Introduction

Nutrition is an important adjunct to medical therapy in cardiac disease. In patients with cardiac disease, nutrition can not only make the patient feel better but also can help to modulate the underlying disease. One concept that is becoming increasingly important is to feed animals with cardiac disease according to the underlying disease and individual patient characteristics. Not all dogs or cats with congestive heart failure (CHF), for example, are the same or require the same diet. Some patients with CHF will be overweight and some will have lost weight, some will be hypokalemic while others will be hyperkalemic, and a small number will have specific nutrient deficiencies. Therefore, the same diet will not meet the requirements of all patients with cardiac disease.

Nutritional Issues of Concern in Cardiac Disease

Body Composition

Cardiac cachexia, a loss of lean body mass, is common in patients with CHF and has deleterious effects on strength, immune function, and survival. Anorexia, increased energy requirements, and metabolic alterations all contribute to the syndrome of cardiac cachexia. However, the inflammatory cytokines (eg, tumor necrosis factor, interleukin-1) appear to be the primary mediators of cachexia. These cytokines directly cause anorexia, increase energy requirements, and loss of lean body mass. Therefore, a logical approach to treating patients would be to block these cytokines. One approach to reducing inflammatory cytokines is supplementation of fish oil, which is high in omega-3 fatty acids. Fish oil decreases cachexia and in some animals with CHF-induced anorexia, fish oil supplementation improves food intake.

Sodium

For patients in International Small Animal Cardiac Health Council (ISACHC) Stage 1, the author recommends < 100 mg/100 kcal sodium. Owners should be specifically counseled to avoid diets, treats, and table foods high in sodium. For ISACHC Stage 2, the goal should be for < 80 mg/100 kcal in the pet food. In ISACHC Stage 3, further sodium restriction may be useful. Controlling sodium intake from other foods (e.g., treats, table food, foods used for medication administration) is important as these can be major sources of sodium.

Potassium

Angiotensin converting enzyme (ACE) inhibitors and spironolactone can increase potassium retention and some animals receiving these drugs can develop hyperkalemia. As some commercial cardiac diets contain increased potassium concentrations, these diets can contribute to hyperkalemia.

Nutritional Deficiencies/Nutritional Pharmacology

Nutritional deficiencies are now uncommon (unless an animal is eating a homemade or otherwise unbalanced diet. However, there may be a number of examples in animals (e.g., taurine) which still are important. There also are some nutritional deficiencies that can develop secondary to the cardiac disease and its treatment. Finally, supplementing certain nutrients may provide benefits above and beyond their nutritional effects (i.e., nutritional pharmacology). It is not always clear whether the benefits of a nutrient are the result of correcting a deficiency or pharmacologic effects.

Restriction of dietary protein intake used to be made for animals with CHF. However, there is no evidence that protein restriction is necessary for patients with CHF and, in fact, it probably is deleterious since these patients are predisposed to loss of lean body mass. Unfortunately, some clinicians recommend a renal diet for patients with heart disease because many renal diets are restricted in sodium. Unless severe renal dysfunction is present, high-quality protein should be fed to at least meet canine (5.1 g/100 kcal) or feline (6.5 g/100 kcal) maintenance requirements.

There has been a dramatic reduction in cases of feline dilated cardiomyopathy (DCM) since the late 1980's when increased dietary supplementation of taurine of commercial foods was instituted. Most of the current cases of feline DCM are not taurine deficient but taurine deficiency should be suspected in all cases of feline DCM. Cats that have been fed a poor quality, homemade, vegetarian, or otherwise unbalanced diets are at risk for taurine deficiency. Taurine deficiency may be present in some dogs with DCM. Typical breeds (e.g., Dobermans, Boxers) are highly unlikely to be taurine deficient. I currently recommend measuring plasma and whole blood taurine concentrations in dogs with DCM that are of high risk (e.g., Cocker spaniel, Newfoundland, golden retriever, Newfoundland) or atypical (e.g., Corgi, Bassett hound) breeds. In addition, taurine concentrations should be measured in dogs with DCM that are eating lamb meal and rice-based diets, high-fiber diets, or diets that are highly protein restricted. Although the extent of benefits of supplementation is not yet clear, I recommend taurine supplementation until plasma and whole blood taurine concentrations are available. The optimal dose of taurine for correcting a deficiency has not been determined, but the dosage currently recommended is 250 to 1000 mg q 8–12 hrs.

The omega-3 polyunsaturated fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are normally in low concentrations in the cell membrane but levels can be increased by a food or supplement enriched in omega-3 fatty acids. There are a number of potential benefits of omega-3 fatty acids, including a reduction in inflammation, improvement in appetite, and suppression of arrhythmias. Fish oil supplements (fish oil concentrate capsules with vitamin E but no other ingredients at a concentration of 180 mg EPA + 120 mg DHA per 1 gm capsule) can be prescribed at a dose of 1 capsule/10 pounds body weight. Flax seed oil or cod liver oil should not be used.

Some cardiac medications are associated with magnesium depletion so animals with CHF can be at increased risk for hypomagnesemia. Hypomagnesemia can increase the risk of arrhythmias, decrease cardiac contractility, cause muscle weakness, contribute to renal potassium loss, and can potentiate the adverse effects of certain cardiac medications. Animals with low serum magnesium concentrations should be fed a diet higher in magnesium or may require magnesium supplementation.

General Dietary Issues for Animals with Cardiac Diseases

The process of choosing an optimal diet for a patient with cardiac disease involves evaluation of the patient, the diet, and the owner's feeding practices. Generally, there is not a single "best" diet for all animals with cardiac disease. What might be the best diet for one patient may be contraindicated in another. So, it is important to assess a number of factors to determine which diet or diets might best suit a particular patient.

The Patient

In general, the nutrients of concern in cardiac patients are calories, sodium and chloride, protein, potassium, and magnesium. However, patients with cardiac disease vary tremendously in terms of their clinical signs, laboratory parameters, and food preferences and these will all affect diet selection. For example, cats with asymptomatic heart disease require less severe sodium restriction than those with CHF. Overweight dogs require a less calorically dense diet than would a dog with weight loss and/or muscle wasting. Laboratory results (e.g., hypo- vs hyperkalemia) and concurrent diseases also influence diet choice.

The Diet

Based on these and other patient parameters, a diet or diets can be matched to the individual patient. For example, in an animal with cardiac disease without CHF (e.g., an asymptomatic cat with hypertrophic cardiomyopathy), I recommend only mild sodium restriction and counsel the owner to avoid diets, treats, and table foods high in sodium. Most owners are unaware of the sodium content of pet and human foods and need very specific instructions for which foods are appropriate. When CHF first arises, additional sodium restriction is recommended.

Feeding Practices

Meeting the owner's expectations in terms of diet is important for animals with cardiac disease. Their pet's quality of life is of tremendous importance to owners so providing diets that are palatable and readily eaten is critical. Some animals receive treats and some (although not as many for cats as for dogs) receive their medications with "people food." Including this information in the overall diet plan is important to achieve success with nutritional modification. Also, cost preferences should be considered as veterinary therapeutic diets may be out of the price range for long term use by some owners; in this case, lower priced alternatives should be offered.

Key Points

 Optimal nutrition is an important part of the overall medical treatment for animals with cardiac disease.

 Alterations in body composition are common and important issues in patients with heart failure and can negatively affect the outcome and quality of life.

 Every patient with cardiac disease should have a thorough nutritional assessment to determine whether the overall diet is optimized. This includes the main pet food being provided, but also treats, table food, dietary supplements, and medication administration.

 Careful monitoring and clear client communication are key to optimal outcomes in patients with cardiac disease.

References

1.  Freeman LM, Rush JE. Nutritional management of cardiac disease. In: Ettinger SJ, ed. Textbook of Veterinary Internal Medicine. 7th ed. St Louis: Elsevier; 2010: 579–583.

2.  Freeman LM, Rush JE. Nutritional management of cardiovascular diseases. In: Fascetti AJ, Delaney S, eds. Applied Veterinary Clinical Nutrition. West Sussex: Blackwell; 2012:301–313.

3.  Freeman LM. Beneficial effects of omega-3 fatty acids in cardiovascular disease. J Small Anim Pract. 2010;51:462–470.

4.  Freeman LM. Cachexia and sarcopenia: Emerging syndromes of importance in dogs and cats. J Vet Intern Med. 2012;26:3–17.

5.  Tufts HeartSmart website (information on heart disease for pet owners, including nutrition). www.tufts.edu/vet/heartsmart

6.  WSAVA Nutritional Assessment Guidelines Taskforce: Freeman L, Becvarova I, Cave N, MacKay C, Nguyen P, Rama B, Takashima G, Tiffin R, Van Beukelen P, Yathiraj S. 2011 Nutritional Assessment Guidelines. J Small Anim Pract. 2011; 52: 385–396.