Traditional and nontraditional effective and noneffective therapies for cardiac disease in dogs and cats (original) (raw)
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Journal of Veterinary Internal Medicine, 1997
Fourteen American Cocker Spaniels (ACS) with dilated cardiomyopathy (DCM) were studied to determine if individuals of this breed with DCM are systemically taurine-or carnitinedeficient and to determine if they are responsive to taurine and carnitine supplementation. American Cocker Spaniels with DCM were identified using echocardiography, and plasma was analyzed for taurine and carnitine concentrations. Each dog was randomly assigned to receive either taurine and carnitine supplementation or placebos. Echocardiograms and clinical examinations were repeated monthly for 4 months. During this period, the investigators and owners were blinded with respect to the treatment being administered. Each dog was weaned off its cardiovascular drugs (furosemide, digoxin, and an angiotensin converting enzyme inhibitor) if an echocardiographic response was identified. At the 4-month time period, each investigator was asked to decide whether he or she thought his or her patient was receiving placebo or taurine/ carnitine, based on presence or absence of clinical and echocardiographic improvement. Unblinding then occurred, and dogs receiving placebos were switched to taurine and carnitine supplementation and followed monthly for 4 additional months.
Journal of Veterinary Internal Medicine, 1991
M-mode echocardiography was completed and plasma taurine concentrations were determined in 79 healthy cats and 77 cats with dilated cardiomyopathy (DCM). In healthy cats, a relationship was not observed between plasma taurine concentrations and any M-mode echocardiographic measurement. End-systolic and end-diastolic cardiac chamber dimensions were larger; wall thickness measures were smaller; and calculations of fractional shortening were less in cats with DCM than in healthy cats. Plasma taurine concentrations < 30 nmol/mL were detected in 7/79 healthy cats and in 52/77 cats with DCM. Of the 52 cats with D C M and an initial plasma taurine concentration < 30 nmol/mL, 23 died or were euthanized during the first post-treatment week, 7 were lost to further study, and 22 improved after taurine supplementation. Of the 25 cats with D C M and an initial plasma taurine concentration 2 30 nmol/mL, 9 died or were euthanatized during the first post-treatment week, and 9 were lost to further study. Two cats did not improve, of which one died and one was euthanatized 4 to 8 weeks after initiation of taurine supplementation. Five cats with a plasma taurine concentration 2 30 nmol/mL improved after taurine supplementation. Myocardial function subsequently deteriorated in three of these cats. Two of the three cats had signs of congestive heart failure redevelop.
Taurine's role in clinical practice
Journal of Small Animal Practice, 1990
Dilated cardiomyopathy has been recognised as a significant heart disease and cause of death in pet cats in the United States. The cause of dilated cardiomyopathy which was unknown and the prognosis grave. An association between low plasma taurine concentrations and dilated cardiomyopathy was established. Daily administration of taurine (250-1000 mg) orally increased plasma taurine concentrations and reversed the clinical signs. It was previously thought that cats became taurine deficient when fed commercial dog food or unbalanced home-cooked diets. We found a high association between the type of diet fed, plasma taurine concentrations and the incidence of myocardial failure and feline central retinal regeneration. Many commercial cat foods were found to cause taurine depletion associated with myocardial failure or central retinal degeneration. It is now established that taurine deficiency is a major cause of myocardial failure in cats and that modification of commercial cat food formulations with regard to taurine content has resulted in a dramatic decrease in the incidence of dilated cardiomyopathy in cats in the United States.
Non-taurine responsive dilated cardiomyopathy in 2 cats
Ankara Üniversitesi Veteriner Fakültesi Dergisi, 2020
Feline dilated cardiomyopathy (DCM) is a rare disease characterized by myocardial failure and systolic dysfunction. Taurine deficiency is the most important cause of DCM phenotype in cats. A 2 year-old Scottish fold and a 8 month-old domestic shorthair cat were referred to hospital with anorexia, weakness and increased respiratory effort. Based on electrocardiographic, radiographic and echocardiographic findings, the both cases were diagnosed with DCM. The cases were managed with pimobendan, furosemide, acetylsalicylic acid and taurine. The cats were more active and clinically healthy during 15 days follow-up. No remarkable changes were observed in follow up echocardiographies. The cases presented here reflect the clinical signs, cardiological examination findings, diagnosis and management of idiopathic DCMin 2 cats.
Taurine-Deficient Dilated Cardiomyopathy in a Family of Golden Retrievers
Journal of the American Animal Hospital Association, 2005
A reversible taurine-deficient dilated cardiomyopathy occurred in five related golden retrievers. An apical systolic heart murmur was the most common physical abnormality. According to fractional shortening and end-systolic diameter on echocardiography, significant improvements (P<0.005) were recorded within 3 to 6 months of starting taurine supplementation. The dogs regained substantial systolic function, and four were weaned off all cardiac medications except taurine. This response to therapy was unusual, because canine dilated cardiomyopathy is generally progressive and fatal.
Plasma Taurine Concentrations in Normal Dogs and in Dogs With Heart Disease
Journal of Veterinary Internal Medicine, 1995
Plasma taurine concentrations were determined in 76 dogs with dilated cardiomyopathy (DCM), 28 dogs with acquired valvular disease (AVD), and 47 normal (control) dogs. The data were collected at 2 referral centers, The Animal Medical Center, New York, NY (AMC), and the University of California, Davis (UCD), and the studies were conducted independently. Different anticoagulants (sodium citrate at AMC and lithium heparin at UCD) were used to collect the plasma samples. Paired analysis of samples showed a significant difference in plasma taurine concentrations, depending on the anticoagulant used. Consequently, results from each clinic were analyzed separately. Plasma taurine concentrations were significantly higher in dogs with AVD (median, 133 nmol/mL; range, 25 to 229 nmol/mL) than in control dogs (median, 63 nmol/ml; range 44 to 224 nmol/mL) and dogs with DCM (median, 72 nmol/ mL; range, 1 to247 nmol/mL) at AMC (P< .001). Thenumber of dogs with AVD at UCD was too small to draw meaningful conclusions. At UCD, the median plasma taurine concentration was 98 nmol/mL (range, 28-1 69 nmol/mL) aurine (Zaminoethane sulfonic acid) is the most abun-