Diet and Nutrition

Excessive dietary sodium intake is a common proximate cause of worsening symptoms and hospitalization for HF exacerbation.1-3 Furthermore, dietary sodium restriction typically results in a decrease in the diuretic dose required for maintenance of a euvolemic state and clinical stability. This is important because loop diuretics increase plasma renin activity and may adversely impact clinical outcomes through neurohormonal stimulation.4 Studies of sodium restriction indicate an impact on such parameters as quality of life and even functional status,5 but not mortality. Despite limited clinical trial data, sodium restriction remains an important and common component of HF disease management programs.6

The "average" American diet contains between 8,000 and 10,000 mg sodium; certain ethnic diets are typically several-fold higher. (See Table 3.2 in Section 3 for salt-sodium equivalents.) A "low-sodium" or "no added salt diet" as defined by the American Heart Association is 4000 mg sodium. The current recommendation from the American Heart Association and the United States Department of Agriculture (USDA) for the general population is to limit sodium intake to 2300 mg per day, while the current USDA recommendation for those with hypertension, blacks and middle-aged and older people is 1500 mg per day for hypertension prevention.7 Thus, although there remains no evidence about the ideal level of sodium restriction in patients with HF because of lack of studies on this topic, it is reasonable to recommend that sodium intake be limited to 2000-3000 mg per day.

Because following a low sodium diet is a specific activity, greater patient success can be expected when the clinician provides the patient with a daily sodium intake target and the knowledge and skills to reach that target. It is not enough to simply ask patients to follow a low salt diet. Nor is it sufficient to advise not salting food at the table or while cooking as most (~70%) of our daily sodium intake comes from processed and pre-packaged foods. Appropriate education and counseling regarding the 2000-3000 mg sodium diet recommendation is covered in Section 8.

Additional dietary instruction should be provided to all patients with HF who have comorbid conditions, including arteriosclerosis, diabetes, renal insufficiency, or obesity. Patients with hyperlipidemia or known underlying coronary or peripheral arteriosclerosis should be given specific instruction regarding dietary fat and cholesterol restriction according to national guidelines, such as the National Cholesterol Education Program. Diabetics exhibiting poor glycemic control or with significant albuminuria should receive individualized nutritional counseling regarding protein and carbohydrate consumption and caloric constraints as indicated to reduce risk for morbidity and mortality. Aggressive management of hyperglycemia diminishes osmotic forces leading to water retention and glomerular hyperfiltration, while reducing infection risk and the long-term risk of additional end-organ damage.8 Patients with significant underlying renal insufficiency may require individualized instruction regarding protein, potassium, phosphorus, or other dietary constraints to preserve electrolyte and acid-base homeostasis.

Obesity is independently associated with HF and contributes to the development of additional HF risk factors, including hypertension, LV hypertrophy and diastolic filling abnormalities. Obesity is linked to insulin resistance and glucose intolerance, hyperaldosteronism, salt sensitivity, and plasma volume expansion, creating both pressure and volume overload stressors with increased systemic vascular resistance. The metabolic demand of excessive adipose tissue increases cardiac output requirements, making cardiomyopathy with HF the leading cause of death in patients with severe obesity. Arrhythmia risk is increased in association with prolongation of the QT interval frequently seen in the setting of morbid obesity. Sleep-disordered breathing is linked to pulmonary hypertension, right ventricular failure, and hypoxemia. For both obesity-cardiomyopathy and obesity-hypoventilation syndromes, weight loss and sodium restriction are effective measures to improve symptoms and prognosis.9

A number of recent studies evaluating the relationship between body mass index (BMI) and mortality have suggested that overweight (BMI 25-29.9 kg/m2) and obese (BMI >=30 kg/m2) people with HF have a better survival than healthy weight people (BMI 18.5-24.9 kg/m2) with HF.10-13 Reasons for this "obesity paradox" remain unexplained. Low BMI (<18.5 kg/m2) subjects with HF appear to have the highest mortality.11-14 At least one study suggests that severely obese subjects (BMI >=35 kg/m2) also have a higher mortality than normal weight or mild to moderately obese people with HF, resulting in a "J" shaped curve for the BMI-mortality relationship.14

When risk of death was assessed in 359,387 people from the general population using BMI, waist circumference and waist-hip ratio, general and abdominal obesity were associated with risk of death.15 In patients with HF, central adiposity, assessed by waist-hip ratio, but not BMI, was predictive of all-cause mortality independent of age and gender.16 Of note, waist-hip ratio was more strongly associated with LV diastolic function as well. After adjustment for LVEF and diastolic function, waist-hip ratio was no longer a risk factor for mortality. Thus, ventricular dysfunction may be an important mediating factor between waist-hip ratio and mortality.16 Another explanation for the "obesity paradox" may be that it is the change in weight over time, not the specific weight at any given time, that predicts mortality. Normal weight people with HF may have been overweight or obese and are actively losing weight.11 It is also possible that HF is detected earlier in overweight and obese people due to symptom exacerbation caused by excess weight.12 Other explanations include the use of higher doses of beneficial medications or the benefits of elevated TNF-? receptor levels in the obese.17,18 Although it seems unlikely that there is a beneficial effect of obesity in people with HF, the explanation for the "obesity paradox" remains uncertain. Until further data are available, caloric restriction as part of the treatment of the severely obese patient with HF and weight stabilization or reduction in overweight and mildly obese patients seems reasonable.

There are defined risks of extreme calorie and carbohydrate restriction that may be increased in patients with HF. Electrolyte abnormalities and ketosis may occur with these diets and require frequent monitoring and physician oversight.

For HF patients with a BMI >35, gastrointestinal surgery is an option, with operative risk dependent on clinical symptoms, hemodynamic stability, and stability of coronary artery disease.19 Surgical intervention is the only weight loss therapy with reasonable long-term result maintenance, although operative morbidity and mortality are substantial.20 One recent study found that weight reduction after bariatric surgery in subjects with morbid obesity may reverse LV hypertrophy.19 Preliminary data also suggest that in subjects with morbid obesity and reduced systolic function, bariatric surgery may lead to improvements in cardiac function.21-23 It is therefore a consideration in morbidly obese patients for whom all other weight loss measures have failed.

Fluid restriction is indicated in the setting of symptomatic hyponatremia (serum sodium <130 mEq/L), whether or not it is precipitated by pharmacologic therapy. Concomitant dietary sodium restriction facilitates maximal diuresis and may reduce hospital length of stay. In the outpatient setting, fluid restriction generally is reserved for advanced HF refractory to high doses of oral diuretic agents. Fluid restriction in the outpatient setting has many inherent logistical difficulties, often leading to increased stress, anxiety, and poor adherence with therapy. Most disease management programs monitor patient volume status reliably and effectively through the attainment of daily morning weight, rather than through patient measurement of daily intake and output.24

Apparent diuretic refractoriness is most often a reflection of nonadherence with dietary sodium restriction or prescribed pharmacologic therapy, unrecognized drug interactions (eg, nonsteroidal anti-inflammatory agents [NSAIDs] and glitazones) or the uncommon patient with excessively high fluid intake (>6 L/day). Physiologic diuretic refractoriness can be observed with chronic loop diuretic administration, primarily from distal renal tubular hypertrophy that facilitates enhanced sodium reabsorption. On the other hand, "true" diuretic refractoriness may reflect underlying disease progression with reduced cardiac output and effective renal plasma flow, development of significant intrinsic renal insufficiency, or nephrosis.

Cardiac cachexia is a well-described phenomenon that is associated with intense activation of the cytokine, tumor necrosis factor-α, or chronically low cardiac output states. Similar features are observed in patients with terminal cancer, acquired immunodeficiency syndrome (AIDS), and chronic inflammatory diseases. Such patients are at extremely high risk for serious morbidity, such as infection, hospitalization and impaired wound healing.

In HF patients with reduced LVEF, tumor necrosis factor-α, levels are highest in advanced disease and correlate with the highest risk of mortality. Formal metabolic evaluation and determination of minimal nutritional requirements should be strongly considered for patients demonstrating this muscle-wasting syndrome. Specific recommendations have been made for these patients, including altering the size and frequency of meals and ensuring a high-energy diet.25

There are no data to support the use of anabolic steroids or human growth hormone supplementation in patients with cardiac cachexia and skeletal muscle wasting. Initial enthusiasm for this approach was based on data suggesting that small doses of testosterone have a beneficial effect on dysfunctional myocardium.26 However, long-term exposure to these compounds has been reported to increase ischemia risk and to promote adverse ventricular remodeling risk. Fluid retention and electrolyte abnormalities are frequently observed with the use of this therapy. Additional serious risks include increased thrombogenicity and erythrocytosis, as well as benign prostatic hypertrophy and prostate cancer.

Based on research, dietary guidelines for individuals at risk for developing HF are more established than for those who already have the condition.27 Balanced nutrition with multivitamin/mineral supplementation to fulfill the recommended daily value of essential nutrients is prudent for persons with any chronic disease, including HF. Multivitamin/mineral supplementation may offset nutritional imbalances from early satiety and altered digestive efficiency related to decreased absorption, enhanced water-soluble vitamin and mineral loss from diuretic administration, and increased utilization due to oxidative stress.28 It should also be recognized that population-related issues, such as old age or other chronic conditions, rather than HF itself, can be responsible for nutritional deficiencies in patients with HF.29

In general, for most patients with HF, a prudent diet providing adequate protein, carbohydrate, and calories according to age, gender, and activity level is advisable. Dietary supplementation consisting of a daily multiple-vitamin should be considered, given that most American diets are inadequate in providing the recommended basic nutrient requirements.

Studies estimate that approximately 50% of patients with HF consume herbal, megavitamin, or other dietary supplements.30 The likelihood of an adverse reaction or vitamin toxicity increases with consumption of multiple supplements, the safety and efficacy of which are not well documented. It is therefore important to ask patients with HF about supplements they are already taking before recommending a daily multiple vitamin.

Naturoceutical use cannot be recommended for the relief of HF symptoms or for the secondary prevention of cardiovascular events. Given the paucity of efficacy data about naturoceutical products, reporting suspected adverse effects or drug interactions to the Food and Drug Administration is strongly encouraged.

There are several agents with documented potential to do harm. Natural or synthetic catecholamine-like products containing ephedra (ma huang), ephedrine metabolites, or imported Chinese herbs are specifically contraindicated in HF. Hawthorne (Cratageus) products appear to have inodilator activity, increasing the risk of orthostatic hypotension and possibly arrhythmia. Hawthorne potentiates the action of vasodilator medications and increases serum digoxin levels. One recent long-term placebo-controlled trial failed to show any incremental benefit when hawthorn extract was given with standard drug therapy to patients with chronic HF. It did show, however, that the drug appeared safe to use with angiotensin converting enzyme (ACE) inhibitors, beta blockers, and other standard HF medications.31 Many other naturoceutical products, including garlic, gingko biloba, and ginseng, have antiplatelet effects or potential anticoagulant interactions.32