Objective—To determine survival times in dogs with
severe subvalvular aortic stenosis (SAS) treated by
means of balloon valvuloplasty or with atenolol, a
β-adrenoceptor blocking drug.
Animals—38 dogs < 24 months old with severe SAS
(peak systolic pressure gradient ≥ 80 mm Hg).
Procedure—10 dogs underwent balloon valvuloplasty
and were reexamined 6 weeks later to determine the
feasibility of the procedure. The remaining 28 dogs
were randomly assigned to undergo balloon valvuloplasty
(n = 15) or to be treated with atenolol long term
(13) and were reexamined annually for 9 years or until
the time of death.
Results—For the first 10 dogs, mean pressure gradient
6 weeks after balloon valvuloplasty (mean ± SD,
119 ± 32.6 mm Hg) was significantly decreased, compared
with mean baseline pressure gradient (167 ±
40.1 mm Hg). Median survival time for dogs that
underwent balloon valvuloplasty (55 months) was not
significantly different from median survival time for
dogs treated with atenolol (56 months).
Conclusions and Clinical Relevance—Results suggest
that balloon valvuloplasty can result in a significant
decrease in the peak systolic pressure gradient
in dogs with severe SAS, at least for the short term.
No clear benefit in survival times was seen for dogs
that underwent balloon valvuloplasty versus dogs that
were treated with atenolol. (J Am Vet Med Assoc
Objective—To measure QT interval duration and QT
dispersion in Boxers and to determine whether QT
variables correlate with indices of disease severity in
Boxers with familial ventricular arrhythmias, including
the number of ventricular premature complexes per
day, arrhythmia grade, and fractional shortening.
Animals—25 Boxers were evaluated by ECG and
Procedure—The QT interval duration was measured
from 12-lead ECG and corrected for heart rate (QTc),
using Fridericia's formula. The QT and QTc were calculated
for each lead, from which QT and QTc dispersion
were determined. Echocardiography and 24-hour
ambulatory ECG were performed to evaluate for
familial ventricular arrhythmias. Total number of ventricular
premature complexes, arrhythmia grade, and
fractional shortening were determined and used as
indices of disease severity.
Results—There was no correlation between any QT
variable and total number of ventricular premature
complexes, arrhythmia grade, or fractional shortening.
No difference between QT dispersion and QTc
dispersion was identified, and correction for heart rate
did not affect the results.
Conclusions and Clinical Relevance—QT interval
duration and dispersion did not correlate with indices
of disease severity for familial ventricular arrhythmias.
Heart rate correction of the QT interval did not appear
to be necessary for QT dispersion calculation in this
group of dogs. QT dispersion does not appear to be a
useful noninvasive diagnostic tool in the evaluation of
familial ventricular arrhythmias of Boxers.
Identification of affected individuals at risk for sudden
death remains a challenge in the management of this
disease. (Am J Vet Res 2001;62:1481–1485)
Objective—To evaluate the coding region of the cardiac
actin gene in Doberman Pinschers with dilated
cardiomyopathy (DCM) for mutations that could be
responsible for the development of the condition
Animals—28 dogs (16 Doberman Pinschers with
DCM and 12 mixed-breed control dogs).
Procedure—Ten milliliters of blood was collected
from each dog for DNA extraction.
Polymerase chain reaction (PCR) primers were
designed to amplify canine exonic regions, using the
sequences of exons 2 to 6 of the cardiac actin gene.
Single-stranded conformational polymorphism analysis
was performed for each exon with all samples.
Autoradiographs were analyzed for banding patterns
specific to affected dogs. The DNA sequencing was
performed on a selected group of affected and control
Results—Molecular analysis of exons 2 to 6 of the
cardiac actin gene did not reveal any differences in
base pairs between affected dogs and control dogs
selected for DNA evaluation.
Conclusions—Mutations in exons 5 and 6 of the cardiac
actin gene that have been reported in humans
with familial DCM do not appear to be the cause of
familial DCM in Doberman Pinschers. Additionally,
evaluation of exons 2 to 6 for causative mutations did
not reveal a cause for inherited DCM in these
Doberman Pinschers. Although there is evidence that
DCM in Doberman Pinschers is an inherited problem,
a molecular basis for this condition remains unresolved.
Evaluation of other genes coding for
cytoskeletal proteins is warranted. ( Am J Vet Res
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 evaluate the potential importance of
dystrophin, α-sarcoglycan (adhalin), and β-dystroglycan,
by use of western blot analysis, in several breeds
of dogs with dilated cardiomyopathy.
Sample Population—Myocardial samples obtained
from 12 dogs were evaluated, including tissues from
7 dogs affected with dilated cardiomyopathy, 4 control
dogs with no identifiable heart disease (positive control),
and 1 dog affected with Duchenne muscular dystrophy
(negative control for dystrophin). Of the affected
dogs, 4 breeds were represented (Doberman
Pinscher, Dalmatian, Bullmastiff, and Irish
Procedure—Western blot analysis was used for evaluation
of myocardial samples obtained from dogs
with and without dilated cardiomyopathy for the presence
of dystrophin and 2 of its associated glycoproteins,
α-sarcoglycan and β-dystroglycan.
Results—Detectable differences were not identified
between dogs with and without myocardial disease in
any of the proteins evaluated.
Conclusions and Clinical Relevance—Abnormalities
in dystrophin, α-sarcoglycan, and β-dystroglycan proteins
were not associated with the development of
dilated cardiomyopathy in the dogs evaluated in this
study. In humans, the development of molecular biological
techniques has allowed for the identification of
specific causes of dilated cardiomyopathy that were
once considered to be idiopathic. The use of similar
techniques in veterinary medicine may aid in the identification
of the cause of idiopathic dilated cardiomyopathy
in dogs, and may offer new avenues for therapeutic
intervention. ( Am J Vet Res 2001;62:67–71)
Objective—To determine whether serum N-terminal pro-B-type natriuretic peptide (NT-proBNP) concentration is useful in discriminating between cardiac and noncardiac (ie, primary respiratory tract disease) causes of respiratory signs (ie, coughing, stertor, stridor, excessive panting, increased respiratory effort, tachypnea, or overt respiratory distress) in dogs.
Design—Multicenter cross-sectional study.
Animals—115 dogs with respiratory signs.
Procedures—Dogs with respiratory signs were solicited for study. Physical examination, thoracic radiography, and echocardiography were used to determine whether respiratory signs were the result of cardiac (ie, congestive heart failure) or noncardiac (ie, primary respiratory tract disease) causes. Serum samples for NT-proBNP assay were obtained at time of admission for each dog. Receiver-operating characteristic curves were constructed to determine the ability of serum NT-proBNP concentration to discriminate between cardiac and noncardiac causes of respiratory signs.
Results—Serum NT-proBNP concentration was significantly higher in dogs with cardiac versus noncardiac causes of respiratory signs. In dogs with primary respiratory tract disease, serum NT-proBNP concentration was significantly higher in those with concurrent pulmonary hypertension than in those without. A serum NT-proBNP cutoff concentration > 1,158 pmol/L discriminated between dogs with congestive heart failure and dogs with primary respiratory tract disease with a sensitivity of 85.5% and a specificity of 81.3%.
Conclusions and Clinical Relevance—Measuring serum NT-proBNP concentration in dogs with respiratory signs helps to differentiate between congestive heart failure and primary respiratory tract disease as an underlying cause.
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.