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Objective: To evaluate plasma taurine concentrations (PTC), whole blood taurine concentrations (WBTC), and echocardiographic findings in dogs fed 1 of 3 protein-restricted diets that varied in fat and L-carnitine content., Animals: 17 healthy Beagles., Design: Baseline PTC and WBTC were determined, and echocardiography was performed in all dogs consuming a maintenance diet. Dogs were then fed 1 of 3 protein-restricted diets for 48 months: a low-fat (LF) diet, a high-fat and L-carnitine supplemented (HF + C) diet, or a high-fat (HF) diet. All diets contained methionine and cystine concentrations at or above recommended Association of American Feed Control Officials (AAFCO) minimum requirements. Echocardiographic findings, PTC, and WBTC were evaluated every 6 months., Results: The PTC and WBTC were not significantly different among the 3 groups after 12 months. All groups had significant decreases in WBTC from baseline concentrations, and the HF group also had a significant decrease in PTC. One dog with PT and WBT deficiency developed dilated cardiomyopathy (DCM). Taurine supplementation resulted in significant improvement in cardiac function. Another dog with decreased WBTC developed changes compatible with early DCM., Conclusions and Clinical Relevance: Results revealed that dogs fed protein-restricted diets can develop decreased taurine concentrations; therefore, protein-restricted diets should be supplemented with taurine. Dietary methionine and cystine concentrations at or above AAFCO recommended minimum requirements did not prevent decreased taurine concentrations. The possibility exists that AAFCO recommended minimum requirements are not adequate for dogs consuming protein-restricted diets. Our results also revealed that, similar to cats, dogs can develop DCM secondary to taurine deficiency, and taurine supplementation can result in substantial improvement in cardiac function.

Turnover of carnitine in the body is primarily the result of renal excretion, and high-fat (HF) diets have been shown to increase urine carnitine excretion in healthy people. Recently, increased renal excretion of carnitine was observed in dogs diagnosed with cystinuria and carnitine deficiency. Carnitine deficiency has been linked to dilated cardiomyopathy and lipid storage myopathies in dogs and humans, and low-fat (LF) diets have been beneficial in some human patients with carnitine deficiency. In addition, HF, protein-restricted diets are often recommended for management of cystinuria in dogs. However, whether HF diets increase renal carnitine excretion in dogs or whether dogs with carnitine deficiency would benefit from LF diets remains unknown. Therefore, the purpose of this study was to determine the influence of dietary fat and carnitine on renal carnitine excretion in healthy dogs. Results from this study revealed that an HF diet increased urine carnitine excretion in dogs; however, carnitine excretion with the HF diet was not significantly different from that in dogs consuming an LF diet. Nonetheless, these results raise the possibility that increased renal carnitine excretion associated with HF diets could be one risk factor for development of carnitine deficiency in dogs with an underlying disorder in carnitine metabolism, and some dogs with carnitine deficiency may benefit from an LF diet. Another important observation in this study was that renal excretion of carnitine exceeded dietary intake in all diet groups, confirming previous reports that concluded that canine renal tubular cells reabsorb carnitine poorly when compared with those of humans.

Five client owned dogs with cystinuria were diagnosed with carnitine and taurine deficiency while participating in a clinical trial that used dietary management of their urolithiasis. Stored 24-hour urine samples collected from the cystinuric dogs before enrollment in the clinical diet trial were quantitatively evaluated for carnitine and taurine. These results were compared to those obtained from 18 healthy Beagles. Both groups of dogs were fed the same maintenance diet for a minimum of 2 weeks before 24-hour urine collection. The protocol used for 24-hour urine collections was the same for cystinuric dogs and healthy Beagles except that cystinuric dogs were catheterized at baseline, 8 hours, 12 hours, and at the end of the collection, whereas Beagles were catheterized at baseline, 8 hours, and at the end of the collection. Three of 5 dogs with cystinuria had increased renal excretion of carnitine. None of the cystinuric dogs had increased renal excretion of taurine, but cystinuric dogs excreted significantly less (P < .05) taurine in their urine than the healthy Beagles. Carnitinuria has not been recognized previously in either humans or dogs with cystinuria, and it may be 1 risk factor for developing carnitine deficiency. Cystinuric dogs in this study were not taurinuric; however, cystine is a precursor amino acid for taurine synthesis. Therefore, cystinuria may be 1 risk factor for developing taurine deficiency in dogs. We suggest that dogs with cystinuria be monitored for carnitine and taurine deficiency or supplemented with carnitine and taurine.

Clinical studies of a family of Saluki dogs demonstrated a spectrum of cardiac malformations, which ranged from mild thickening of a pulmonic valve leaflet to a complex condition composed of tricuspid valve insufficiency, pulmonic stenosis, patent ductus arteriosus, and mitral valve insufficiency. All affected dogs had patent ductus arteriosus or ductus diverticulum, which is an incomplete or atypical form of patent ductus arteriosus. The clinical findings varied with the type of cardiac lesion(s) found. Pedigree evaluation suggested a genetic cause, though environmental factors could not be excluded.

A case of permanent atrial standstill is described in a 10-month-old dog with ascites as a presenting complaint. The patient had absence of P waves in all leads in numerous ECG's and had a regular idioventricular rhythm. Pathologically, the patient had multiple areas of atrial and ventricular myocardial necrosis and fibrosis, with chronic active myocarditis and obliteration of the SA and AV node and AV bundle.

A 2-year-old Old English Sheepdog had right-side congestive heart failure characterized by pericardial effusion, pleural effusion, ascites, and increased pulmonary wedge pressure. A diagnosis of atrial septal defect was made by means of cardiac catheterization and angiography. Surgical correction initially was deferred because of pulmonary hypertension. However, when congestive heart failure could not be managed adequately, surgical correction was attempted. Postsurgically, thrombocytopenia developed and that led to bleeding, oliguira, and pulmonary edema. The bleeding was controlled by whole blood transfusion, but the oliguria and pulmonary edema were not resolved, even with intensive diuretic therapy. The dog died 24 hours after surgery.

Acetohydroxamic acid (AHA), a potent urease inhibitor used for treatment of infection-induced struvite urolithiasis, was teratogenic after administration of 25 mg of AHA/kg of body weight/day orally to 5 clinically normal Beagles from the onset of proestrus until parturition. Thirty pups exposed to AHA in utero developed anomalies of the skeletal system, heart, and ventral midline. Cardiac anomalies included atrial septal defects (20%), ventricular septal defects (3%), and atrial and ventricular septal defects (3%). Skeletal anomalies included coccygeal hemivertebrae and fused coccygeal vertebrae (50%), supernumerary vertebrae (67%), supernumerary ribs (50%), duplicated sternebrae (3%), and lumbar hemivertebrae (3%). Defects of the ventral midline of the abdominal wall occurred in 20% of AHA-exposed pups. Other abnormalities included retarded growth, high neonatal mortality, and a decreased number of circulating RBC, compared with those in 30 control pups born to 5 Beagles given a placebo. Adverse effects of AHA in pregnant Beagles were limited to morphologic alterations (Howell-Jolly bodies, spherocytes, and target cells) in a small number of circulating RBC. Slight neutrophilic leukocytosis and monocytosis occurred between 0 and 30 days of pregnancy in dogs given AHA, compared with those in controls. Seemingly, AHA did not influence fertility, conception rate, or length of gestation.

Basic differences were observed in the elctrocardiographic and vectorcardiogrpahic response to RVH in goats when compared to man and dogs. Instead of RVH inducing a redistribution of major fronts of electrical activity which result in profound QRS complex alterations as in man and dogs, it appears to produce no significant alteration of the QRS complex or major vector orientation in goats. Although slight reorientation of sagittal and horizontal vector forces occurred during development of RVH, no statistically significant changes could be detected.

In a case of double outlet right ventricle in a cat, initial examination revealed a holosystolic murmur and right-sided heart enlargement, as deduced from electrocardiography and thoracic radiography. On cardiac catheterization, it was determined that pressure in the right ventricle equaled that of the left ventricle. Angiography revealed a large ventricular septal defect, with prodominant left-to-right shunt and some right-to-left component. The cat lived for 3 1/2 years. During this period, the cat would become cyanotic only under stressful situations. At necropsy, the diagnosis was further refined to that of a double outlet right ventricle, as both the aorta and pulmonary artery originated from the right ventricle.