Royal Canin Nutritional Information

Royal Canin Nutritional Information

The majority of cardiac dogs suffer from systolic failure due either to acquired chronic valvular disease (endocardiosis) or dilated cardiomyopathy (DCM). The former disease very often affects small-breed dogs. DCM is most common in large-breed dogs. (© Lanceau).

Key Points to Remember:

The Role of Nutrition in Cardiac Disease

• One of the main goals of dietetic strategy is to achieve optimal body weight whatever the initial situation: obesity (especially in case of a subclinical disease) or cachexia in some severe cardiac diseases. Anorexia is a common phenomenon in cardiac patients that needs to be given due consideration: it is one of the main reasons for the request to euthanize patients with severe cardiac disease. It may be directly linked to respiratory problems, to fatigue accompanying heart failure, to nausea induced by medication or to poor palatability of certain cardiac diets, containing low sodium and protein content.
  Selecting a palatable food, giving frequent small meals and encouraging the dog to eat are all measures that should not be neglected in therapeutic management.
• Cardiac dogs often suffer from a deficiency of EPA-DHA, long-chain n-3 fatty acids. A food with a higher EPA-DHA content facilitates the treatment of cardiac cachexia.
• Severe sodium restriction has been inappropriately recommended for far too long. Its application is unwarranted in the initial stages of heart failure, as it risks hastening the progression of the cardiac disease by activating the renin-angiotensin system, especially when angiotensin converting enzyme (ACE) inhibitors are simultaneously prescribed.
  A moderate restriction of sodium content (< 80 - 100 mg/100 kcal) is sufficient for stages I and II of heart failure. Only severe heart failure justifies restricting sodium content to 50 mg/100 kcal.
• A cardiac dog must receive a normal intake of high quality proteins to combat cardiac cachexia. Limiting the protein intake is not indicated, except for concomitant hepatic encephalopathy or kidney disease that demands such a restriction. Taurinesupplementation is recommended as this sulfated amino acid has positive properties that can prove effective in the prevention and treatment of dilated cardiomyopathy.
• Arginine is a precursor of nitric oxide (NO), which has been identified as a relaxation factor for the smooth muscle of blood vessels. Supplementary arginine intake will indirectly help combat hypertension.
• L-carnitine is concentrated in the striated muscles and the heart where it plays a key role in providing energy to the cells. L-carnitine deficiency has been suggested in connection with dilated cardiomyopathy. Clinical improvements have been reported after the administration of a supplement, although several months of treatment are necessary to achieve changes that can be detectable by echocardiography.
• Free radicals, which are responsible for oxidation of membranous phospholipids, aggravate cardiac lesions. Oxidative stress is a causal factor of dilated cardiomyopathy. The daily administration of antioxidants in the food is one of the main ways of combating the progression of heart failure.

Focus on: The Importance of Taurine Intake to Encourage Optimal Cardiac Contractility

Taurine accounts for at least 40% of the pool of free amino acids in the heart. This amino acid is normally synthesized in the dog from methionine and cystine. The taurine concentration can be limited in certain conditions such as when the animal receives a food with reduced protein content or when taurine synthesis is insufficient, as is the case in some breeds and some lines. The synthesis of taurine appears to be much less efficient in large-breed dogs (> 35 kg) compared to Beagles (Ko et al., 2005).

A simple blood sample will help determine whether the dog has taurine deficiency. Taurine analysis should be performed on whole blood as taurine is stored predominantly in blood cells. The plasma taurine concentration does not properly reflect the muscular and cardiac storage of taurine.

Taurine is essential to the contractility of the heart muscle.

1. It has a positive or negative inotropic effect depending on whether calcium is abundant or not in the cells; taurine protects the myocytes against the effects of excess calcium (Satoh & Sperelakis, 1998).
2. It has an antiarrhythmic role (Satoh & Sperelakis, 1998).
3. It helps preserve the integrity of cardiac muscle cells: in vitro taurine prevents myocyte hypertrophy induced by angiotensin II (Takahahsi et al., 1998).

It has long been known that taurine deficiency can provoke degeneration of the retina and slow down growth. Only recently has DCM in dogs been associated with extremely low plasma taurine levels.

The correlation has especially been shown in Newfoundland dogs in the United Kingdom (Dukes-McEwan et al., 2001). Positive responses to taurine supplementation have been noted in Boxers suffering from DCM. It is therefore advisable to provide sufficient quantities of taurine in the food to prevent any risk of deficiency.

Lateral thoracic radiograph of a large-breed dog with dilated cardiomyopathy. Generalized cardiomegaly during cardiomyopathy with clinical signs. (© Bussadori).

Summary of Select Publications...

There is a hypothesis associating dilated cardiomyopathy (DCM) in dogs, especially large breeds, with taurine deficiency. This study was designed to evaluate the taurine status of a group of Newfoundland dogs in the United Kingdom. One hundred and four Newfoundlands underwent clinical and echocardiography examinations. The evaluation of taurine status was based on total blood analysis (nmol/mL). In addition, a detailed dietary history was obtained for each dog. The echocardiography examinations permited the classification of dogs as normal, dogs with dilated cardiomyopathy, dogs with a reduction in shortening fraction or dogs presenting with dilatation of the left ventricle.

A low taurine concentration is considered less than 200 nmol/mL, and a very low taurine level is less than 130 nmol/mL.

(© Psaila).

A low taurine concentration has been shown in a significant number of Newfoundland dogs. In this study population, the taurine values tended to be lower than in dogs with dilated cardiomyopathy (DCM). The purpose of this study was to test the impact of taurine or methionine supplementation in correcting taurine deficiency.

Forty-eight dogs with a blood taurine value less than 200 nmol/mL were identified. Echocardiography examination enabled the establishment of three categories of dogs: normal, echocardiography anomalies without clinical signs (e.g. reduced contractility or dilatation of the left ventricle) and dogs with clinical DCM.

The dogs with clinical DCM received 1000 mg of taurine by mouth twice a day. The remaining dogs were matched by age and sex and then received 250 mg of taurine or 750 mg of methionine per os twice a day. Four dogs were fed with a specific food for very-large dogs.

The blood and urine taurine concentration, as well as the urine creatinine concentration were measured after three and six months of supplementation and compared with the initial values.

The blood taurine concentration increased in all the dogs. It rose from 144 ± 8 nmol/mL at the start of the study to 324 ± 14 nmol/mL after three months of supplementation and 275 ± 10 nmol/mL after six months of supplementation. No differences could be distinguished with respect to the type or dose of supplementation.

The urine taurine/creatinine ratio was minimal at the start of the study, increasing significantly with supplementation of methionine or taurine, more makedly with the highest taurine concentration.

These results suggest that 250 mg of taurine or 750 mg of methionine per os twice a day, and a diet providing 1000 mg of taurine/kg normalizes the taurine concentration in taurine deficient Newfoundland dogs. For the dogs in this study, a low taurine status cannot be explained by greater taurine losses or an inability to utilize methionine as a taurine precursor.

(© Lenfant).