a secondary analysis of the EFFORT (Effect of early nutritional support on Frailty, Functional Outcomes, and Recovery of malnourished medical inpatients Trial) including 645 hospitalized patients with HF and malnutrition revealed that a dietitian-led inpatient intervention to reach daily calorie and protein goals was associated with lower all-cause 30-day mortality compared to control with a median intervention time of only 10 days (OR: 0.44; 95% CI: 0.26–0.75).34 Despite these results, there are no specific recommendations to treat malnutrition in the major HF guidelines, likely because of underdiagnosis and heterogeneity of intervention strategies to date.46 A suggested approach to the diagnosis and treatment of malnutrition in HF is depicted in Figure 2.50

FIGURE 2. Approach to the Management of Malnutrition in Heart Failure.

FIGURE 2

Suggested considerations for screening, diagnostics, and intervention with regard to malnutrition in heart failure. DXA = dual-energy X-ray absorptiometry; MR = magnetic resonance.

DIETARY PATTERNS.

Although there are no guideline recommendations to endorse a specific diet in the management of HF, there are data in support of specific dietary patterns. The most well researched are the DASH (Dietary Approaches to Stop Hypertension) and the Mediterranean diet, which entail a base of fruits, vegetables, whole grains, unsalted nuts, legumes, and seafood, as well as low intake of processed foods and red meats. In a cohort of more than 16,000 healthy adults enrolled in the REGARDS (REasons for Geographic and Racial Differences in Stroke) study, adherence to a plant-based diet was inversely associated with HF risk over 8.7 years of median follow-up (HR: 0.49; 95% CI: 0.41–0.86).35 Among those with established HF, women enrolled in the Women’s Health Initiative had lower mortality risk with greater adherence to the DASH diet in a dose-dependent manner (most adherent HR: 0.84; 95% CI: 0.70–1.00).36 In the GOURMET-HF (Geriatric Out-of-Hospital Randomized Meal Trial in Heart Failure) trial in which patients ≥65 years were randomized to 4 weeks of home-delivered DASH-compliant meals following an HF hospitalization, those randomized to the intervention experienced benefit with regard to symptoms, functional capacity, and hospitalizations.37 It is notable that in a study examining the impact of several dietary patterns on HF risk, certain patterns were associated with the development of heart failure reduced ejection fraction but not HFpEF (ie, a “Southern” high-saturated fat/high-sugar diet).35 Whether specific dietary patterns can be used for the precision prevention of HF based on etiology and other phenotypic features is an important subject for future research.51

MACRONUTRIENT AND MICRONUTRIENT SUPPLEMENTATION.

Micronutrient supplementation is a subject of great interest in HF, given the association between micronutrient deficiencies and poor outcomes.52 Micronutrient deficiencies in HF can result from inadequate dietary intake as well as urinary losses with diuretic agents.3,26 Although the quantity and quality of evidence for micronutrient supplementation in HF is highly variable, iron supplementation with iron deficiency is one strategy with a robust research base to date.38 Although oral iron supplementation does not improve clinical outcomes, intravenous iron has shown benefit for functional capacity and quality of life.38 To date, the evidence for improvement in mortality and hospitalization rates are less clear, although one trial is ongoing for these endpoints (FAIR-HF2 [Intravenous Iron in Patients With Systolic Heart Failure and Iron Deficiency to Improve Morbidity and Mortality; NCT03036462). The evidence for other micronutrient supplementation in HF is limited to date, and further large-scale trials are needed to establish their particular role in HF pathogenesis (Table 3).1,3,38,42,5254 Overall, it is likely that most micronutrient deficiencies can be mitigated by a well-rounded diet.

TABLE 3.

Key Micronutrient Deficiencies With Potential Involvement in HF Pathogenesis and Considerations for Supplementation

Micronutrient Deficiency Significance in HF Evidence for a Direct HF Benefit with Supplementatioa

Minerals
Calcium Most common micronutrient deficiency in HF52 Severe hypocalcemia (but not calcium deficiency) can lead to cardiac dysfunction53 Antioxidant activity Not applicable
Coenzyme Q Antioxidant activity
Deficiency associated with worse cardiac function and worse biomarker profile1
Reduction in major adverse cardiovascular events (all-cause mortality, cardiovascular mortality, and hospitalizations for HF) at 2-y follow-up in a randomized trial among patients with HFrEF and HFpEF42
Folate Common micronutrient deficiency in HF52 May consider supplementation if on diuretic agents and restricted diets3
Iron Iron deficiency anemia common and compounds reduced exercise capacity in HF38 Intravenous but not oral iron supplementation improved HF functional status, objective exercise capacity, and quality of life1,38
Magnesium Common micronutrient deficiency in HF52 May consider in high burden of ventricular arrhythmia or prolonged QT interval
Selenium Deficiency common in HF52 Severe deficiency can lead to reversible cardiomyopathy (Keshan disease) Some evidence for improvement in cardiac function with supplementation3
Zinc Common deficiency in HF52 Modulates oxidative stress Susceptible with angiotensin-converting enzyme and aldosterone receptor blockers associated with reduced serum zinc because of increased urinary excretion3 Trial results pending for a prospective study on zinc supplementation in nonischemic cardiomyopathy (NCT00696410)
Water-soluble vitamins
Vitamin B1 (thiamine) Common deficiency in HF52 Severe deficiency can lead to reversible cardiomyopathy (wet beriberi)
Susceptible with renal excretion of water-soluble vitamins in the setting of diuretic use3 Less common deficiency
Susceptible with renal excretion of water-soluble vitamins in the setting of diuretic use3
In select observational (n < 30) and randomized control trials (n < 50), thiamine supplementation improved ejection fraction1
Vitamin B6 (pyridoxine) Less common deficiency
Increased renal excretion of water-soluble vitamins in the setting of diuretic use3
May consider supplementation if on diuretic agents and restricted diets3
Vitamin B12 Less common deficiency
Increased renal excretion of water-soluble vitamins in the setting of diuretic use3
May consider supplementation if on diuretic agents and restricted diets3
Vitamin C Deficiency common in HF52 Oxidative stress is involved in the pathogenesis of HF, and vitamin C is an antioxidant1 May improve endothelial function in HF1
Fat-soluble vitamins
Vitamin D Lower vitamin D associated with increased mortality in HF1 No major improvements in symptoms or outcomes with supplementation
Susceptible with decreased exercise tolerance and less sun exposure May increase the incidence of mechanical circulatory support with supplementation (possible confounding by critical
illness)54
Vitamin E Oxidative stress is involved in the pathogenesis of HF, and vitamin E is an antioxidant1 Possible role in improvements in markers of oxidative stress1
Vitamin K Common deficiency in HF52 Not applicable
a

None of the micronutrients listed in this table are currently recommended for routine use with the exception of intravenous iron in cases of deficiency

HF = heart failure.

In terms of macronutrient supplementation, there have been data supporting a benefit with unsaturated fatty acid (UFA) supplementation. Supplementation with omega-3 polyunsaturated fatty acid (n-3 PUFA) has been shown to improve CRF, ejection fraction, and reduced rates of HF hospitalizations compared to placebo in randomized trials.55 In the GISSI-HF (Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto miocardico-Heart Failure) trial, >7,000 patients with HF were randomized to n-3 PUFA or placebo with a significant reduction in all-cause mortality over a mean follow-up of 3.9 years (HR: 0.91; 95% CI: 0.83–1.00).40 However, a recent meta-analysis demonstrated increased risk for incident atrial fibrillation with n-3 PUFA in patients with established or at high risk for cardiovascular disease (incidence rate ratio: 1.37; 95% CI: 1.22–1.54).43 Therefore, further studies, particularly in patients with HFpEF at highest risk for atrial fibrillation, are needed. UFA supplementation through dietary sources, such as extra-virgin olive oil, canola oil, and nuts, has also been demonstrated as a feasible and effective intervention to improve CRF in patients with HFpEF and obesity in a single-arm pilot study.41 A randomized controlled trial is ongoing (UFA-Presewrved2 [Unsaturated Fatty Acids to Improve Cardiorespiratory Fitness in Obesity and HFpEF]; NCT03966755). Finally, supplementation with amino acids and/or protein has shown modest benefits in CRF among patients with sarcopenia and/or cardiac cachexia, although to date this is not recommended routinely.1

CHALLENGES IN IMPLEMENTATION OF NUTRITIONAL INTERVENTIONS

As the body of evidence for nutrition interventions in HF continues to expand over time, it is important to recognize the challenges in implementation. In this section, we outline potential barriers and offer potential solutions that may improve the detection and management of nutrition disorders in HF (Table 4). Overall, it is likely that involvement of a multidisciplinary care team is the best approach to the care of complex nutrition-related disorders among patients with HF (Figure 3).

TABLE 4.

Barriers to Implementation for Nutrition Interventions in Heart Failure and Potential Solutions

Access Adherence Practicality Education

Patient-Level barriers Insurance coverage
Affordability of nutrition interventions
Preference for high-sodium foods
Cultural preferences at odds with prescribed nutrition interventions
Potential side effects of nutrition interventions (ie, nausea or diarrhea with supplements)
Time and financial investment associated with nutrition interventions Lack of nutrition education at all age levels
Lack of culturally sensitive nutrition education
Health care provider-level barriers Lack of nutrition-related resources
Insufficient number of trained dietitians
Lack of adherence measurement techniques Time limits preventing nutrition counseling
Lack of clear referral patterns to dietitians
Lack of nutrition education
Low awareness of certain nutritional disorders
Societal-Level barriers Disparities in access to care for those of racial and ethnic minorities
Disparities in insurance coverage Low availability of fresh fruit and vegetables Neighborhoods and regions designated as “food deserts”
Strong emphasis on pharmacologic and invasive solutions and lower emphasis on prevention Strong emphasis on efficiency in patient-provider interactions Lack of nutrition-related guidelines in HF
Potential solutions Programs to reduce racial and ethnic bias in nutrition- related HF care
Increase insurance coverage for effective nutrition interventions
Routine integration of registered dietitians into the development of HF clinical programs
Leverage remote delivery of meals
Programs to adapt diets consistent with patient preferences
Improve technologies to measure adherence
Incentives or compensation for physician nutrition counseling
Electronic medical record prompt for referral to dietitians
Telehealth dietitian visits
Patient education initiatives regarding the importance of nutrition
Nutrition education curricula in medical school
Specific nutrition-related HF guidelines

HF = heart failure.

FIGURE 3. Multidisciplinary Care Team for Nutrition Disorders in Heart Failure.

FIGURE 3

Suggested members of the multidisciplinary team and potential contributions for the care of patients with HF and nutritional disorders. HF ¼ heart failure.

EDUCATION.

A lack of population nutrition education may hinder the implementation of nutrition interventions in HF. In U.S. schools that offer nutrition curricula, of which there are few, those with long-term programs (≥1 year) have shown reduction in overweight/obesity among students.56 Culturally relevant nutrition education is necessary to make information more accessible for diverse populations. Additionally, from a provider standpoint, there is an overall lack of nutrition education in medical school and throughout postgraduate training. A meta-analysis of 24 studies from diverse countries reported that nutrition is insufficiently incorporated into medical education regardless of country, setting, or year of medical education, despite students’ desire to develop their skills in the field.57 Therefore, education reform is necessary from both the patient and provider standpoint to maximize the effectiveness of all dietary interventions in HF.

PRACTICALITY.

All health-related interventions, including those for nutrition, require time and financial investment. Types of interventions that have been studied to date include intensive inpatient interventions, meal preparation and distribution, prescription of supplements, and nutrition education and/or counseling, all of which vary widely in their practicality. In the outpatient setting, time constraints on provider-patient interactions may limit the time available to dedicate to nutrition counseling. Additionally, from a patient standpoint, nutrition interventions that require meal preparation and/or repeated in-person visits to the dietitian may be impractical in the context of other work- and family-related responsibilities.

ADHERENCE.

Measuring adherence is a major obstacle to determine the efficacy of any nutrition intervention, and there is no gold standard assessment tool. Methods that involve self-report are used most frequently, including 24-hour dietary recalls, 3-day food diaries, and food frequency questionnaires; however, these are subject to significant recall bias.58 Whether photography methods using mobile phone capabilities can be used as a more accurate measure of adherence is a subject of ongoing research. Measuring biomarkers that reflect recent intake is another candidate method; however, there are no validated protocols. In a recent pilot trial studying UFA supplementation in HFpEF, plasma UFA were measured to assess compliance and increased with reported intake of supplemental UFA, providing both memory-based and objective operator-independent measures of adherence.41

It is also important to consider patient-related barriers to adherence with nutrition interventions. In the NOURISH trial, despite finding a reduction in all-cause mortality with protein supplementation, 45% of participants self-reported <25% adherence.33 Potential reasons may include cultural and/or personal preferences that are inconsistent with prescribed diets. HF-related symptoms, such as nausea, fatigue, and low exercise tolerance, as well as non-HF-related conditions, such as depression and anxiety, may also contribute.59 Additionally, older patients with limited functional and/or cognitive capacity may be unable to acquire or prepare food that complies with dietary recommendations.

ACCESS.

Lack of access to resources that are necessary for a particular nutrition intervention may limit its efficacy. We must keep in mind disparities in access to quality care for racial and ethnic minority as well as socioeconomically disadvantaged populations that may limit access to nutrition-related resources. Previous studies have shown that community-level engagement targeting nutrition-related cardiovascular risk factors such as hypertension can be highly successful in high-risk minority populations.60 Other access issues include environmental factors such as neighborhood, which influences access to fresh fruits and vegetables, with large disparities in the distribution of such resources by location. For older adults with mobility disorders, the inability to travel because of physical or cognitive limitations must be considered. Lack of physician access to registered dietitians also limits the ability of patients with HF to receive adequate nutritional support.

CONCLUSIONS

Because of a lack of clinically accepted and reliable measures of nutritional status and ongoing controversy regarding the most effective interventions on a variety of nutritional disorders, nutrition-related recommendations are lacking in the current HF guidelines. Barriers related to education, practicality, adherence, and access on the patient, provider, and societal levels have also contributed. There is a need to develop multimodal dietary interventions involving HF, nutrition, metabolism, and implementation science so that we can most effectively target nutritional disorders to affect HF morbidity and mortality.

Supplementary Material

Supplemental document

HIGHLIGHTS.

  • Nutritional disorders are often overlooked in patients with heart failure because of a paucity of standardized definitions and accurate tools to assess nutritional status in this population.

  • Evidence is controversial for interventions targeting nutrition issues pertinent to patients with heart failure, including sodium restriction, obesity, malnutrition, dietary patterns, and micronutrient supplementation.

  • There are several patient, provider, and societal barriers to the implementation of effective nutrition interventions in the management of heart failure.

FUNDING SUPPORT AND AUTHOR DISCLOSURES

Dr Gallagher has received grant support from National Institutes of Health (UG3 DK128302-01, P30 DK26687-41 and 5T32DK007559-31). Dr Karmally is a health advisor at Sesame Workshop; and is a member of Heali Diet Advisory Group and a member of the Abbott Diversity Council. Dr Maddox has received grant funding from the National Institutes of Health National Center for Advancing Translational Sciences (1U24TR002306-01: A National Center for Digital Health Informatics Innovation); has received honoraria and/or expense reimbursement in the past 3 years from the Henry Ford health system (March 2019), the University of California, San Diego (January 2020), the University of Chicago (January 2021), George Washington University (January 2021), Baylor College of Medicine (April 2021), and the New York Cardiological Society (May 2021); has received compensation and travel expense reimbursement for American College of Cardiology leadership roles and meetings; is currently employed as a cardiologist and vice president of digital products and innovation at BJC HealthCare/Washington University School of Medicine, and in this capacity is advising Myia Labs, for which his employer is receiving equity compensation in the company (he is receiving no individual compensation from the company); and is a compensated director for a New Mexico-based foundation, the J.F. Maddox Foundation. Dr Hummel has grant support from the National Institutes of Health (R01-HL39813, R01-AG062582, R61-HL155498), American Heart Association (20-SFRN35370008), and Veterans Affairs Clinical Science Research & Development (CARA-009-16F9050); has received previous grant support from PurFoods, LLC; and has institutional support in the form of clinical trial funding from Pfizer, Novartis, Corvia, and Axon Therapeutics. Dr Carbone is supported by a Career Development Award (19CDA34660318) from the American Heart Association and by the Clinical and Translational Science Awards Program (UL1TR002649) from the National Institutes of Health to Virginia Commonwealth University. Dr Maurer has grant support from the National Institutes of Health (R01HL139671, R21AG058348, and K24AG036778); has received consulting income from Eidos, Prothena, Akcea, Alnylam, Intellia, and GlaxoSmithKline; and has received institutional support in the form of clinical trial funding from Pfizer, Ionis, Eidos, and Alnylam. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.

ABBREVIATIONS AND ACRONYMS

BMI

body mass index

CRF

cardiorespiratory fitness

DASH

Dietary Approaches to Stop Hypertension

FFM

fat free mass

HF

heart failure

HFpEF

heart failure preserved ejection fraction

n-3 PUFA

omega-3 polyunsaturated fatty acids

UFA

unsaturated fatty acids

Footnotes

The authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the Author Center.

APPENDIX For supplemental methodology, please see the online version of this paper.

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