Right axis deviation in the canine electrocardiogram for predicting severity of pulmonic stenosis: a retrospective cohort analysis.

OBJECTIVE: To investigate the predictive value of right axis deviation of the mean electrical axis (MEA) in assessing the severity of pulmonic stenosis (PS) in dogs. ANIMALS: Records for 218 client-owned dogs diagnosed between 2014 and 2020 with PS as determined by Doppler echocardiography. PROCEDURES: University of Florida Small Animal Clinic medical records were reviewed, and signalment and clinical risk variables (murmur grade and clinical signs) were extracted. MEA was determined from ECG records by use of leads I and III. Predictive potential of MEA and associated risk factors to diagnose PS severity (mild [< 50 mm Hg], moderate, or severe [> 75 mm Hg]) were assessed by receiver-operating characteristic curve analysis and quantile regression. RESULTS: Records for 88 dogs were eligible for analysis. Greater PS severity was associated with smaller breeds presenting with ECG abnormalities, overt clinical signs, and high-category murmur grades (IV and V). Mean MEA increased with stenosis severity category, with an average of 62° for mild, 113° for moderate, and 157° for severe. Each 10° increase in MEA corresponded to an approximately 5-mm Hg increase in PG. Increasing PS severity was associated with MEA right axis deviation > 100° and the more severe cases (PG > 75 mm Hg) with MEA right axis deviation > -180°. CLINICAL RELEVANCE: Mean electrical axis right axis deviation may be a useful screening metric for dogs with suspected moderate to severe PS.

Evaluation of benazepril in cats with heart disease in a prospective, randomized, blinded, placebo-controlled clinical trial.

BACKGROUND: Heart disease is an important cause of morbidity and mortality in cats, but there is limited evidence of the benefit of any medication. HYPOTHESIS: The angiotensin-converting enzyme inhibitor benazepril would delay the time to treatment failure in cats with heart disease of various etiologies. ANIMALS: One hundred fifty-one client-owned cats. METHODS: Cats with heart disease, confirmed by echocardiography, with or without clinical signs of congestive heart failure, were recruited between 2002 and 2005 and randomized to benazepril or placebo in a prospective, multicenter, parallel-group, blinded clinical trial. Benazepril (0.5-1.0 mg/kg) or placebo was administered PO once daily for up to 2 years. The primary endpoint was treatment failure. Analyses were conducted separately for all-cause treatment failure (main analysis) and heart disease-related treatment failure (supportive analysis). RESULTS: No benefit of benazepril versus placebo was detected for time to all-cause treatment failure (P = .42) or time to treatment failure related to heart disease (P = .21). Hazard ratios (95% confidence interval [CI]) from multivariate analysis for benazepril compared with placebo were 1.00 (0.57-1.74) for all-cause failure, and 0.99 (0.50-1.94) for forward selection and 0.93 (0.48-1.81) for bidirectional selection models for heart disease-related failure. There were no significant differences between groups over time after administration of the test articles in left atrium diameter, left ventricle wall thickness, quality of life scores, adverse events, or plasma biochemistry or hematology variables. CONCLUSIONS AND CLINICAL RELEVANCE: Benazepril was tolerated well in cats with heart disease, but no evidence of benefit was detected.

Barium toxicosis in a dog.

CASE DESCRIPTION: A 2-year-old 14.9-kg (32.8-lb) neutered female Shetland Sheepdog was admitted to the University of Liverpool Small Animal Teaching Hospital for evaluation of acute collapse. CLINICAL FINDINGS: At admission, the dog was tachypneic and had reduced limb reflexes and muscle tone in all limbs consistent with diffuse lower motor neuron dysfunction. The dog was severely hypokalemic (1.7 mEq/L; reference range, 3.5 to 5.8 mEq/L). Clinical status of the dog deteriorated; there was muscle twitching, flaccid paralysis, and respiratory failure, which was considered a result of respiratory muscle weakness. Ventricular arrhythmias and severe acidemia (pH, 7.18; reference range, 7.35 to 7.45) developed. Intoxication was suspected, and plasma and urine samples submitted for barium analysis had barium concentrations comparable with those reported in humans with barium toxicosis. Analysis of barium concentrations in 5 control dogs supported the diagnosis of barium toxicosis in the dog. TREATMENT AND OUTCOME: Fluids and potassium supplementation were administered IV. The dog recovered rapidly. Electrolyte concentrations measured after recovery were consistently unremarkable. Quantification of plasma barium concentration 56 days after the presumed episode of intoxication revealed a large decrease; however, the plasma barium concentration remained elevated, compared with that in control dogs. CLINICAL RELEVANCE: To our knowledge, this case represented the first description of barium toxicosis in the veterinary literature. Barium toxicosis can cause life-threatening hypokalemia; however, prompt supportive treatment can yield excellent outcomes. Barium toxicosis is a rare but important differential diagnosis in animals with hypokalemia and appropriate clinical signs.