Objective—To determine the clinical usefulness of
cardiac event recording in evaluating dogs and cats
with unexplained syncope, episodic collapse, or intermittent
Animals—58 dogs and 2 cats.
Procedure—Medical records and electrocardiographic
rhythm strips obtained by cardiac event recordings
were reviewed. Cardiac rhythm data from the event
recordings were classified as diagnostic or nondiagnostic.
Diagnostic yield was calculated by dividing the
number of animals for which cardiac event recording
was diagnostic by the total number of animals undergoing
cardiac event recording.
Results—For 51 animals, cardiac event recording was
classified as diagnostic; therefore, overall diagnostic
yield was 85%. Diagnostic yield was lower for animals
without underlying structural heart disease
(75.5%) than for animals with structural heart disease
(95.6%). A specific arrhythmia was identified as the
cause of clinical signs in 18 of the 51 (35%) animals
for which cardiac event recording was diagnostic.
Cardiac arrhythmia was definitively excluded as the
cause of clinical signs in the remaining 33 (65%) animals
in which cardiac event recording was diagnostic.
Conclusions and Clinical Relevance—Results indicate
that cardiac event recording had a high diagnostic
yield in dogs and cats examined because of unexplained
syncope, episodic collapse, or transient weakness
and ataxia, regardless of whether animals did or
did not have an underlying structural heart disease.
Diagnostic yield of cardiac event recording was higher
than that reported previously for Holter monitoring.
(J Am Vet Med Assoc 2000;216:1110–1114)
OBJECTIVE To determine pharmacokinetic and pharmacodynamic properties of the novel factor Xa inhibitor apixaban in clinically normal cats.
ANIMALS 5 purpose-bred domestic shorthair cats.
PROCEDURES A single dose of apixaban (0.2 mg/kg, PO) was administered to each cat (time 0), and blood samples were obtained at 0, 15, 30, 45, 60, 120, 240, 360, 480, and 1,440 minutes. After a 1-week washout period, another dose of apixaban (0.2 mg/kg, IV) was administered to each cat, and blood samples were obtained at 0, 5, 10, 15, 30, 45, 60, 120, 240, 360, 480, and 1,440 minutes. Apixaban concentrations in plasma were measured via liquid chromatography–tandem mass spectrometry. Pharmacodynamic effects of apixaban were determined with a commercial assay for factor × activity, which measures endogenous factor Xa activity chromogenically.
RESULTS Factor Xa was inhibited as a function of time after a single dose of apixaban administered orally or IV, and a direct inverse correlation with the plasma apixaban concentration was detected. Pharmacokinetic analysis revealed moderate clearance, short half-life, and high bioavailability for apixaban. A 2-compartment model was fit to the IV pharmacokinetic data; compartmental modeling could not be used to adequately describe the oral data because of substantial interindividual variability.
CONCLUSIONS AND CLINICAL RELEVANCE Results inticated that apixaban was an effective inhibitor of factor Xa in cats. Further studies will be needed to determine pharmacokinetics and pharmacodynamics after multidose administration, effects of cardiac disease on pharmacokinetics and pharmacodynamics, dosing recommendations, and efficacy of apixaban for use in the treatment and prevention of thromboembolic disease in cats.
Case Description—A 20-year-old sexually intact female African Grey parrot (Psittacus erithacus) was evaluated to determine the cause of lethargy, hyporexia, weight loss, and persistent ascites of 21 days' duration.
Clinical Findings—Physical examination revealed a markedly distended abdomen and systolic heart murmur. Thoracic radiography revealed cardiomegaly and hepatomegaly. Doppler echocardiography revealed severe eccentric and concentric hypertrophy of the right ventricle with systolic dysfunction, moderate regurgitation through the right atrioventricular valve, a substantial increase in estimated systolic pulmonary arterial pressure, hepatic venous congestion, and coelomic effusion. A clinical diagnosis of chronic cor pulmonale was established.
Treatment and Outcome—The parrot was initially stabilized by use of coelomocentesis. During the next month, the parrot was treated by administration of furosemide, hydrochlorothiazide, spironolactone, benazepril, and pimobendan. The parrot appeared to be responding well to treatment but was found dead in its cage 35 days following initial examination. Postmortem examination revealed substantial atherosclerosis of the large pulmonary arteries, with lesions extending into the medium-size arteries. Pulmonary atherosclerosis was suspected as a cause of the severe pulmonary hypertension.
Clinical Relevance—Although atherosclerosis most commonly affects the systemic and coronary arteries of parrots, sclerotic changes within the pulmonary vasculature should be considered as a possible cause of pulmonary hypertension and as a differential diagnosis for right-sided congestive heart failure in psittacine species.