Nutritional Management of Heart Disease

Chapter 168

Nutritional Management of Heart Disease

General Nutritional Issues for Animals with Heart Disease

For many years the role of nutrition in the management of heart disease consisted primarily of feeding a low-sodium diet. We now know that severe sodium restriction is not necessary in all animals with heart disease. It also is becoming apparent that supplementation of certain nutrients, either to correct a deficiency or to provide pharmacologic effects, may have profound benefits in animals with heart disease. Research now is beginning to show that nutrition can modulate heart disease by slowing the progression, minimizing the number of medications required, improving quality of life, and in rare cases actually curing the disease. Therefore attention to diet at all stages of heart disease is critical for optimal care of the cardiac patient.

A single diet does not work for all animals with heart disease, and dietary modifications need to be individualized. Patients with heart disease vary in their clinical signs, laboratory parameters, and food preferences, all of which affect diet selection. For example, more severe sodium restriction would be required for a cat with congestive heart failure (CHF) than for a cat with asymptomatic heart disease. Animals with heart disease may be hyperkalemic, hypokalemic, or normokalemic, which influences the choice of diet. Concurrent diseases also alter diet choice and are present in many animals with heart disease (61% of dogs and 56% of cats) (Freeman et al, 2003; Torin et al, 2007).

Based on patient characteristics, one or more diets can be selected. Currently at least two commercial veterinary cardiac diets are available in the United States. The specific characteristics of each diet differ, but both are moderately to severely sodium restricted (i.e., 17 to 50 mg/100 kcal). One cardiac diet also includes supplemental taurine, carnitine, arginine, antioxidants, and omega-3 fatty acids.

In some cases a veterinary diet designed for another disease or an over-the-counter diet may have the nutritional properties desired for an individual patient. Having a number of choices is particularly beneficial for animals with severe CHF, a condition in which loss or change of appetite is common. I generally try to recommend multiple diets so the owner can determine which is most palatable to the pet.

In addition to the pet food selected, the owner also must receive careful instructions on treats and table food. In some cases animals may be eating an ideal pet food but are obtaining large amounts of sodium from treats. Over 90% of dogs and 30% of cats with heart disease received treats (Freeman et al, 2003; Torin et al, 2007). Examples of appropriate treats are given in Table 168-1. Including all sources of dietary sodium in the overall diet plan is important to achieve success with nutritional modifications.

Although a diet must be selected based on desired nutritional properties and palatability, it also is important to devise an overall dietary plan that includes an effective method for administering medications. Most dog owners (57%) and many cat owners (34%) use food for medication administration, and the most commonly used foods are high in sodium (e.g., cheese, hot dogs, lunch meats) (Freeman et al, 2003; Torin et al, 2007). Therefore examples of appropriate methods for administering medications should be provided (Box 168-1).

All dietary changes should be made gradually over a period of 3 to 5 days. However, major dietary changes should not be instituted while the patient is sick or hospitalized. Usually it is better to wait several days until the patient’s condition has improved before initiating the change. Food aversions may develop and prevent adequate intake of the food over the long term. It also is important to instruct the owner to notify the veterinarian if the patient does not eat adequate amounts of the new food so that other options can be devised.

Nutritional Modifications Based on Severity of Disease

Asymptomatic Heart Disease

Over the years, recommendations for nutritional therapy for dogs and cats with asymptomatic heart disease have resembled a pendulum. Initially very-low-sodium diets were recommended when a heart murmur was first detected. Veterinarians then moved toward the approach that severe sodium restriction may not be ideal at this stage of disease because of early activation of the renin-angiotensin-aldosterone (RAA) system. This led to the idea that no nutritional modifications can or should be made for animals with asymptomatic heart disease. Veterinarians are now swinging back toward the middle because new research is supporting the idea that dietary modification in early heart disease might be beneficial and the nutritional management of animals with asymptomatic heart disease should not be ignored.

One of the earliest and major compensatory responses in heart disease is activation of the RAA system, and sodium restriction can further elevate renin, angiotensin, and aldosterone concentrations. Thus severe sodium restriction in animals with early heart disease theoretically could be detrimental by triggering early and excessive activation of the RAA system. I recommend only mild sodium restriction in asymptomatic heart disease (<100 mg/100 kcal for animals with International Small Animal Cardiac Health Council [ISACHC] class 1a or 1b heart disease; see Chapter 176). However, this is also an opportune time to begin talking to the owner about the animal’s overall dietary patterns (e.g., the pet’s food, treats, table food, and methods of administering medications), since it is generally much easier to institute dietary modifications when the animal is asymptomatic.

In addition to mild sodium restriction, another important goal is to achieve or maintain optimal body condition. Goals for body condition in animals with CHF may be different (see later), but in asymptomatic heart disease, veterinarians should assess the animal’s body weight, body condition score, and muscle condition score at every visit as part of nutritional screening (which should be performed on every patient at every visit [World Small Animal Veterinary Association, 2011; World Small Animal Veterinary Association website]). If the animal is above the weight for an optimal body condition, a gradual and comprehensive weight-loss program should be instituted with careful monitoring.

Finally, there is the potential for benefit from nutritional modification in the asymptomatic animal. One study compared a moderately reduced-sodium cardiac diet that was enriched with omega-3 fatty acids, antioxidants, arginine, taurine, and carnitine with a placebo diet in dogs with asymptomatic chronic valvular disease (CVD) (Freeman et al, 2006). The cardiac diet increased circulating levels of key nutrients (e.g., antioxidants, omega-3 fatty acids) and also reduced cardiac size. This reduction in cardiac size did not appear to be an effect of sodium restriction. In addition, one retrospective study showed a significantly longer survival time in dogs with cardiac disease that were receiving omega-3 fatty acid supplementation (Slupe et al, 2008). Future prospective studies are needed to confirm such findings and to provide a better understanding of the role of nutritional modification in this early stage of disease.

Mild to Moderate Congestive Heart Failure

When CHF develops, additional nutritional concerns arise. Maintaining optimal body condition is of primary importance in the animal with CHF. Although obesity still can be present at this stage, animals with CHF more commonly begin to demonstrate weight loss. This weight loss, or cardiac cachexia, is unlike that seen in a healthy animal, which loses primarily fat. In an animal with CHF, the primary tissue lost is lean body mass. The term cachexia does not necessarily imply an emaciated, end-stage patient; there is a spectrum of severity of cachexia. In the early stages it can be very subtle and even may occur in obese animals (i.e., an animal may have excess fat stores but still lose lean body mass). Loss of lean body mass usually is noted first in the epaxial, gluteal, scapular, or temporal muscles. Cardiac cachexia can occur with any underlying cause of CHF (e.g., dilated cardiomyopathy [DCM], CVD, congenital heart diseases) but typically does not occur until CHF has developed (although it can occur in dogs with advanced CVD with severe left atrial enlargement). Cardiac cachexia is a common finding in animals with CHF and has deleterious effects on strength, immune function, and survival; thus it is important to recognize cachexia at an early stage and seize opportunities to manage it effectively.

The loss of lean body mass in cardiac cachexia is a multifactorial process caused by anorexia, increased energy requirements, and increased production of inflammatory cytokines such as tumor necrosis factor (TNF) and interleukin-1 (IL-1). These cytokines cause anorexia, increase energy requirements, and increase the catabolism of lean body mass. In addition, TNF and IL-1 also cause cardiac myocyte hypertrophy and fibrosis and have negative inotropic effects.

The nutritional management of cardiac cachexia consists primarily of providing adequate calories and protein and modulating cytokine production. One of the most important issues in managing anorexia (which is defined here to include either complete or partial loss of appetite) is to optimize medical therapy. An early sign of worsening CHF or the need for medication adjustment is a reduction in food intake in an animal that has previously been eating well. Medication adverse effects such as digoxin toxicity or azotemia secondary to angiotensin-converting enzyme (ACE) inhibitors or diuretic use also can cause anorexia. Providing a more palatable diet can help to improve appetite. This might involve switching from a dry food to a canned food, changing to a different brand, or feeding a balanced, cooked homemade diet formulated by a veterinary nutritionist. It also may be helpful to use flavor enhancers to increase food intake (e.g., yogurt, maple syrup, or applesauce in dogs; small amounts of home-cooked meats or fish in cats). Modulation of cytokine production also can be beneficial for managing cardiac cachexia. Supplementation of fish oil, which is high in omega-3 fatty acids, can decrease inflammatory cytokine production and improve cachexia (see later).

Unlike in the healthy animal or the asymptomatic person, dog, or cat with cardiac disease, obesity actually may be associated with a protective effect once CHF is present; this is known as the obesity paradox (Finn et al, 2010; Slupe et al, 2008). Although there are a number of hypothesized reasons for the obesity paradox, the benefit of obesity in CHF likely is due more to a lack of cachexia than to the obesity per se, given the adverse effects associated with cachexia.


As early as the 1960s, protein restriction was recommended for animals with CHF to reduce the metabolic load on the kidneys and liver. Restricting protein actually is detrimental because it can contribute to lean body mass loss and malnutrition. Animals with CHF should not be protein restricted unless they have concurrent advanced renal disease. Some diets designed for dogs with cardiac disease are very low in protein. Similarly, protein-restricted renal diets are sometimes recommended for animals with heart disease because these diets often (but not always) are moderately sodium restricted. Unless concurrent disease dictates otherwise, high-quality protein should be fed to meet minimum requirements for dogs (5.1 g/100 kcal) or cats (6.5 g/100 kcal). This should be a primary goal in animals with heart disease, particularly as CHF becomes more severe.

Another important issue with regard to protein is the still widespread misconception that dietary protein should be restricted in early renal disease. Some dogs receiving ACE inhibitors develop azotemia. Azotemia occurs more frequently when ACE inhibitors are used in conjunction with diuretics, but in a small number of dogs azotemia can develop from ACE inhibitors alone. When concurrent ACE inhibitor and diuretic use causes azotemia, reduction of the diuretic dose and/or temporary cessation of the ACE inhibitor is indicated. A protein-restricted diet is not recommended in this situation unless medication changes do not correct the problem and renal disease progresses.

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Jul 18, 2016 | Posted by in PHARMACOLOGY, TOXICOLOGY & THERAPEUTICS | Comments Off on Nutritional Management of Heart Disease

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