OBJECTIVE To assess signalment and concurrent disease processes in dogs with aortic thrombotic disease (ATD).
DESIGN Retrospective case-control study.
ANIMALS Dogs examined at North American veterinary teaching hospitals from 1985 through 2011 with medical records submitted to the Veterinary Medical Database.
PROCEDURES Medical records were reviewed to identify dogs with a diagnosis of ATD (case dogs). Five control dogs without a diagnosis of ATD were then identified for every case dog. Data were collected regarding dog age, sex, breed, body weight, and concurrent disease processes.
RESULTS ATD was diagnosed in 291 of the 984,973 (0.03%) dogs included in the database. The odds of a dog having ATD did not differ significantly by sex, age, or body weight. Compared with mixed-breed dogs, Shetland Sheepdogs had a significantly higher odds of ATD (OR, 2.59). Protein-losing nephropathy (64/291 [22%]) was the most commonly recorded concurrent disease in dogs with ATD.
CONCLUSIONS AND CLINICAL RELEVANCE Dogs with ATD did not differ significantly from dogs without ATD in most signalment variables. Contrary to previous reports, cardiac disease was not a common concurrent diagnosis in dogs with ATD.
A 12-year-old 23.0-kg (50.6-lb) neutered male mixed-breed dog was referred to the Veterinary Teaching Hospital at Colorado State University for evaluation of a chronic cough. For approximately 2 months prior to the referral evaluation, the dog had had daily episodes of nonproductive coughing, which had recently increased in frequency. During this period, the dog had been taken on 2-hour-long walks daily without any problems, and the owner reported no additional concerns.
At the evaluation, the dog was quiet and alert. Respiratory abnormalities were not discernible during thoracic auscultation, and a cough could not be elicited via tracheal palpation. The dog
A 9-year-old 21.7-kg (47.7-lb) spayed female Rottweiler was evaluated because of progressive weakness, lethargy, and diarrhea. Signs of weakness became noticeable approximately 4 weeks prior to evaluation. The dog's weakness progressively worsened, and the diarrhea had been unsuccessfully treated several times during that period. Several days prior to evaluation, the dog developed ascites. The dog was not receiving any medications other than a flea, tick, and heartworm preventative. On physical examination, bradycardia was detected and prompted echocardiographic and ECG examinations to be performed.
An initial lead II ECG tracing revealed an underlying sinus rhythm that was conducted with
A 4-year-old 31.0-kg (68.2-lb) castrated male mixed-breed dog was examined by the cardiology service at the Colorado State University Veterinary Teaching Hospital for a scheduled recheck examination and pacemaker interrogation. Previous diagnoses include bartonellosis; severe, chronic hepatitis; and third-degree (ie, complete) atrioventricular (AV) block. Intermittent atrial standstill attributable to some degree of sinoatrial dysfunction was also present. Two weeks prior to the recheck examination, a pacemaker with transdiaphragmatic epicardial leads had been placed in response to a 3-month history of labored breathing, lethargy, and syncope. Epicardial leads had been selected, rather than transvenous, endocardial leads, because the previously diagnosed
A 5-year-old 28.9-kg (63.6-lb) neutered male Boxer was referred to the Veterinary Medical Teaching Hospital at Texas A&M University for evaluation of an arrhythmia that was ausculted during routine physical examination. Two episodes of syncope had occurred 2 days prior to the evaluation. Additionally, occasional instances of cough were reported. The dog was successfully treated for heartworm infection 4 years earlier and had been given monthly heartworm preventative regularly since that time. The owner reported that the dog had a history of extreme anxiety during each visit to a veterinary hospital.
A 2-year-old 24-kg (53-lb) spayed female American Staffordshire Terrier was referred to the Texas A&M Veterinary Medical Teaching Hospital for potential pacemaker placement. Six days prior, the dog began to vomit persistently and became lethargic, anorectic, and hypodipsic. Results of a CBC (performed at the referring veterinary clinic) were within reference ranges. An abbreviated serum biochemical profile performed at the referring clinic revealed high BUN (66.4 mg/dL; reference range, 9.0 to 29.0 mg/dL) and creatinine (1.8 mg/dL; reference range, 0.4 to 1.4 mg/dL) concentrations; serum electrolyte concentrations were not measured. The referring veterinarian had administered a dose of barium contrast
A 5.0-kg (11.0-lb) 3-year-old sexually intact male Shih Tzu was referred for investigation of an enlarged heart that had been observed on routine thoracic radiographs by the referring veterinarian. When the patient was a puppy, medical records from the referring veterinarian indicated that a loud left-sided heart murmur was auscultated (murmur timing was not documented). This heart murmur decreased in intensity and was no longer present by 6 months of age. The patient had a recent history of gastrointestinal upset, but had been otherwise apparently healthy.
On physical examination, the patient was bright, alert, and responsive, with a heart
A 17-year-old 513-kg (1,129-lb) gray Holsteiner gelding was presented for evaluation of lethargy of indeterminate duration. On examination, the horse was markedly lethargic with dull attitude and exercise intolerance when walking. It was thin (body condition score, 3/9). Mucous membranes were pink and moist with a capillary refill time < 2 seconds. Heart rate was 28 beats/min, respiratory rate was 20 breaths/min, and rectal temperature was 37.6°C (99.8°F). Cardiac auscultation revealed a grade 3/6 left-sided, apical, systolic murmur as well as an irregularly irregular arrhythmia. Frequent pauses with presumptive S4 heart sounds were auscultated. Gastrointestinal sounds and digital pulses were
To investigate the effects of recombinant equine IL-1β on function of equine endothelial colony-forming cells (ECFCs) in vitro.
ECFCs derived from peripheral blood samples of 3 healthy adult geldings.
Function testing was performed to assess in vitro wound healing, tubule formation, cell adhesion, and uptake of 1,1′-dioctadecyl-3,3,3′,3′ tetramethylindocarbocyanine perchlorate–labeled acetylated low-density lipoprotein (DiI-Ac-LDL) by cultured ECFCs. Cell proliferation was determined by 2,3-bis-(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide assay. Effects on function test results of different concentrations and exposure times of recombinant equine IL-1β were assessed.
Challenge of cultured ECFCs with IL-1β for 48 hours inhibited tubule formation. Continuous challenge (54 hours) with IL-1β in the wound healing assay reduced gap closure. The IL-1β exposure did not significantly affect ECFC adhesion, DiI-Ac-LDL uptake, or ECFC proliferation.
CONCLUSIONS AND CLINICAL RELEVANCE
These results suggested a role for IL-1β in the inhibition of ECFC function in vitro. Functional changes in ECFCs following challenge with IL-1β did not appear to be due to changes in cell proliferative capacity. These findings have implications for designing microenvironments for and optimizing therapeutic effects of ECFCs used to treat ischemic diseases in horses.
To compare pharmacokinetics of levetiracetam in serum and CSF of cats after oral administration of extended-release (ER) levetiracetam.
9 healthy cats.
Cats received 1 dose of a commercially available ER levetiracetam product (500 mg, PO). Thirteen blood and 10 CSF samples were collected over a 24-hour period for pharmacokinetic analysis. After 1 week, cats received 1 dose of a compounded ER levetiracetam formulation (500 mg, PO), and samples were obtained at the same times for analysis.
CSF concentrations of levetiracetam closely paralleled serum concentrations. There were significant differences between the commercially available product and the compounded formulation for mean ± SD serum maximum concentration (Cmax; 126 ± 33 μg/mL and 169 ± 51 μg/mL, respectively), Cmax corrected for dose (0.83 ± 0.10 μg/mL/mg and 1.10 ± 0.28 μg/mL/mg, respectively), and time to Cmax (5.1 ± 1.6 hours and 3.1 ± 1.5 hours, respectively). Half-life for the commercially available product and compounded formulation of ER levetiracetam was 4.3 ± 2.0 hours and 5.0 ± 1.6 hours, respectively.
CONCLUSIONS AND CLINICAL RELEVANCE
The commercially available product and compounded formulation of ER levetiracetam both maintained concentrations in healthy cats 12 hours after oral administration that have been found to be therapeutic in humans (ie, 5 μg/mL). Results of this study supported dosing intervals of 12 hours, and potentially 24 hours, for oral administration of ER levetiracetam to cats. Monitoring of serum concentrations of levetiracetam can be used as an accurate representation of levetiracetam concentrations in CSF of cats.