A 56-year-old woman was brought to the cardiologist office for routine clinical examination. The patient showed signs of peripheral edema, denied dyspnea, New York Heart Association functional class II, and was on the following cardiac medications: angiotensin-converting enzyme (ACE) inhibitors, beta blockers, statins, mineralocorticoid receptor antagonists, and furosemide. Her focused past cardiac history is that of a prior myocardial infarction, coronary artery bypass surgery, prior heart failure hospitalizations, and a known ejection fraction of 35%. She also notes medical compliance but not dietary compliance and does not feel that her muscle strength is being maintained. Serum electrolytes were: sodium, 140 mmol/L; potassium ranges from 4.9 to 5.8 mmol/L; and creatinine, 62 μmol/L. The woman’s weight was 80 kg; height was 169 cm; body mass index (BMI) was 28 kg/m². She and her clinical team wonder if a better focus on diet may play a role.

Chronic heart failure (HF) is a major and growing public health problem, with a tremendous impact on patients’ quality of life and a broader economic burden. Approximately 5.7 million Americans ≥20 years of age have HF, and prevalence has been projected to increase 46% from 2012 to 2030 as patients survive acute myocardial infarction, live to an older age, and have best medical and nonpharmacologic care available. Survival after HF diagnosis has improved over time; however, HF carries a 5-year mortality rate of ~50% after diagnosis, and total direct medical cost of HF was estimated to be $21 billion in 2012.

HF is a clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood.¹ The most common etiologies are ischemic heart disease, hypertension (HTN), and diabetes. Less common causes of HF are cardiomyopathies, infections (eg, viral myocarditis, Chagas disease), toxins (eg, alcohol, cytotoxic drugs), valvular disease, and prolonged arrhythmias.²

HOW DOES DIET PLAY A ROLE IN HEART FAILURE?

HF may be associated with reduced cardiac output, which leads to a decrease in mean arterial pressure and diminished renal perfusion and causes to neurohormonal activation characterized by an overexpression of the sympathetic nervous system and the renin angiotensin aldosterone system to maintain optimal tissue perfusion to vital organs. This set of complex compensatory mechanisms causes vasoconstriction and renal sodium and water retention. Chronic neurohormonal activation exacerbates the hemodynamic abnormalities present in HF, producing further remodeling and neurohormone release and progressive cardiac impairment, causing excessive sodium and fluid retention.^2,3 This pathophysiologic process is in part responsible for HF signs and symptoms such as dyspnea and fatigue, which may limit exercise tolerance, and fluid retention, which may lead to pulmonary congestion and peripheral edema, all of which affect functional capacity and quality of life.¹

DIETARY SODIUM INTAKE

Patients with chronic HF often have exacerbations requiring an emergency department visit and/or a hospital admission—often precipitated by excess sodium intake.⁴ Recognizing the importance of achieving sodium balance in HF, dietary sodium restriction has been suggested as a major component of self-care management in HF. Dietary sodium recommendations for HF management typically call for a reduction in dietary sodium, because most individuals consume excessive amounts of dietary sodium. However, there is a lack of consistency for dietary sodium intake recommendations among the major guidelines for the management of HF.^1,5-10 Recommendations provided by the Canadian Cardiovascular Society (CCS),⁵ the Heart Failure Society of America (HFSA),⁶ the National Heart Foundation of Australia, and the Cardiac Society of Australia and New Zealand,⁸ range from less than 2000 mg to 3000 mg per day, without identifying any safe lower level of consumption; whereas the National Institute for Health and Care Excellence (NICE),⁷ the European Society of Cardiology (ESC),⁹ and the American College of Cardiology and the American Heart Association (ACC/AHA),¹ on their most recent guidelines for the management of HF, do not provide any precise recommendation for sodium restriction.

Inconsistency in dietary sodium recommendations for HF is due to a lack of conclusive evidence on the impact of decreased dietary sodium on clinical events in the HF population.^3,11 Additionally, it has been suggested that a low-sodium diet may have detrimental effects in patients with HF due to its association with further neurohormonal activation in these patients.¹¹

Clinical Studies on Sodium Restriction in Heart Failure

During the last decade, both observational and experimental studies evaluating the effects of sodium restriction in HF population have shown mixed results.³ A small clinical trial suggested that a sodium intake less than 1500 mg/day may have a beneficial impact on B-type natriuretic peptide (BNP) levels and quality of life in ambulatory patients with chronic HF on optimal medical treatment.¹² However, 3 of the largest randomized controlled trials (RCTs)^13-15 testing the effects of sodium restriction on outcomes in HF showed that among patients with systolic HF, a low-sodium diet (80 mmol [1800 mg] sodium/day) was associated with higher mortality and readmission rates compared with a moderate-sodium diet (120 mmol [2800 mg] sodium/day) in combination with an aggressive diuretic regimen (250-1000 mg/day of furosemide) and fluid restriction (1 L/day). Though these trials tested the effect of dietary sodium restriction, the concomitant treatments administered make it challenging to elucidate the independent effects of dietary sodium on clinical outcomes. The aggressive doses of loop diuretics and fluid restriction likely also resulted in hypovolemia, which explains the adverse outcomes observed.

Overall, there are limitations to the quality of clinical and observational data that limit their use in developing evidence-based clinical practice guidelines. These include clinical studies that have small sample sizes and that administered aggressive cointerventions that prohibit the independent analysis of the effect of sodium restriction on clinical outcomes, making it challenging to compare data and draw definitive conclusions. However, a sodium restriction between 2000 and 3000 mg/day appears to be safe in this patient population, based on expert concensus. Further reduction to less than 1500 needs to be tested in large pragmatic RCTs.³

How Do We Assess Sodium Intake in Heart Failure?

Sodium restriction is a recommended dietary strategy for patients with symptomatic HF to reduce congestive symptoms.^1,9 Therefore, estimating dietary sodium intake is a key component of the dietary assessment in the clinical setting of HF to effectively implement appropriate dietary interventions for sodium reduction and monitor adherence to the dietary treatment. Current available sodium intake assessment methods include 24-hour urine collection, spot urine collections, multiple-day food records, food recalls, and food frequency questionnaires. Some of these methods have questionable validity at estimating individual intakes (ie, spot urine collection), require moderate to high participant burden, and do not provide timely feedback to guide dietary counseling in the clinical setting. Importantly, HF-related factors, such as the use of loop diuretics, may impede the utility of 24-hour urinary sodium excretion for estimating sodium intake in this patient population, and its use should be discouraged in the context of patients with HF on diuretics.^16,17 The use of high-quality dietary surveys, such as 3-day food records, might be an alternative to overcome this issue. Future research in this area is needed in order to identify the best method to assess dietary sodium intake in patients with HF.

WHAT ABOUT FLUID INTAKE?

Routine strict fluid restriction in all patients with HF regardless of symptoms or other considerations does not appear to result in significant benefit. Fluid restriction of 1.5 to 2 L/day may be considered in patients with severe HF, especially in those with hyponatremia, to relieve symptoms and congestion.^1,9

ARE THERE OTHER DIETARY STRATEGIES TO CONSIDER BEYOND SODIUM?

Energy and Protein

Total energy expenditure in healthy subjects is the sum of resting energy expenditure (REE) and energy expenditure induced by physical activity. In patients with chronic HF, compared to healthy subjects, the REE is initially increased about 10% due to hypermetabolism,¹⁸ which should be considered when estimating energy requirements in these patients; however, it is important to consider that physical activity may also be decreased in these same patients.

Negative calorie and nitrogen balances have been reported in patients with chronic HF, despite having similar calorie and nitrogen intakes, as compared to controls, suggesting that HF is a hypercatabolic state requiring increased calorie and protein needs. Therefore, it has been recommended that clinically stable malnourished patients with chronic HF have a daily intake of at least 31.8 kcal/kg + 1.37 grams protein/kg, and normally nourished patients a daily intake of at least 28.1 kcal/kg + 1.12 grams protein/kg in order to preserve their body weight and lean body mass, limiting the effects of hypercatabolism.¹⁹

Fats

The relationship of dietary fats to clinical outcomes or biochemical measures in patients with HF is scarce. Given that one of the most important risk factors for HF is coronary heart disease (CHD), the general dietary recommendations to reduce saturated fat intake for CHD risk reduction may be extrapolated to the HF population.²⁰ Current American Heart Association recommendation for saturated fat intake for cardiovascular risk reduction is to aim for a dietary pattern that achieves 5% to 6% of calories from saturated fat.²¹ Additionally, there is increasing interest on the effects of omega-3 polyunsaturated fatty acids (n-3 PUFAs) in patients with HF. Results of the GISSI-HF trial, the larger clinical trial assessing the effects of n-3 PUFAs in HF, suggested a modest survival advantage from dietary supplementation with 1 g/day of n-3 PUFAs on mortality and cardiovascular hospital admission in patients with HF.^22,23 However, recent clinical trials and meta-analysis have not shown clear evidence of benefit from the supplementation with n-3 PUFAs on mortality in patients at risk for or with established cardiovascular disease (CVD).^24,25 Therefore, even though its supplementation seems to be reasonable as adjunctive therapy in patients with chronic HF, there is still a need to better define optimal dosing and formulation of omega-3 PUFA supplements.¹

Micronutrients

There is concern that micronutrient needs may be higher in patients with HF compared to the general population due to oxidative stress.²⁶ Also, use of prescribed HF medications, such as loop diuretics, may alter the requirements of certain nutrients due to increased urinary excretion of thiamine, potassium, magnesium, and calcium.²⁷ It is important to consider that if a potassium-losing diuretic is used in combination with an ACE inhibitor and a mineralocorticoid receptor antagonist (MRA) or an angiotensin receptor blocker (ARB), potassium replacement is usually not required. Also, serious hyperkalemia may occur if potassium-sparing diuretics or supplements are taken in addition to the combination of an ACE inhibitor (or ARB) and MRA.⁹

In order to prevent serious micronutrient deficiencies, it is important to ensure that patients meet the Dietary Reference Intake (DRI) for micronutrients,^28,29 especially for those most likely to be deficient in patients with HF, as described below (Table 25-1). Currently, the most recent ACC/AHA guidelines do not recommend nutritional supplements in the treatment of HF.¹

MICRONUTRIENT DEFICIENCY IN HEART FAILURE

Dietary inadequacies (eg, calories, protein, and several vitamins and minerals) are common in patients with HF.^30-36 It has been shown that more than 50% of HF patients have inadequate dietary intakes of several nutrients, including calcium, magnesium, potassium, folate, vitamin E, vitamin D, and zinc.^30,37 Factors associated with deceased food intake in this patient population include decreased hunger sensations, fatigue, shortness of breath, nausea, anxiety, sadness, and medically recommended diet restrictions.^38,39

A dietary sodium consumption of <2000 mg/day has also been linked to poor overall nutrient intake in these patients.^40,41 A sodium-restricted diet is often described as unpalatable and subsequently related to decreased appetite, leading to higher risk of poor nutritional intake.³⁸ It was reported that among patients who were prescribed a <2000 mg/day sodium-restricted diet for 1 week, a 49% reduction in dietary sodium (3626-1785 mg/day) was associated with a significant reduction in calorie, carbohydrate, calcium, thiamine, and folate intakes. Also, there was a decrease in saturated fat.⁴² However, results of a recent study suggested that dietary sodium reduction in these patients may be achieved without greatly compromising overall dietary intake and nutritional status when an individualized dietary approach, considering the whole diet, is used. Nonetheless, calcium intake was still negatively affected.⁴³