Page 179 - Small Animal Internal Medicine, 6th Edition
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CHAPTER 7   Myocardial Diseases of the Dog   151


            and biologic toxins (wasp or scorpion stings, snake venom,   trial  of supplemental  taurine  for  3  to 4  months  is  recom-
            spider bites).                                       mended (see p. 73 for supplementation guidelines). However,
  VetBooks.ir  METABOLIC AND NUTRITIONAL                         the effect of taurine supplementation on disease progression
                                                                 is unclear. Taurine-deficient dogs may show echocardio-
            DEFICIENCY
              L-carnitine                                        graphic improvement after supplementation; however, some
                                                                 degree of cardiac abnormality often persists, and there is
              L-carnitine is an essential component of the mitochon-  questionable effect on survival time.
            drial membrane transport system for fatty acids, which are   Other factors
            the heart’s most important energy source. It also transports   Myocardial injury induced by free radicals may play a role
            potentially toxic metabolites out of the mitochondria in the   in a number of diseases. Evidence for increased oxidative
            form of carnitine esters. L-carnitine-linked defects in myo-  stress has been found in dogs with CHF and myocardial
            cardial metabolism have been found in some dogs with   failure, but the clinical ramifications of this are unclear. Dis-
            DCM.  Rather  than  simple  L-carnitine  deficiency,  one  or   eases such as hypothyroidism, pheochromocytoma, and dia-
            more underlying genetic or acquired metabolic defects are   betes mellitus have been associated with reduced myocardial
            suspected. There may be an association between DCM and   function, but clinical CHF is unusual in dogs secondary to
            carnitine deficiency in some families of Boxers, Doberman   these conditions alone. Excessive sympathetic stimulation
            Pinschers, Great Danes, Irish Wolfhounds, Newfoundlands,   stemming from brain or spinal cord injury results in myo-
            and Cocker Spaniels. L-carnitine is mainly present in foods   cardial hemorrhage, necrosis, and arrhythmias (brain-heart
            of animal origin. DCM has developed in some dogs fed strict   syndrome). Muscular dystrophy of the fasciohumoral type
            vegetarian diets.                                    (reported in English Springer Spaniels) can result in atrial
              Plasma carnitine concentration is not a sensitive indicator   standstill and heart failure. Canine X-linked (Duchenne)
            of myocardial carnitine deficiency. Most dogs with myocar-  muscular dystrophy in Golden Retrievers and other breeds
            dial carnitine deficiency, diagnosed via endomyocardial   also has been associated with myocardial fibrosis and min-
            biopsy, have had normal or high plasma carnitine concentra-  eralization, with subsequent LV systolic dysfunction and
            tions. Furthermore, the response to oral carnitine supple-  CHF. Rarely, nonneoplastic (e.g., glycogen storage disease)
            mentation is inconsistent. Subjective improvement may   and neoplastic (metastatic and primary) infiltrates interfere
            occur, but few dogs have echocardiographic evidence of   with normal myocardial function. Immunologic mecha-
            improved function. Dogs that do respond show clinical   nisms also could play an important role in the pathogenesis
            improvement within the first month of supplementation;   of myocardial dysfunction in some dogs with myocarditis.
            there may be some degree of improvement in echo param-
            eters after 2 to 3 months. L-carnitine supplementation does   ISCHEMIC MYOCARDIAL DISEASE
            not suppress preexisting arrhythmias or prevent sudden   Acute myocardial infarction resulting from coronary embo-
            death. See p. 73 for supplementation guidelines.     lization is uncommon. An underlying disease associated
              Taurine                                            with increased risk for thromboembolism, such as bacterial
              Although most dogs with DCM are not taurine deficient,   endocarditis, neoplasia, protein-losing nephropathy or
            low plasma taurine concentration has been documented in   enteropathy, immune-mediated hemolytic anemia, acute
            some and appears particularly common in certain breeds.   pancreatitis, disseminated intravascular coagulopathy, and/
            Low taurine, and sometimes carnitine, concentrations occur   or corticosteroid use, underlies most cases. Sporadic reports
            in Cocker Spaniels with DCM. Oral supplementation of   of myocardial infarction have been associated with con-
            these amino acids can improve LV size and function, as well   genital ventricular outflow obstruction, patent ductus arte-
            as reduce the need for heart failure medications in this breed.   riosus, hypertrophic cardiomyopathy, and mitral insufficiency.
            Low taurine concentrations have also been found in some   Atherosclerosis of the major coronary arteries, which can
            Newfoundlands, Golden Retrievers, Labrador Retrievers,   accompany severe hypothyroidism in dogs, rarely leads to
            Saint Bernards, and other dogs with DCM. Some such dogs   acute  myocardial  infarction.  Clinical  signs  of  acute  major
            have been fed low-protein lamb meal and rice, or vegetarian   coronary  artery  obstruction  are  likely  to  include  arrhyth-
            diets; others have been consuming diets with adequate   mias, pulmonary edema, marked ST segment change on
            taurine content. In particular, DCM has been identified in   ECG, and evidence of regional or global myocardial contrac-
            Dalmatians fed protein-restricted diets for prevention of   tile dysfunction on echocardiogram. High circulating cardiac
            breed-related urate urolithiasis.                    troponin concentrations and possibly creatine kinase activity
              Assessment of plasma or whole blood taurine concentra-  occur after myocardial injury and necrosis.
            tion should be considered in “atypical” breeds affected with   Disease of small coronary vessels is recognized as well.
            DCM or any dog with concern for nutritional deficiency   Nonatherosclerotic narrowing of small coronary arteries
            based on diet history. Plasma taurine concentrations less   could be more clinically important than previously assumed.
            than 40 nmol/mL and blood taurine concentrations less than   Hyalinization of small coronary vessels and intramural myo-
            150 nmol/mL are generally considered deficient. Specific col-  cardial infarctions have been described in dogs with chronic
            lection and submission guidelines should be obtained from   degenerative mitral valve disease; however, they can occur
            the laboratory used. If taurine deficiency is documented, a   in older dogs without valve disease as well. Fibromuscular
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