Linda Arndt ~ Canine Nutritional Consultant

Efficacy of Oral L-Carnitine Supplementation for

Dilated Cardiomyopathy in Great Danes

The L-Carnitine supplementation that I use is made by Lonza Corporation and it is affordable - 1 tablespoon = 1000 mg of Carnitine. I purchase it from Dr. Wagner's


Cecilia Quintavalla, Danitza Pradelli, Giuseppe Zannetti - Istituto di Clinica Medica Veterinaria – Università di Parma


Dilated cardiomyopathy (DCM) is a primary myocardial disease characterised by progressive systolic dysfunction due to impaired myocardial contractility and cardiac chamber dilatation (usually all four chambers to some degree, but sometimes predominantly left or more rarely predominantly right)1,10. Diastolic dysfunction also occurs in DCM, but it is less notable than the characteristically severe systolic dysfunction2.

The disease was first described by Ettinger et al. in 1970 as congestive heart failure in conjunction with dilation of cardiac chambers and absence of other congenital or acquired heart diseases3. Since this first description, DCM has been widely observed in the dog.

DCM is considered one of the most common acquired heart diseases in the dog and it has been recognised in many medium-sized, large and giant breed dogs, notably English4 and American Cocker Spaniels9, Boxers5, Dalmatians6, Doberman Pinschers7, Newfoundlands8, Irish Wolfhounds, Great Danes, Saint Bernards, Old English Sheepdogs, Scottish Deerhounds1. However, the prevalence of the disease in most affected breeds shows wide differences related to geographic locations. Whether this variability reflects genetic or environment differences is unknown.

Despite the differences in breed distribution, the disease is rarely identified in dogs less than 12 kg, and male dogs are overrepresented in most demographic investigations on the disease1.

Many efforts have been spent to identify the causes of the disease.

A lot of theories have been proposed, taurine9 e/o carnitine5 deficiency, antibodies against beta-receptors11 or the adenine nucleotide translocator12, mutations in the cardiac actin gene13 or dystrophin abnormalities15, infectious agents, toxins1 and even pregnancy14, but the cause in most cases remains unknown.

Despite the variety of potential causes of DCM, a relative morphologic, histologic and ultrastructural homogeneity of patients with DCM has been observed. This suggests the existence of similarities in the response of the myocardium to different types of injuries and that some common cellular pathways that respond to those injuries cause and/or exacerbate the structural and functional changes typical of DCM1.

This paper relates about two cases of dilated cardiomyopathy in a family of Great Danes and the successful use of oral L-carnitine in the management and in the clinical course of the disease.

Case history

Three 2-year-old Great Danes, one male (dog A) and two females (dogs B and C), have been presented at the Institute of Veterinary Internal Medicine of the University of Parma on May 1997 for cardiovascular examination because of a familial history of sudden death. Their 4-year-old father died suddenly a few days before without showing overt clinical signs of heart disease. No necroscopic examination had been performed on this dog, belonging to a different owner. A physical and electrocardiographic examination performed by a practitioner on dogs’ mother did not reveal signs of congenital or acquired heart diseases. At the time of writing the mother is still healthy.

The three dogs belonged to a litter of 7 puppies. Three littermates, two males and a female, died suddenly at 1 year of age, but the cause of the death is still unknown because necroscopic examination has not been performed. A 18-month-old male littermate died of cardiovascular collapse because of severe dehydration due to haemorragic gastroenteritis. Microbiological culture of faecal samples revealed an high titre of Salmonella spp. and protozoa.

At the time of presentation, the three Great Danes were asymptomatic. Dogs’ growth was normal, as well as the level of activity and major organic functions. Dogs had been regularly vaccinated and submitted to prophylaxis against heartworm disease.

Cardiovascular physical examination

Dogs underwent a complete cardiovascular physical examination revealing a normal mucous membrane colour and normal capillary refilling times (< 2 sec).

In two dogs out of 3 (A and B) a rapid, irregular arterial pulse of variable strength was felt. Cardiac auscultation revealed tachycardia with irregular rhythm. Heart sounds varied in intensity beat by beat. A olosystolic, 3/6 heart murmur, best heard on the left apex, was audible in dogB.

In dog C, the pulse was regular but tachysphygmic. On cardiac auscultation heart sounds were normal and only tachycardia was present.

The auscultatory findings were consistent with atrial fibrillation in dogs A and B and with tachycardia in dog C.

An electrocardiographic examination has been performed on the three dogs in order to characterise the existing arrhythmias (Fig.1).

Dog A showed a low frequency atrial fibrillation with an average heart rate of 150 bpm, dog B a high frequency atrial fibrillation with an average heart rate of 200 bpm and dog C a sinus tachicardia with an average heart rate of 190 bpm.

EchocardiographyUltrasound imaging was performed with a SIM 7000 Challenge CFM machine and a 2.5-3.5 MHz transducer with conscious dogs restrained on an appropriate scanning table with a cutout.

Standard images have been obtained from the right and left parasternal views according to the guide-lines of Thomas et al., 199420.

Dog A

B-mode echocardiography showed a mild increase in left atrial diameter, as shown by an increased left atrium/aorta diameter ratio (LA/Ao = 2.1) measured from the right parasternal short-axis view at the heart base level. The right atrium appeared similarly enlarged. A mild dilation of ventricular chambers was apparent and a marked septal and parietal hypokinesis was appreciated (Fig. 2).

On Duplex echocardiography, a reduction of fractional shortening (FS) to value in the lower limit of the range reported for the breed has been observed: the FS, measured on 6 cardiac cycles to reduce the influence of ventricular rate and diastolic pause on ventricular filling, averaged 16%. Other relevant finding were an increased EPSS (13.8 mm) (Fig.3) and a slight increase of endo-diastolic (70 mm) and end-systolic (54.2 mm) diameters, as compared to normal values for Great Danes21,22.

Doppler evaluation of transvalvular flows was normal, with exception for predictable flow velocity variations related to variable ventricular filling due to atrial fibrillation.

Echocardiographic findings were consistent with dilated cardiomyopathy.

Dog B

Echocardiographic examination of dog B showed similar findings: increased end-diastolic (77 mm) and end-systolic (60 mm) left ventricle diameters, increased EPSS (15 mm), reduced FS (15%) and increased left atrium/aortic diameter ratio (LA/Ao = 3). Moreover, an high velocity regurgitant flow was registered at mitral level on spectral echocardiography (Fig. 4).

Echocardiographic findings were consistent with dilated cardiomyopathy.

Dog C

All measured parameters fell into normal range for this breed.

Treatment and follow-upDogs A an B have been allocated in Class I of heart failure according to the guide-lines of the NYHA and of the International Small Animal Cardiac Council.

To both dogs a therapy with ACE-inhibitors (enalapril: 0.5 mg/kg/b.i.d.) associated with digoxin (0.22 mg/m2/b.i.d.) and beta-blockers (propranolol: 0.5 mg/kg/t.i.d.) has been prescribed. Moreover, oral L-carnitine has been administered (5 grams/die).

At the 10-day follow-up, the owner reported weakness, lethargy and anorexia of dog A. Electrocardiographic tracing showed a persistent atrial fibrillation with marked reduction of ventricular rate (70 bpm). Digoxin administration has been discontinued and the dog has been maintained under beta-blocking therapy at the same dosage.

Dog B was still asymptomatic and the EKG showed a slowing of ventricular rate to 140 bpm. No therapy adjustment has been applied.

At the 15-day follow-up dog A showed an increase of heart rate to 80-100 bpm and the vanishing of previous clinical signs.

At the 8-month follow-up, echo-Doppler parameters were stable as compared to previous data for both dogs, A and B. EKG tracings showed atrial fibrillation with an heart rate of 100 and 140 bpm, respectively.

Dygoxinemia of dog B fell into normal range (1.2 ng/ml).

At 14-month follow-up a slight increase in EPSS (13.5 mm) and of LA/Ao ratio (2.7) has been observed in dog A. Atrial fibrillation was still present.

At 2-year follow-up dog A showed an increase in left ventricle end-diastolic (77 mm) and end-systolic (63.7 mm) diameters, an increase of EPSS (14.5 mm) and a slight decrease in FS (14%) as compared to previous controls, but clinical conditions were stable and no signs of heart failure have been manifested.

Dog B did not show consistent alterations in echo-Doppler and EKG parameters as compared to previous control.

Dog C has not been treated and at the time of writing it has not showed overt clinical signs of heart failure nor alterations of echocardiographic patterns.


DCM has been long suspected to be a familial disease in the dog with a possible genetic basis because of a high prevalence of the disease in certain breeds and specific families. Familial DCM has been demonstrated in Boxers5,10, Dobermans16, Irish Wolfhounds17, Portoguese water dog puppies18 and Newfoundlands19. In most cases the mode of inheritance has proved difficult to conclusively elucidate although most Authors suspect an autosomal dominant transmission (with the exception of Portoguese water dog pups DCM which is autosomal recessive).

The familial nature, male predominance and geographic variation in breed prevalence rates suggest that genes play an important role in the pathogenesis of DCM in dogs or initiating inherited DCM and/or influencing the progression of DCM caused by environmental (not genetic) factors.

Myocardial L-carnitine deficiency has received considerable attention as a possible cause of or contributor to cardiomyopathy in dogs and humans5,9,24-27. Carnitine plays important roles in mitochondrial metabolism, including transporting long-chain free fatty acids into the inner mitochondrial membrane where beta oxidation occurs. Because fatty acids are the heart’s major metabolic fuel, it is theorised that inadequate amounts of free L-carnitine could cause myocardial damage as a result of altered energy metabolism1,28.

In normal mammals, plasma and myocardial concentrations of carnitine are strictly related. However, reduced concentrations of myocardial L-carnitine have been measured in several canine breeds with DCM, including Boxers, Doberman Pinschers and American Cocker Spaniels. Dogs with low myocardial L-carnitine concentrations usually have normal plasma concentrations, suggesting the possibility of a membrane transport defect. Has been reported that the 80% of dogs with DCM have a myocardial deficiency of carnitine but normal to increased L-carnitine plasmatic level, while both myocardial and systemic L-carnitine deficiency is registered only in the 20 % of dogs with DCM26. As a result, the dosage of plasma concentration of carnitine is a specific but insensitive indicator for myocardial carnitine deficiency.

The response of dog with DCM to oral carnitine supplementation is also variable. In some dogs a dramatic improvement has been observed5 while in other cases of DCM a clinical subjective improvement has been noted, not supported by improved cardiac function as assessed by echocardiography24,26. Dogs with proved L-carnitine deficiency may not experience benefits from supplementation29.The supplementation with L-carnitine and taurine has been proved as beneficial in experimental study in American Cocker Spaniel with decreased plasma concentrations of both carnitine and taurine9.

As the natural history of dilated cardiomyopathy is variable and the most part of clinicians prescribe a combination of drugs to treat heart failure and arrhythmias associated to the disease, it is difficult to objectively evaluate the effects of carnitine supplementation on survival or on other clinical and cardiac function parameters29.

The early clinical benefits observed in the most part of dogs treated with oral L-carnitine were an increase of appetite and of activity level, as reported by the owners 1-4 weeks after starting supplementation. Cardiac function, as assessed by ultrasonography, showed a variable improvement only after 2-3 months of oral L-carnitine therapy. The clinical improvement could go on for 6-8 months until a "plateau" stage was reached, even if cardiac function remained depressed on echocardiography and no effects were noted on cardiac arrhythmias29.

The evidence suggests that L-carnitine deficiency is not the primary cause of most cases of canine DCM but it could occur secondary to other genetic or acquired abnormalities in approximately 40% of canine cases1,30.

As in most cases the primary cause of DCM can not be established and as myocardial L-carnitine deficiency can not be surely confirmed by blood examination but only by endomyocardial biopsy, it is a matter of discussion whether oral supplementation with L-carnitine should be given beside conventional therapy in dog with DCM, or not.

In three recently published papers, the percentage of survival of dogs affected from overt DCM at 1 year from the diagnosis was 37.5%31, 17.5%32 e 12%23, respectively. Lifespan dramatically decreases in Doberman Pinscher, where a mean survival time of 9.5 weeks has been reported after the occurrence of an episode of pulmonary edema33. According to Tidholm et al.32,1997, the worst prognostic factors are the young age, followed by the presence of ascites and dyspnea. According to Monnet et al.31,1995, pleural effusion and pulmonary oedema are the major negative prognostic elements. According to Calvert et al.33,1997, in Doberman Pinschers atrial fibrillation is associated with a shorter time of survival. According to Borgarelli et al.23,1998, major negative prognostic factors are the peak velocity of mitral regurgitation (MR) (lower chance of survival for dogs with MR < 4 m/sec as compared to dogs with MR > 4 m/sec: 54% vs 23% at 6 months; 31% vs. 15% at 1 year) and end-systolic left ventricular index (ESV-I) (the cumulative chance surviving at 12 months was 36% in dogs with ESV-I < 140 ml/m2 and 1% in dogs with ESV-I > 140 ml/m2).

In our experience, reported in this paper, affected dogs are still healthy at 2 year and 7 months from the diagnosis of DCM and the progression of the disease appears slowed down, as attested by the only slight variations in echocardiographic para-meters of systolic and diastolic function. Moreover, no dog has by now shown overt clinical signs of DCM, in spite of the young age and the presence of atrial fibrillation.

In these dogs oral L-carnitine has been administered without a preliminary evaluation of blood or byoptic endomyocardial carnitine contents. Moreover, supplementation has been associated with standard therapy of the disease based on the administration of ACE-inhibitors and anti-arrhythmc drugs, so it could be difficult to attribute the relative efficacy of L-carnitine integration on the course of the disease.

However, described cases have shown a better clinical course of the disease, as compared with the prognosis of DCM reported for dogs in recent literature. No objective improvement of cardiac function has been noticed in serial echocardiographic examinations, but the progression of the disease seems slowed down with reference to normal clinical history of DCM in absence of oral L-carnitine therapy.


The lack of an apparent univocal cause of DCM in the dog makes prevention and treatment of the disease a challenge for the clinician. In most cases, as it is impossible to demonstrate the initiating event causing DCM, only a symptomatic treatment is allowed, but the progression of the disease can not be avoided.

Ideally, carnitine supplementation should be instituted only if myocardial carnitine deficiency is certainly documented. Unfortunately, endomyocardial biopsy is a technique difficult to perform, invasive and hazardous. Moreover, plasma concentration of L-carnitine is an insensitive indicator of myocardial deficiency.

According to available statistical survey, at least 40% of dogs with heart failure secondary to DCM seems to have also a L-carnitine deficiency in association to other congenital or acquired defects. Probably, the most part of these dogs could take advantage from L-carnitine supplementation.

It is difficult to state if L-carnitine supplementation could be useful in all Great Danes with DCM or if this should be considered an isolated case. However, according to our observations, even in lack of diagnostic confirmation of endomyocardial carnitine deficiency, oral L-carnitine therapy could be reccomended in young dogs with familial CDM and with highly motivated clients who wish to pursue every treatment avenue.

Key words: dog, Great Dane, dilated cardiomyopathy, L-carnitine, therapy

Summary - Authors describe two cases of dilated cardiomyopathy in Great Danes belonging to the same litter and with a familial history of sudden death. The clinical course of the disease is discussed on the basis of given therapy, with particular reference to oral L-carnitine administration.

Reserach References Below Editorial Comment.

Editorial Comment:

Heart Problems: If you own a giant breed or one prone to heart problems it is recommended that you use the highest quality protein food and supplement with these components. These are nutritional substances from food sources and do not conflict with medications or each other and are good to use for heart disease.

1) Co-enzyme-Q-10 - 30 mg daily for maintenance dose - if one has heart problems then the dosage is more, see my article on Supplements for the Heart.

2) Taurine & L- Carnitine - Most dog foods now have high taurine levels it is L-Carnitine that is more of an issue today. If you want to supplement Taurine, pick a good brand from your health food store. For L- Carnitine - 100 mg for puppies - 200 - 1000 mg for adults and 3000 - 6000 mg is recommended for dogs with cardiomyopathy.

Dr. Wagner now carries a terrific and affordable liquid L-Carnitine - 1000 mg in 1 tablespoon.

These dosages are taken from the newest textbook Small Animal Clinical Nutrition and would be increased if the dog had been diagnosed with actual cardiomyopathy.


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18) Dambach D.M. et al.: Familial dilated cardiomyopathy of young Portoguese water dogs. J. Vet. Int. Med., 13, 65, 1999
19) Dukes Mc Ewan J.: The genetics of dilated cardiomyopathy in Newfoundland dogs. Proceedings 9th ESVIM Congress, Perugia, 60, 1999
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21) De Majo M., Masucci M., Pantano V.: Misurazioni ecocardiografiche in cani di razza Alano Tedesco: valori normali. Atti S.I.S.Vet., 51, 591, 1997
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24) Keene B.W., Kittleson M.D., Rush J.E.: Myocardial carnitine deficiency associated with dilated cardiomyopathy in Doberman Pinschers. Journal of Veterinary Internal Medicine, 3, 126, 1989
25) Gilbert E.F.: Carnitine deficiency. Pathology, 17, 161, 1985
26) Keene B.W.: L-carnitine deficiency in canine dilated cardiomyopathy. In Kirk R.W., Bonagura J.D. (Eds.): Kirk’s Current Veterinary Therapy, XI, W.B. Saunders Co., Philadelphia, 780, 1992
27) Keene B.W.: L-carnitine supplementation in the therapy of canine dilated cardiomyopathy. Veterinary Clinics of North America, Small Animal Practice, 21, 1005, 1991
28) Scholte H.R.: The role of the carnitine system in myocardial fatty acid oxidation: carnitine deficiency, failing mitochondria and cardiomyopathy. Basic Res Cardiol, 82 (Suppl. 11), 63, 1987
29) Costa N.D., Labuc R.H.: Case report: efficacy of oral carnitine therapy for dilated cardiomyopathy in Boxer dogs. J. Nutr., 124, 268, 1994
30) Keene B.W. et al.: Frequency of myocardial carnitine deficiency associated with spontaneous canine dilated cardiomyopathy. Proceedings of the 6th Annual Veterinary Medical Forum, 757, 1988
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32) Tidholm A., Svensson H., Sylvén C.: Survival and prognostic factors in 189 dogs with dilated cardiomyopathy. Journal of American Animal Hospital Association, 33, 544, 1997
33) Calvert C.A., Pickus C.W., Jacobs G.J. et al.: Signalement, survival and prognostic factors in Doberman Pinschers with end-stage cardiomyopathy. Journal of Veterinary Internal Medicine,11, 323, 1997

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