Objective—To compare results of 3 commercial
heartworm antigen test kits performed on serum
samples from dogs infected with low numbers of
adult female heartworms.
Design—Blinded laboratory evaluation.
Sample Population—Serum samples from dogs (n =
208) proven at necropsy to be infected with 1 to 4
adult female heartworms and from dogs (32) without
Procedure—Samples were sequentially tested with
each test kit, following the manufacturers' instructions,
by licensed veterinary technicians in private
practice who were not aware of infection status of
the dogs. The order of test kit evaluations was randomly
chosen. For each test kit, sensitivity, specificity,
accuracy, positive predictive value, and negative
predictive value were evaluated.
Results—All tests yielded some false-negative
results, and there were significant differences among
tests in regard to ability to detect low heartworm burdens.
Sensitivity of the test kits ranged from 78 to
84%. For all test kits, sensitivity increased as number
of female heartworms increased. All 3 test kits had
high specificity (97%).
Conclusions and Clinical Relevance—Results indicated
that sensitivity of the 3 commercially available
heartworm antigen test kits ranged from 78 to 84%
when used to test serum samples from dogs with
low heartworm burdens, and that sensitivity varied
among test kits. For all 3 test kits, specificity was
97%. All 3 test kits yielded false-positive and false-negative
results for some dogs with low heartworm
burdens. (J Am Vet Med Assoc 2003;222:1221–1223)
Objective—To determine whether a high dosage of pimobendan, when administered concurrently with moderate-dosage furosemide to healthy dogs, would activate the renin-angiotensin-aldosterone system (RAAS) more than furosemide alone.
Animals—12 healthy dogs.
Procedures—6 dogs received furosemide (2.0 mg/kg, PO, q 12 h) only, as an RAAS activator, for 10 days. The other 6 dogs received furosemide (2.0 mg/kg, PO, q 12 h) and pimobendan (0.6 mg/kg, PO, q 12 h) for 10 days. The effect of these drugs on the RAAS was determined by measurement of the aldosterone-to-creatinine ratio (A:C) in urine collected in the morning and evening of study days −2, −1, 1, 5, and 10.
Results—Although there was an increase in the urine A:C during the study period in both groups, it was significant only for dogs that received both drugs. The urine A:C only differed significantly between groups on day 1, at which time A:C was greater in the group that received both drugs.
Conclusions and Clinical Relevance—High-dosage pimobendan administration neither substantially suppressed nor potentiated the RAAS when administered with furosemide in healthy dogs.
OBJECTIVE To determine whether high doses of enalapril and benazepril would be more effective than standard doses of these drugs in suppressing the furosemide-activated renin-angiotensin-aldosterone system (RAAS).
ANIMALS 6 healthy Beagles.
PROCEDURES 2 experiments were conducted; each lasted 10 days, separated by a 2-week washout period. In experiment 1, all dogs received furosemide (2 mg/kg, PO, q 12 h) and enalapril (1 mg/kg, PO, q 12 h) for 8 days (days 0 through 7). In experiment 2, dogs received furosemide (2 mg/kg, PO, q 12 h) and benazepril (1 mg/kg, PO, q 12 h) for 8 days. Effects on the RAAS were determined by assessing serum angiotensin-converting enzyme (ACE) activity on days −1, 3, and 7; serum aldosterone concentration on days −2, −1, 1, 3, and 7; and the urinary aldosterone-creatinine ratio (UAldo:C) in urine collected in the morning and evening of days −2, −1, 1, 3, and 7.
RESULTS High doses of enalapril and benazepril caused significant reductions in serum ACE activity on all days but were not more effective than standard doses used in other studies. Mean UAldo:C remained significantly higher on days 2 through 7, compared with baseline values. Serum aldosterone concentration also increased after drug administration, which mirrored changes in the UAldo:C.
CONCLUSIONS AND CLINICAL RELEVANCE In this study, administration of high doses of enalapril and benazepril significantly inhibited ACE activity, yet did not prevent increases in mean urine and serum aldosterone concentrations resulting from furosemide activation of RAAS. This suggested that aldosterone breakthrough from ACE inhibition was a dose-independent effect of ACE inhibitors.
Objective—To perform polymerase chain reaction
(PCR) analysis on paraffin-embedded myocardium
from dogs with dilated cardiomyopathy (DCM) and
dogs with myocarditis to screen for canine parvovirus,
adenovirus types 1 and 2, and herpesvirus.
Sample Population—Myocardial specimens from 18
dogs with an antemortem diagnosis of DCM and 9
dogs with a histopathologic diagnosis of myocarditis
Procedure—Paraffin-embedded myocardial specimens
were screened for viral genome by PCR analysis.
Positive-control specimens were developed from
cell cultures as well as paraffin-embedded tissue
specimens from dogs with clinical and histopathologic
diagnoses of viral infection with canine parvovirus,
adenovirus types 1 and 2, and herpesvirus. The histologic
characteristics of all myocardial specimens were
classified regarding extent, location, and type of
inflammation and fibrosis.
Results—Canine adenovirus type 1 was amplified
from 1 specimen from a dog with DCM. Canine parvovirus,
adenovirus type 2, and herpesvirus were not
amplified from any myocardial specimens. Histologic
analysis of specimens from dogs with DCM revealed
variable amounts of fibrosis; myocardial inflammation
was observed in 1 affected dog. Histopathologic analysis
of specimens from dogs with myocarditis disclosed
variable degrees of inflammation and fibrosis.
Conclusions and Clinical Relevance—Viral agents
canine parvovirus, adenovirus types 1 and 2, and herpesvirus
are not commonly associated with DCM or
active myocarditis in dogs. Additional studies evaluating
for nucleic acid from viruses that less commonly
affect dogs or different types of infectious agents may
be warranted to gain insight into the cause of DCM
and myocarditis in dogs. ( Am J Vet Res 2001;62:
Objective—To determine the usefulness of echocardiography
in the diagnosis of heartworm disease in cats and to compare this modality with other tests.
Animals—43 cats with heartworm infection that had echocardiographic examinations at 2 veterinary teaching hospitals between 1985 and 1997. Twenty-two of these 43 cats also underwent radiography of the thorax and heartworm antibody and heartworm antigen testing.
Procedure—Cats were determined to be infected with Dirofilaria immitis infection on the basis of 1 or more of the following findings: positive modified Knott or antigen test result, echocardiographic evidence of heartworm disease, or confirmation of the disease on postmortem examination. The percentage of echocardiographs in which heartworms were evident was compared with the percentage of radiographs in which pulmonary artery enlargement was evident and results of antigen or antibody tests in cats in which all tests were performed.
Results—Overall, heartworms were detectable by use of echocardiography in 17 of 43 cats, most often in the pulmonary arteries. In the 22 cats in which all tests were performed, antibody test results were positive in 18, antigen test results were positive in 12, and pulmonary artery enlargement was evident radiographically and heartworms were identifiable echocardiographically in 14. Heartworm infection was diagnosed exclusively by use of echocardiography in 5 cats in which the antigen test result was negative.
Conclusions and Clinical Relevance—Although echocardiography was less sensitive than antigen testing, it was a useful adjunctive test in cats that had negative antigen test results in which there was a suspicion of heartworm disease. The pulmonary arteries should be evaluated carefully to increase the likelihood of detection of heartworms echocardiographically. ( J Am Vet Med Assoc2001;218:66–69)
Objective—To characterize clinical and clinicopathologic
findings, response to treatment, and causes of
systemic hypertension in cats with hypertensive
Animals—69 cats with hypertensive retinopathy.
Procedure—Medical records from cats with systemic
hypertension and hypertensive retinopathy were
Results—Most cats (68.1%) were referred because
of vision loss; retinal detachment, hemorrhage,
edema, and degeneration were common findings.
Cardiac abnormalities were detected in 37 cats, and
neurologic signs were detected in 20 cats.
Hypertension was diagnosed concurrently with chronic
renal failure (n = 22), hyperthyroidism (5), diabetes
mellitus (2), and hyperaldosteronism (1). A clearly
identifiable cause for hypertension was not detected
in 38 cats; 26 of these cats had mild azotemia, and 12
did not have renal abnormalities. Amlodipine
decreased blood pressure in 31 of 32 cats and
improved ocular signs in 18 of 26 cats.
Conclusions and Clinical Relevance—Retinal
lesions, caused predominantly by choroidal injury, are
common in cats with hypertension. Primary hypertension
in cats may be more common than currently
recognized. Hypertension should be considered in
older cats with acute onset of blindness; retinal
edema, hemorrhage, or detachment; cardiac disease;
or neurologic abnormalities. Cats with hypertensioninduced
ocular disease should be evaluated for renal
failure, hyperthyroidism, diabetes mellitus, and cardiac
abnormalities. Blood pressure measurements
and funduscopic evaluations should be performed
routinely in cats at risk for hypertension (preexisting
renal disease, hyperthyroidism, and age > 10 years).
Amlodipine is an effective antihypertensive agent in
cats.(J Am Vet Med Assoc 2000;217:695–702)
Objective—To evaluate the effect of administration of the labeled dosage of pimobendan to dogs with furosemide-induced activation of the renin-angiotensin-aldosterone system (RAAS).
Animals—12 healthy hound-type dogs.
Procedures—Dogs were allocated into 2 groups (6 dogs/group). One group received furosemide (2 mg/kg, PO, q 12 h) for 10 days (days 1 to 10). The second group received a combination of furosemide (2 mg/kg, PO, q 12 h) and pimobendan (0.25 mg/kg, PO, q 12 h) for 10 days (days 1 to 10). To determine the effect of the medications on the RAAS, 2 urine samples/d were obtained for determination of the urinary aldosterone-to-creatinine ratio (A:C) on days 0 (baseline), 5, and 10.
Results—Mean ± SD urinary A:C increased significantly after administration of furosemide (baseline, 0.37 ± 0.14 μg/g; day 5, 0.89 ± 0.23 μg/g) or the combination of furosemide and pimobendan (baseline, 0.36 ± 0.22 μg/g; day 5, 0.88 ± 0.55 μg/g). Mean urinary A:C on day 10 was 0.95 ± 0.63 μg/g for furosemide alone and 0.85 ± 0.21 μg/g for the combination of furosemide and pimobendan.
Conclusions and Clinical Relevance—Furosemide-induced RAAS activation appeared to plateau by day 5. Administration of pimobendan at a standard dosage did not enhance or suppress furosemide-induced RAAS activation. These results in clinically normal dogs suggested that furosemide, administered with or without pimobendan, should be accompanied by RAAS-suppressive treatment.