Objective—To characterize risk factors, clinical findings,
usefulness of diagnostic tests, and prognosis in
cats with naturally occurring heartworm infection (HWI).
Animals—50 cats with Dirofilaria immitis infection.
Procedure—Medical records, thoracic radiographs,
and echocardiograms were reviewed and findings
compared with appropriate reference populations.
Results—Findings suggested that male cats were
not predisposed to HWI, domestic shorthair cats
were at increased risk, and indoor housing was only
partially protective. Fewer cases of HWI were identified
in the final quarter of the year, compared with
other periods, and prevalence is not apparently
increasing. Signs of respiratory tract disease were
most common, followed by vomiting. Infection was
diagnosed incidentally in > 25% of cats; conversely,
10% of infected cats died suddenly without other
clinical signs. Serologic tests were most useful for
diagnosis, followed by radiography and echocardiography.
Eosinophilia supported the diagnosis.
Overall median survival time was 1.5 years but
exceeded 4 years in cats surviving beyond the day
Conclusions and Clinical Relevance—Sex does not
appear to be a risk factor for HWI in cats, and indoor
housing provides only incomplete protection. Signs
of respiratory tract disease (dyspnea and cough) are
the strongest indicators of HWI in cats, and some
radiographic evidence of infection is detected in
most cases. Antibody screening for HWI in cats is
efficacious, and antigen testing and echocardiography
are most useful for making a definitive antemortem
diagnosis. (J Am Vet Med Assoc 2000;217:
Case Description—2 full-sibling male German Shorthaired Pointer (GSHP) puppies (dogs 1 and 2) with X-linked muscular dystrophy and deletion of the dystrophin gene (gene symbol, DMD) each had poor growth, skeletal muscle atrophy, pelvic limb weakness, episodic collapse, and episodes of coughing.
Clinical Findings—Initial examination revealed stunted growth, brachygnathism, trismus, and diffuse neuromuscular signs in each puppy; clinical signs were more severe in dog 2 than in dog 1. Immunohistochemical analysis revealed a lack of dystrophin protein in both dogs. During the next 3 years, each dog developed hyperinflation of the lungs, hypertrophy of the cervical musculature, and hypertrophy of the lateral head of the triceps brachii muscle.
Treatment and Outcome—Monitoring and supportive care were provided at follow-up visits during an approximately 7-year period. No other specific treatment was provided. Neuromuscular signs in both dogs remained stable after 3 years of age, with dog 2 consistently more severely affected than dog 1. The dogs had multiple episodes of aspiration pneumonia; dogs 1 and 2 were euthanatized at 84 and 93 months of age, respectively.
Clinical Relevance—The clinical course of disease in these dogs was monitored for a longer period than has been monitored in previous reports of dystrophin-deficient dogs. The clinical progression of muscular dystrophy in the 2 GSHPs was compared with that for other breeds and species with dystrophin-deficient conditions, and the potential basis for the phenotypic variation observed between these littermates, along with potential therapeutic ramifications for dogs and humans, was evaluated.
Objective—To determine the effect of long-term
administration of enalapril on renal function in dogs
with severe, compensated mitral regurgitation.
Design—Randomized controlled trial.
Animals—139 dogs with mitral regurgitation but
without overt signs of heart failure.
Procedure—Dogs were randomly assigned to be
treated with enalapril (0.5 mg/kg [0.23 mg/lb], PO,
q 24 h) or placebo, and serum creatinine and urea
nitrogen concentrations were measured at regular
intervals for up to 26 months.
Results—Adequate information on renal function
was obtained from 132 dogs; follow-up time ranged
from 0.5 to 26 months (median, 12 months). Mean
serum creatinine and urea nitrogen concentrations
were not significantly different between dogs receiving
enalapril and dogs receiving the placebo at any
time, nor were concentrations significantly different
from baseline concentrations. Proportions of dogs
that developed azotemia or that had a ≥ 35% increase
in serum creatinine or urea nitrogen concentration
were also not significantly different between groups.
Conclusions and Clinical Relevance—Results suggest
that administration of enalapril for up to 2 years
did not have any demonstrable adverse effects on
renal function in dogs with severe, compensated
mitral regurgitation. (J Am Vet Med Assoc 2002;221:
Animals—124 dogs with compensated mitral valve regurgitation (MR).
Procedures—Dogs randomly assigned to receive enalapril or placebo were monitored for the primary endpoint of onset of CHF for ≤ 58 months. Secondary endpoints included time from study entry to the combined endpoint of CHF-all-cause death; number of dogs free of CHF at 500, 1,000, and 1,500 days; and mean number of CHF-free days.
Results—Kaplan-Meier estimates of the effect of enalapril on the primary endpoint did not reveal a significant treatment benefit. Chronic enalapril administration did have a significant benefit on the combined endpoint of CHF-all-cause death (benefit was 317 days [10.6 months]). Dogs receiving enalapril remained free of CHF for a significantly longer time than those receiving placebo and were significantly more likely to be free of CHF at day 500 and at study end.
Conclusions and Clinical Relevance—Chronic enalapril treatment of dogs with naturally occurring, moderate to severe MR significantly delayed onset of CHF, compared with placebo, on the basis of number of CHF-free days, number of dogs free of CHF at days 500 and study end, and increased time to a combined secondary endpoint of CHF-all-cause death. Improvement in the primary endpoint, CHF-free survival, was not significant. Results suggest that enalapril modestly delays the onset of CHF in dogs with moderate to severe MR.