Nutrition and the Heart

Chapter 38. Nutrition and the Heart

There are several requirements for normal cardiac function. First, there needs to be adaptable coronary circulation. The vessels that supply oxygen and nutrients to the heart must be functional and capable of adapting to meet increased demands when needed. There also must be a flexible response by myocardial contractile cells so that when the animal needs additional cardiac output during stress or exercise, the cells of the heart can provide for a higher heart rate and cardiac output. The valves of the heart must function normally and maintain healthy blood flow. Finally, normal peripheral vascular response is needed to maintain normal blood pressure under a variety of physiological states.

When any of these functions is impaired, the heart begins to undergo a state of imbalance, eventually resulting in congestive heart failure (CHF). Clinically, animals with heart disease may show signs of syncope, coughing or respiratory difficulty, exercise intolerance, and cyanosis. Additional signs include cardiac murmurs, rhythm disturbances, cardiac enlargement, and/or excessively weak or strong arterial pulses.


Heart disease is one of the most commonly diagnosed diseases of dogs in the United States and Europe. 1 In dogs, heart disease can be either congenital or acquired. Common congenital heart conditions include aortic stenosis (AS), patent ductus arteriosis (PDA), ventricular septal defect (VSD), and pulmonic stenosis (PS). Some of these conditions appear to have a hereditary component and are found more frequently in certain breeds or lines of purebred dogs. Acquired heart disease is more common than congenital disease in dogs and cats. However, companion animals rarely suffer from atherosclerosis and coronary disease. 2 The most common form of acquired heart disease in dogs is chronic valvular disease. There are many different types of valvular diseases; chronic mitral insufficiency, tricuspid insufficiency, mitral stenosis, aortic insufficiency, pulmonic insufficiency, and bacterial endocarditis are the most common forms that are diagnosed in dogs. Of these, chronic mitral insufficiency is the most common and is typically observed in middle- to older-age dogs. It also appears more often in certain breeds such as the Cavalier King Charles Spaniel, Dachshund, Miniature and Toy Poodles, Chihuahuas, and many of the Terrier breeds. 3 In chronic mitral insufficiency, there is retrograde flow of blood from the left ventricle to the left atrium during ventricular systole or contraction. This results in reduced flow to the peripheral circulation, an increased backflow to the atrium, and blood volume overload in the heart. Dogs with this heart problem usually eventually develop CHF.

Acquired heart disease is more common than congenital heart disease in dogs and cats. However, companion animals rarely suffer from atherosclerosis and coronary disease. Chronic mitral insufficiency is one of the most common heart problems in dogs and is seen in middle- to older-age dogs. It occurs more often in Cavalier King Charles Spaniels, Dachshunds, Miniature and Toy Poodles, Chihuahuas, and some Terrier breeds.

Another common heart problem in dogs is dilated cardiomyopathy (DCM). This disease typically occurs in dogs that are middle-aged to older; however, some breeds have been reported to develop it early in life. For example, Portuguese Water Dogs can develop DCM and show clinical signs of CHF as young as 2 to 3 months of age. 4 There also appears to be a genetic predisposition in several large- and giant-breed dogs. Irish Wolfhounds, Great Danes, Saint Bernards, Newfoundlands, Doberman Pinschers, and Boxers are breeds that show an increased incidence of DCM. 5. and 6. Over half of all Dobermans and one third of Boxers are estimated to develop the disease in their lifetime. 5. and 6. Although they are not considered a large- or giant-breed dog, Cocker Spaniels also have a tendency to develop a form of DCM that previously was considered only a feline cause of cardiomyopathy; DCM in Cocker Spaniels can be caused by a taurine deficiency.

DCM is a primary myocardial disease characterized by cardiac chamber enlargement, arrhythmias, and diminished cardiac contractility. Eventually these dogs show signs of CHF, if not managed properly. Clinically, these dogs can show signs of weakness, collapse, lethargy, abdominal distention, tachycardia, tachypnea, dyspnea, coughing, syncopy, weight loss, anorexia, and sudden death. Two multibreed studies done on dogs with DCM demonstrated survival after 1 year of being diagnosed with DCM at only 17.5% and 37.5%, respectively, with the median survival times of only 27 and 65 days, respectively. 7. and 8.

In cats, DCM used to be the most common type of heart disease. However, in the late 1980s Pion et al. 9 reported an association with DCM and taurine deficiency in cats. Fortunately, it was found that administration of taurine to cats’ diets could reverse the myocardial changes seen. 9 Since that finding was demonstrated, commercial cat food manufacturers have increased the amount of taurine in their products, and there has been a dramatic reduction in the incidence of feline DCM. Although it is possible to still see a case of DCM in cats fed a poor-quality homemade, vegetarian, or unbalanced diet, most cases of feline DCM are seen as a taurine-independent variant of DCM, or seen as end-stage hypertrophic cardiomyopathy (HCM). 10

Currently in cats, the most common heart disease is HCM. Its incidence appears to be increasing. A recent publication reported 21% of overtly healthy cats had heart murmurs, and 86% of these cats, when evaluated using echocardiography, had structural cardiac disease, primarily HCM. 11 This is in comparison to studies conducted in the 1970s and 1980s where only 1.6% of all cats referred to a veterinary hospital were reported to have HCM. 12 Although most cats listed to be at risk for this condition include domestic long- and short-haired cats, in purebred lines, Maine Coon cats seem to have a heritable or familial tendency toward the disease. 13

Cats with HCM have a symmetrical or asymmetrical hypertrophy of the left ventricular wall, papillary muscles, and septum restricting the size of the left ventricular lumen. The myocardial cells are enlarged, and the left ventricular filling is impaired from reduced left ventricular compliance. There often is a secondary left atrial enlargement present. If there is atrial enlargement, arrhythmias may be more commonly detected. Cat with HCM usually develop CHF and arterial thromboembolism (ATE) with ATE reportedly developing in up to 48% of affected cats. and 17. Clinically, cats with HCM demonstrated signs of weakness, labored breathing, lethargy, syncope, arrhythmias, and hindlimb pain or paralysis if ATE was present. Cats with HCM have a mean survival time of less than 2 years. 14

The most common heart disease in cats is hypertrophic cardiomyopathy (HCM). Cats with HCM usually develop congestive heart failure and approximately half will develop arterial thromboembolism (ATE). Clinically, cats with HCM demonstrated signs of weakness, labored breathing, lethargy, syncope, arrhythmias, and hindlimb pain or paralysis if ATE was present.


Cardiac cachexia is defined as muscle wasting and weight loss that commonly occurs in humans, dogs, and cats with cardiac disease. For example, one study reported that more than 50% of dogs with DCM showed some degree of cardiac cachexia. 18 Similar to cancer cachexia, the weight loss that occurs with cardiac cachexia includes a substantial and unusually high loss of lean body tissue. Although many veterinarians consider cachexia to be an end-stage development in animals with CHF, it can occur in early stages of CHF. 19 Similar to cancer cachexia, the metabolic changes may precede obvious physical changes. The loss of lean body mass can affect many different systems and is associated with shortened survival time. As muscle tissue is metabolized, the animal experiences muscle wasting, a loss of strength, and eventually compromised immune function. For example, dogs with cardiac cachexia have lower CD4+ lymphocytes and are at increased risk for anemia. 20

Anorexia is a very common problem in pets with CHF and contributes to the onset of cardiac cachexia. It has been reported to occur in up to 84% of dogs with CHF and in at least 38% of cats with cardiac disease. 21.22. and 23. Reduced appetite may be secondary due to the fatigue and respiratory dyspnea commonly seen with CHF, but it can also be due to side effects of medications or feeding a new food that may be less palatable. 24 An increase in energy requirements is also a factor that needs to be evaluated when considering the loss of lean body mass. In humans, it has been documented that some may need up to a 30% increase in overall energy requirements when diagnosed with CHF. 25 This increase in energy requirements may be due to tachycardia or tachypnea. 10 Therefore dogs and cats may also benefit from increasing the total energy in their diet. Metabolic alterations may also contribute to the loss of lean body mass. Cytokine elevation, tumor necrosis factor, and interleukin-1 occur in patients with CHF. 24 These inflammatory mediators can increase energy requirements, increase breakdown of lean body mass, and directly cause anorexia. 24 Interestingly, in 68% of dogs with CHF, anorexia was a contributing factor for owners opting to euthanize their pets. 21 Therefore controlling, or at least addressing, the issue of cardiac cachexia and anorexia nutritionally is important to prolong survival time in dogs and cats with CHF.

Cardiac cachexia and anorexia are common in pets with congestive heart failure (CHF). The resultant loss of lean body mass can affect many different systems and is associated with shortened survival time. Decreased interest in food may be secondary to fatigue and respiratory dyspnea, but may also be due to side effects of medications or feeding a new food that is less palatable. Therefore nutritional management of cardiac cachexia and anorexia is important to prolong survival time and improve the quality of life for pets with CHF.


Medical treatment goals for cats with HCM are those that include reducing heart rate, management of CHF when present, and either treating or preventing ATE. Common medications to achieve this include diltiazem, beta-blockers, furosemide, and angiotensin-converting enzyme (ACE) inhibitors. To prevent or treat ATE, aspirin, warfarin, dalteparin or enoxaparin, and clopidigrel are common options. Dogs with DCM are often prescribed medications such as ACE inhibitors, beta-blockers, pimobendan, digoxin, antiarrhythmics, and diuretics such as furosemide.


In addition to medical therapy, nutritional modification is an important component of treatment protocols for dogs and cats with CHF. Nutritional modification can support a good quality of life, and, in some cases, may ameliorate some of the clinical effects of heart disease.

In many cases, preventing or reversing anorexia is part of nutritional treatment. Because some medications given to heart patients can cause anorexia as a side effect, reducing the dose or altering the number of doses per day may be helpful. Food palatability is an important consideration. Many therapeutic foods are available in both a canned and dry form, so switching between the two may be beneficial. Warming the food in a microwave (either canned foods or wetted dry foods) and offering small, frequent meals throughout the day can also help with acceptance. Additionally, adding small amounts of certain flavor enhancers such as honey, yogurt, or diluted tuna juice may improve acceptance of the food.

Specific Nutritional Modifications in Managing Cardiovascular Disease

A variety of nutritional modifications may help to slow progression of cardiac disease and improve the quality of life in animals with cardiovascular disease. Specific nutrients of interest include sodium, taurine, carnitine, fatty acids, antioxidants, and protein.


Animals with cardiovascular disease have impaired ability to excrete sodium in the urine because of decreased cardiac output. 26 Therefore dietary salt restriction is typically recommended as an aid to control fluid accumulation. The degree of sodium restriction should be dependent on the stage of heart failure and is directed at controlling sodium-responsive clinical signs. Restricting sodium too extensively, especially in asymptomatic dogs, may lead to increased blood pressure via an activated renin-angiotensin-aldosterone system. 27 Although this may not have negative long-term effects, early neuroendrocrine activation may not be desirable. 28 Therefore a food containing maintenance levels of sodium can be fed to pets with early-stage cardiovascular disease (sodium <0.40% dry matter). High-salt table scraps or treats should be avoided. For example, a study showed that dogs with cardiac disease but without CHF were able to maintain both sodium and potassium levels when fed either a low- or a high-sodium diet. 29 Another study reported that a low-sodium diet fed to dogs with asymptomatic cardiac disease had no beneficial effect on cardiac size or function but, rather, led to increased aldosterone concentration and heart rate. 28

The stage of heart disease at which to institute sodium restriction in dogs and cats is still unclear. A general recommendation is to reduce sodium to less than 0.30% of dry matter when clinical signs appear. 10 This can be accomplished by feeding a pet food that is formulated for senior pets because many of these products contain slightly reduced sodium. Foods should be evaluated individually, or the pet food company should be contacted to ensure that an adequate product is selected. As CHF becomes more severe, veterinary diets specifically formulated for heart patients should be considered because these products are more restricted in sodium. It is also important to assess the food’s palatability because low-sodium foods may not be well accepted by pets with congestive heart disease (CHD).

The sodium content of treats and human foods that may be used to administer medications is also an important consideration. Because pets with CHD often show a reduced interest in food, some owners use dog treats, hot dogs, cheese, peanut butter, or lunch meats to administer pills. All of these foods are high in sodium and so are contraindicated. In one study, although owners reported that they were aware of the importance of sodium, they often failed to consider the type of treats they were using to administer medications. 30 In fact, 92% of the dogs studied were fed high-sodium treats or table scraps. In another study, 62% of pet owners used high-sodium human or pet foods for pill administration. 31 High-sodium foods should be avoided when giving medications to all pets with CHD, regardless of the stage of disease. Other “human” treats that should be avoided include canned fish, margarine or butter, canned vegetables, potato chips, pretzels, pop corn, and other salty snacks. Dog treats and snacks that are specifically formulated to be low in sodium are acceptable, but other over-the-counter pet treats should not be fed.

The degree of sodium restriction for pets with heart disease is directed toward controlling sodium-responsive clinical signs. Foods containing maintenance levels of sodium can be fed to pets with early-stage cardiovascular disease. High-salt table scraps or treats should always be avoided. It is generally recommended to reduce sodium to <0.30% of dry matter when clinical signs appear. As congestive heart failure becomes more severe, veterinary diets specifically formulated for heart patients should be considered.


Taurine is a sulfur-containing amino acid. As discussed in Chapter 4 and Chapter 12 (pp. 22 and 97-100), taurine is found in high concentrations in the myocardium, skeletal muscle, central nervous system, and platelets, and is important for normal heart function. 32 Although the exact mechanisms through which taurine affects heart function are not completely understood, taurine modulates cellular calcium concentrations and availability in heart muscle, directly affects contractile proteins, and serves as a natural antagonist of angiotension II. 32.33.34. and 35. Additionally, taurine may protect the heart by inactivating free radicals and changing cellular osmolality. 36

Taurine is an essential amino acid for the cat, and a deficiency can cause DCM. Until the late 1980s, DCM was one of the most common heart conditions diagnosed in cats. In 1987, an association between clinical cases of DCM in cats and taurine levels in pet food was found; taurine supplementation completely reverses the condition (see Chapter 12, pp. 97-100 for a complete discussion). 9 Commercial pet food companies that increased the concentration of taurine have further supplemented taurine levels in feline diets, and thus there has been a dramatic reduction in cases of DCM in cats. Occasionally a few cases of DCM are reported in cats, but these cases are usually not a result of a taurine-deficient diet. Rather, these cases may represent a taurine-independent variant of DCM in cats or are associated with end-stage HCM. 10

In the dog, taurine is currently classified as a conditionally essential amino acid (see Chapter 12, pp. 99-100 for a complete discussion). Dogs of some breeds that are diagnosed with DCM have been found to have low plasma taurine concentrations. 37.38.39. and 40. Affected breeds include the American Cocker Spaniel, Golden Retriever, Labrador Retriever, Saint Bernard, Newfoundland, and English Setter. Although the underlying causes are not known, it appears that some breeds (or lines) have a naturally occurring higher requirement for taurine or a breed-specific metabolic abnormality that affects taurine need. 41.42. and 43. Taurine deficiency has also been associated with lamb meal and rice diets, soybean-based diets, and high-fiber diets (see Chapter 12, pp. 97-100 for a complete discussion). and 48. Any factor that results in increased colonic bacteria populations leads to increased taurine loss in the feces and thus an increased dietary requirement for this nutrient. 44. and 49. Taurine is found naturally in animal-based proteins; so, providing diets that include a sufficient level of high-quality animal proteins ensures adequate taurine intake.
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Jul 31, 2016 | Posted by in INTERNAL MEDICINE | Comments Off on Nutrition and the Heart

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