32 / / Veterinary Focus / / Vol 18 No 3 / / 2008

Accurate and timely diagnosis of earlystage (Class 1 & 2, Table 1) cardiacdisease historically has been difficult.Most patients show no outward evidence of beingsick. Owners themselves usually do not reportclinical signs related to a cardiac abnormalityuntil later stages occur. Typical treatment of earlystage cardiac disease has largely focused onbenign neglect with subsequent monitoring ofthe patients cardiac rate, rhythm, size andassociated clinical signs at six to twelve monthintervals. The question that must be asked is a topicof much debate within the veterinary community.If a patient shows no outward clinical signs

associated with a disease, such as early cardiacdisease, what if anything should be done clinicallyto aid in the improvement of the animals health?

Through the collaboration with some of the worldsleading cardiologists and nutritionists in conjunc-tion with the innovative research performed atRoyal Canin and the WALTHAM Centre for PetNutrition, we now realize the beneficial effects ofimplementing early nutritional support in patientsfaced with cardiac abnormalities. Nutrition by itselfcan have profound beneficial effects at minimizingmetabolic disturbances, while at the same timeimproving the patients over all quality of life.

Daniel Baker, DVMScientific Communications, Royal Canin USA

Dr. Baker graduated from the University ofMassachusetts-Amherst with a Bachelor of Sciencedegree in biology with Honors in 1999. As anundergraduate he was one of the eighteen membersfrom around the world who took part in the East/Westmarine biology program at Northeastern University,allowing students to compare and contrast marine floraand fauna in three distinct parts of the world. Danielreceived his DVM degree from Ross University in 2003having completed his clinical year at the University ofMinnesota. Following graduation he worked as a smallanimal clinician for 4 years. During this time he focusedmainly in the area of emergency and critical basedmedicine. Daniel is currently a member of the ScientificCommunications team for Royal Canin USA.

Denise Elliott, BVSc (Hons), PhD, Dipl. ACVIM, Dipl. ACVN

Scientific Affairs, Royal Canin USA

Dr. Elliott received her degree in Veterinary medicinewith honors from the University of Melbourne in 1991.

After completing an internship in Small AnimalMedicine and Surgery at the University of Pennsylvania,Denise completed a residency in Small Animal Internal

Medicine and Clinical Nutrition at the University ofCalifornia-Davis. Denise became a Diplomate of theAmerican College of Internal Veterinary Medicine in

1996 and the American College of Veterinary Nutritionin 2001. She received her PhD in Nutrition from the

University of California-Davis in 2001, for her work onmultifrequency bioelectrical impedance analysis in

healthy cats and dogs. Denise is currently the Directorof Scientific Affairs for Royal Canin USA.

Nutritional managementof early cardiac disease:

ACT with SPEED

ROYAL CANIN VIEWPOINT

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Vol 18 No 3 / / 2008 / / Veterinary Focus / / 33

Cardiac disease is now the second leading causeof death in dogs. Chronic valvular disease (CVD)accounts for approximately 75% of these caseswhile dilated cardiomyopathy (DCM) is responsiblefor 10-15% of cases observed. Over the past decademore advanced diagnostic tools such as: electro-cardiography (ECG), Holter monitoring andechocardiography are now available to the generalpractitioner. This allows for early diagnosis andsubsequent intervention of early cardiac disease.

Nutritions primary role in the prevention andtreatment of cardiac disease is multimodal.Through the use of key nutrients, dietaryintervention seeks to provide optimal amountsof energy, minimize oxidative stress, reduceinflammation, balance electrolytes and ultimatelyto improve cardiac performance. Through the useof the ACT with SPEED acronym we can betterunderstand each key nutrients role in slowingthe progression of heart disease.

ACTArginine, an essential amino acid, is the precursorfor endogenously synthesized nitric oxide. Nitricoxide is well known for its role as an endothelium-derived relaxation factor, which in turn isresponsible for maintaining normal vascular tone(1). Endothelial dysfunction has been linked, inhumans and dogs, with congestive heart failure

(CHF) (2). Arginine supplementation appears toimprove cardiac output in patients with cardiacdisease by positively inf luencing preload andafterload (CO = HR x contractility x preload/afterload).

Carnitine, a quaternary amine, is composed of twoessential amino acids, lysine and methionine. It iscommonly found concentrated in both skeletal andcardiac muscle. L-carnitine (the biologically activeform) is critical for oxidation of fatty acids withinmitochondria. It serves as a transport shuttle offatty acids from outside the mitochondria intothe inner membrane and in turn is a key componentin the regulation of the citric acid cycle (3).L-carnitine is also responsible for transportingmetabolic waste products out of the mitochondriathat might otherwise become cardiotoxic.L-carnitine is normally provided to the animal insufficient amounts through intestinal absorption orfollowing hepatic and renal synthesis. In certainbreeds (Boxers, Doberman Pinschers and AmericanCocker Spaniels) there have been reportedmyocardial carnitine deficiencies (4,5). In a greatmany of these cases plasma carnitine levels werewithin normal limits. These findings suggest amembrane transport defect may be presentpreventing L-carnitine from entering into themyocardial cells from the plasma. Providingoptimal amounts of carnitine in the diet mayimprove overall myocardial function.

Taurine, a non-essential amino acid in the dog,is well known for its powerful antioxidant effectsthroughout the body. Taurine also is a key nutrientin the treatment of certain cardiomyopathies (6-8).Recent evidence also suggests that feeding certainlamb-based diets and severely protein restricteddiets, may lead to marked taurine deficiencieswith associated clinical signs (9-10). Breedassociated deficiencies (e.g. American CockerSpaniel, Portuguese Water dog) have manifestedthemselves in the form of dilated cardiomyopathy.Clinical improvement has resulted in severalcases where the proper taurine levels were presentwithin the diet (5-11). Taurine has also provento have positive iontropic effects in animals withexperimentally induced heart failure (12). Thissuggests taurine supplementation may provebeneficial in patients with cardiac disease withouttrue taurine deficiencies.

Table 1. Classification of heart disease

Grade

Class I

Class II

Class III

Class IV

Clinical description

No limitation of physical activity. Ordinary physical activity does not causeundue fatigue, palpitation, or dyspnea.

Slight limitation of physical activity.Comfortable at rest, but ordinary physicalactivity results in fatigue, palpitation, ordyspnea.

Marked limitation of physical activity.Comfortable at rest, but less than ordinaryactivity causes fatigue, palpitation, ordyspnea.

Unable to carry out any physical activitywithout discomfort. Symptoms of cardiacinsufficiency at rest. If any physical activityis undertaken, discomfort is increased.

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34 / / Veterinary Focus / / Vol 18 No 3 / / 2008

With

SPEEDSodium restriction has long been thought of asthe nutritional mainstay of treating cardiacdisease. While sodium restriction has its placeadjunctively along side additional nutritionalmodalities, it is the degree of sodium restrictionbased on the severity of cardiac disease presentthat must be taken into account. Indeed, sodiumrestriction that is too severe early on in thedisease process may lend itself to an exaggeratedresponse by the renin-angiotensin aldosteronesystem (13-18). This can exacerbate clinicalsigns and the progression of the disease itself.The advent of angiotensin converting enzyme(ACE) inhibitors has further decreased the needfor severe sodium restriction in most patients(19). Based on our current understandingof sodiums relationship to cardiac physiologyduring certain stages of cardiac disease, tailoringthe degree of sodium restriction is of the utmostimportance.

Protein restriction has erroneously worked itsway into the management of cardiac disease.Many of todays diets are formulated on the anti-quated thought process that protein restrictionlends itself to reduced metabolic stress on thekidneys and liver (20). No known peer reviewedpublications exist proving this hypothesis.Whats worse is that protein restricted diets favorthe development of cardiac cachexia. This in turnwill lead to the perception by the owner of a poor

quality of life and likely hasten euthanasia. Cardiacdiets should contain optimal amounts of highlydigestible proteins that allow for the preservationof lean body mass.

Energy requirements in patients with cardiacdisease should be considered with both thepatients body condition score (BCS) and degreeof cardiac cachexia (Table 2) in mind. The goalshould be to manage caloric intake to preventboth obesity and emaciation while preservinglean body mass. Special focus needs to be placedon patients with poor BCS and/or cachexiaalready prevalent. Poor doing is often associatedwith anorexia in patients with cardiac disease.A recent study revealed the daily caloric intakein dogs with dilated cardiomyopathy was 72-84%of their expected daily energy requirements (21).Nutrient profiles therefore need be formulatedwith nutrients that are highly digestible andreadily bioavailable.

Eicosapentaenoic acid (EPA)&

Docosahexaenoic acid (DHA) are essentiallong chain fatty acids derived from marinesources that provide profound anti-inflammatoryeffects throughout the body but especially with-in the heart. Studies have revealed that dogswith congestive heart failure have decreasedconcentrations of plasma EPA/DHA in comparisonwith healthy dogs (21). Their combined effectstarget the reduction of pro-inflammatory mediatorsactions on the cardiac infrastructure (21).Supplementation with marine derived omega-3fatty acids have also been shown to improve cardiaccachexia scores in dogs with cardiac disease. Arecent study revealed that EPA/DHA from fishoils given over a six-week period may decrease theseverity and frequency of arrhythmias in Boxerswho suffer from Arrhythmogenic Right VentricularCardiomyopathy (ARVC) (22).

Several other key nutrients related to the heartshould be taken into consideration. For example,vitamin E has positive effects on inhibiting lipidperoxidation of the cellular membranes of cardiaccells. Vitamin E can be looked at as a biomarker ofoxidative stress. In patients with heart disease, low

Cachexiascore

0

1

2

3

4

Description

Good muscle tone with no evidence ofmuscle wasting

Early, mild muscle wasting, especially in thehindquarters and lumbar region

Moderate muscle wasting apparent in allmuscle groups

Marked muscle wasting as evidenced byatrophy of all muscle groups

Severe muscle wasting

*Modified from Freeman (29).

Table 2. Cachexia scoring system

ROYAL CANIN VIEWPOINT

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Vol 18 No 3 / / 2008 / / Veterinary Focus / / 35

1. Palmer RM, Ferrige AG, Moncada S. Nitric oxide release accounts forthe biological activity of endothelium-derived relaxing factor.Nature 1987; 327: 524-526.

2. Wang J, Yi GH, Knecht M, et al. Physical training alters the pathogenesis ofpacing-induced heart failure through endothelium-mediated mechanismsin awake dogs. Circulation 1997; 96: 2683-2692.

3. Rebouche CJ, Paulson DJ. Carnitine metabolism and functions in humans.Annu Rev Nutr 1986; 6: 41-66.

4. Keene BW. L-carnitine deficiency in canine dilated cardiomyopathyIn: R. W. Kirk and J. D. Bonagura, eds. Current veterinary therapy XI.Philadelphia: W. B. Saunders Co, 1992; 780-783.

5. Kittleson MD, Keene B, Pion PD, et al. Results of the multicenter spaniel trial(MUST): taurine- and carnitine-responsive dilated cardiomyopathy inAmerican Cocker Spaniels with decreased plasma taurine concentration.J Vet Intern Med 1997; 11: 204-211.

6. Kramer GA, Kittleson MD, Fox PR, et al. Plasma taurine concentrations innormal dogs and in dogs with heart disease. J Vet Intern Med 1995; 9: 253-258.

7. Alroy J, Rush JE, Freeman LM, et al. Inherited infantile dilatedcardiomyopathy in dogs: genetic, clinical, biochemical and morphologicfindings. J of Med Genet 2000; 95: 57-66.

8. Freeman LM, Rush JE, Brown DJ, et al. Relationship between circulatingand dietary taurine concentrations in dogs with dilated cardiomyopathy.Vet Ther 2001; 2: 370-378.

9. Torres CL, Fascetti AJ, Rogers QR. Taurine and sulphur amino acid status indogs fed dry commercial poultry-by-product meal or lamb meal diets.J Vet Int Med 2000; 14: 364.

10. Sanderson SL, Gross KL, Ogburn PN, et al. Effects of dietary fat andL-carnitine on plasma and whole blood taurine concentrations andcardiac function in healthy dogs fed protein-restricted diets. Am J Vet Res2001; 62: 1616-1623.

11. Gavaghan B, Kittleson MD. Dilated cardiomyopathy in an AmericanCocker Spaniel with taurine deficiency. Aust Vet J 1997; 75: 862-868.

12. Elizarova EP, Orlova TR, Medvedeva NV. Effects on heart membranesafter taurine treatment in rabbits with congestive heart failure.Arzneimittelforschung 1993; 43: 308-312.

13. Koch J, Pedersen HD, Jensen AL, et al. Activation of the renin-angiotensinsystem in dogs with asymptomatic and symptomatic dilatedcardiomyopathy. Res Vet Sci 1995; 59: 172-175.

14. Pedersen HD, Koch J, Poulsen K, et al. Activation of the renin-angiotensinsystem in dogs with asymptomatic and mildly symptomatic mitralvalvular insufficiency. J Vet Intern Med 1995; 9: 328-331.

15. Webester KT, Brilla CG. Pathological hypertrophy and cardiac interstitium.Firbrosis and renin-angiotensin system. Circulation 1991; 83:1849-1865.

16. Tan LB, Jalil JE, Pick R, et al. Cardiac myocycte necrosis induced byangiotension II. Circ Res 1991; 69: 1185-1195.

17. Pedersen HD, Koch J, Jensen AL, et al. Effects of a low sodium diet with ahigh potassium content on plasma endothelin-1, atrial natriuretic peptideand arginine vasopressin in normal dogs. J Vet Med 1994; 41: 713-716.

18. Pedersen HD, Koch J, Jensen AL, et al. Some effects of a low sodium diethigh in potassium on the renin-angiotensin system and plasma electrolyteconcentrations in normal dogs. Acta Vet Scand 1994; 35: 133-140.

19. Kock J, Pedersen HD, Jensen AL, et al. Short term effects of acute inhibitionof the angiotensin-converting enzyme on the renin-angiotension systemand plasma atrial natriuretic peptide in healthy dogs fed a low-sodium dietversus a normal-sodium diet. J Vet Med 1994; 41: 121-127.

20. Pensinger RR. Nutritional management of heart disease In: R. W. Kirk, ed.Current veterinary therapy III. Philadelphia: W. B. Saunders, 1968; 229-232.

21. Freeman LM, Rush JE, Kehayias JJ, et al. Nutritional alterations and theeffect of fish oil supplementation in dogs with heart failure. J Vet Intern Med1998; 12: 440-448.

22. Smith CE, Freeman LM, Rush JE, Cunningham SM, Biourge V. Omega-3fatty acids in Boxer dogs with arrhythmogenic right ventricularcardiomyopathy. J Vet Intern Med 2007; 21: 265-273.

23. Freeman LM, Brown DJ, Rush JE. Assessment of degree of oxidative stressand antioxidant concentrations in dogs with idiopathic dilatedcardiomyopathy. J Am Vet Med Assoc 1999; 215: 644-646.

24. McMichael MA, Freeman LM, Selhub J, et al. Plasma homocysteine, Bvitamins, and amino acid concentrations in cats with cardiomyopathyand arterial thromboembolism. J Vet Intern Med 2000; 14: 507-512.

25. O'Keefe D, Sisson DD. Serum electrolytes in dogs with congestive heartfailure. J Vet Intern Med 1993; 7: 118.

26. Cobb M, Michell AR. Plasma electrolyte concentrations in dogs receivingdiuretic therapy for cardiac failure. J Small Anim Pract 1991; 33: 526-529.

27. Pedersen H, Mow T. Hypomagnesemia and mitral valve prolapse in CavalierKing Charles Spaniels. Zentralbl Veterinarmed 1998; 45: 607-614.

28. Roudebush P, Allen TA, Kuehn NF, et al. The effect of combined therapywith captopril, furosemide, and a sodium-restricted diet on serum electrolyteconcentrations and renal function in normal dogs and dogs with congestiveheart failure. J Vet Intern Med 1994; 8: 337-342.

29. Freeman LM. Nutritional Modulation of cardiac disease. WALTHAM FocusSpecial Edition Advances in Clinical Nutrition, 2000; 36-42.

REFERENCES

Vitamin E concentrations have been negativelycorrelated with the severity of the disease (23).Vitamin B deficiencies have been reported in catswith cardiomyopathy (24). Hypomagnesemia maypotentiate cardiac arrhythmias, decrease myocardialcontractility and contribute to muscle weakness(25,26). This is often observed in the CavalierKing Charles Spaniel (27). Potassium, traditionallyhyper-supplemented in historic cardiac dietformulations to compensate for the urine wastingsecondary to diuretic therapy, is no longer necessary.With the advent of ACE inhibitor therapy thatincreases the renal absorption of potassium,modern cardiac diets should contain normallevels of potassium (28).

In summary, we must first identify early stagecardiac disease in our patients. Then we need toeducate pet owners that early cardiac disease leftuntreated may have drastic life long complications.Many of these consequences stem from a sub-clinical disease process not necessarily manifestingitself as outward clinical signs. As clinicians, wenow have the opportunity to offer our clients earlydietary therapeutic intervention in conjunctionwith close monitoring of their pets disease state.Together we can give owners and their belovedpets, the nutritional tools necessary to aid in themanagement of heart disease and to improve thechance of living longer, healthier lives.

NUTRITIONAL MANAGEMENT OF EARLY CARDIAC DISEASE: ACT WITH SPEED

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