Objective—To evaluate the use of 24-hour ambulatory
electrocardiography (AECG) for the detection of ventricular
premature complexes (VPC) in healthy dogs.
Animals—50 healthy mature dogs.
Procedure—A 24-hour AECG was performed on each
dog and evaluated for the presence of VPC.
Results—Fifty dogs weighing between 18.2 to 40.9 kg
(40 and 90 lb) representing 13 breeds were evaluated;
there were 4 sexually intact females, 21 spayed
females, 4 sexually intact males, and 21 castrated
males. Ages ranged from 1 to 12 years. Thirty-four dogs
had no VPC; 16 dogs had between 1 and 24 VPC. The
grade of arrhythmia ranged from 1 to 4, with 4 dogs
having an arrhythmia with a grade > 1. Significant differences
were not detected between the group of
dogs with VPC and those without VPC with regard to
sex, age, and minimum, maximum, or mean heart rate.
Conclusions and Clinical Relevance—We conclude
that healthy mature dogs have infrequent VPC, as
detected by use of 24-hour AECG. The presence of
numerous or sequential VPC may be suggestive of
cardiac or systemic disease and may indicate the
need for thorough clinical evaluation. (J Am Vet Med
Objective—To evaluate the use of in-hospital electrocardiography
(ECG) for detection of ventricular premature
complexes (VPC), compared with 24-hour
Animals—188 Boxers > 9 months old; 31 had a history
of syncope, and 157 were healthy (no history of
Procedure—In-hospital ECG was performed on all
Boxers for at least 2 minutes. Within 7 days after the
in-hospital ECG was completed, 24-hour ambulatory
ECG was performed.
Results—The specificity of in-hospital ECG was
100% for the detection of at least 50 VPC in a 24-hour
period in dogs with syncope and 93% in healthy dogs.
In-hospital ECG had poor sensitivity, although sensitivity
increased as the number of VPC per 24 hours
Conclusions and Clinical Relevance—Use of in-hospital
ECG is highly specific for detection of at least 50
VPC during a 24-hour period. However, in-hospital
ECG is insensitive, and a lack of VPC does not suggest
that the dog does not have a substantial number
of VPC during that same period. The use of in-hospital
ECG appears to be inadequate for screening purposes
and therapeutic evaluations in mature Boxers with
ventricular arrhythmic disease. (J Am Vet Med Assoc
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 compare plasma fatty acid concentrations and the relationships of fatty acids to arrhythmias in Boxers versus Doberman Pinschers.
Animals—38 Boxers and 13 Doberman Pinschers.
Procedures—Boxers and Doberman Pinschers evaluated via Holter recording and for which a blood sample was available were included. Echocardiograms were performed in 49 of 51 dogs. The number of ventricular premature complexes (VPCs)/24 h was counted and fatty acids analyzed. Plasma fatty acid concentrations and VPCs/24 h, as well as correlations between the 2 variables, were compared between the 2 breeds.
Results—Compared with the Doberman Pinschers, Boxers had significantly higher plasma concentrations of γ-linolenic acid but lower concentrations of arachidonic acid. Total n-6 fatty acids and total polyunsaturated fatty acid concentrations were higher in Doberman Pinschers. There were significant, but weak, positive correlations between VPCs and oleic acid, total n-3 fatty acids, and total n-9 fatty acids in Boxers but not in Doberman Pinschers.
Conclusions and Clinical Relevance—Data suggested that plasma fatty acid concentrations may differ between Boxers and Doberman Pinschers and that the relationship between fatty acid concentrations and VPCs may be different between these 2 breeds.
OBJECTIVE To evaluate a group of related Rhodesian Ridgebacks with a family history of sudden death for the presence of arrhythmia and to identify possible patterns of disease inheritance among these dogs.
DESIGN Prospective case series and pedigree investigation.
ANIMALS 25 Rhodesian Ridgebacks with shared bloodlines.
PROCEDURES Pedigrees of 4 young dogs (1 female and 3 males; age, 7 to 12 months) that died suddenly were evaluated, and owners of closely related dogs were asked to participate in the study. Dogs were evaluated by 24-hour Holter monitoring, standard ECG, echocardiography, or some combination of these to assess cardiac status. Necropsy reports, if available, were reviewed.
RESULTS 31 close relatives of the 4 deceased dogs were identified. Of 21 dogs available for examination, 8 (2 males and 6 females) had ventricular tachyarrhythmias (90 to 8,700 ventricular premature complexes [VPCs]/24 h). No dogs had clinical signs of cardiac disease reported. Echocardiographic or necropsy evaluation for 7 of 12 dogs deemed affected (ie, with frequent or complex VPCs or sudden death) did not identify structural lesions. Five of 6 screened parents of affected dogs had 0 to 5 VPCs/24 h (all singlets), consistent with a normal reading. Pedigree evaluation suggested an autosomal recessive pattern of inheritance, but autosomal dominant inheritance with incomplete penetrance could not be ruled out.
CONCLUSIONS AND CLINICAL RELEVANCE Holter monitoring of Rhodesian Ridgebacks with a family history of an arrhythmia or sudden death is recommended for early diagnosis of disease. An autosomal recessive pattern of inheritance in the studied dogs was likely, and inbreeding should be strongly discouraged.
Objective—To determine whether plasma concentrations
of tumor necrosis factor-α (TNF-α) are increased
in cats with congestive heart failure (CHF) secondary
Animals—26 adult cats with CHF and cardiomyopathy
and 9 healthy control cats.
Procedure—Plasma concentrations of TNF-α were
measured in cats with CHF and cardiomyopathy.
Tumor necrosis factor-α was measured by quantifying
cytotoxic effects of TNF-α on L929 murine fibrosarcoma
Results—Concentrations of TNF-α were increased
(0.13 to 3.6 U/ml) in 10 of 26 cats with CHF but were
undetectable in the other 16 cats with CHF and all
control cats. In 20 of 26 cats with CHF, right-sided
heart failure (RHF) was evident; TNF-α concentrations
were increased in 9 of these 20 cats. The remaining 6
cats had left-sided heart failure (LHF); TNF-α concentrations
were increased in only 1 of these cats. Age of
cats with LHF (mean ± SD, 12.1 ± 6.2 years) was not
significantly different from age of the cohort with RHF
(10.5 ± 5.2 years). Body weight of cats with increased
TNFα concentrations (5.4 ± 1.8 kg) was not significantly
different from body weight of cats with CHF
that did not have measurable concentrations of TNF-α
(4.7 ± 1.6 kg).
Conclusionss and Clinical Relevance—Concentrations
of TNF-α were increased in many cats with
CHF. Cats with RHF were most likely to have
increased TNF-α concentrations. Increased plasma
concentrations of TNF-α in cats with CHF may offer
insights into the pathophysiologic mechanisms of
heart failure and provide targets for therapeutic interventions.
(Am J Vet Res 2002;63:640–642)
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 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 determine electrocardiographic parameters
in healthy llamas and alpacas.
Animals—23 llamas and 12 alpacas.
Procedure—Electrocardiography was performed in
nonsedated standing llamas and alpacas by use of multiple
simultaneous lead recording (bipolar limb, unipolar
augmented limb, and unipolar precordial leads).
Results—Common features of ECGs of llamas and
alpacas included low voltage of QRS complexes, variable
morphology of QRS complexes among camelids,
and mean depolarization vectors (mean electrical
axes) that were directed dorsocranially and to the
right. Durations of the QT interval and ST segment
were negatively correlated with heart rate.
Conclusions and Clinical Relevance—ECGs of
acceptable quality can be consistently recorded in
nonsedated standing llamas and alpacas. Features of
ECGs in llamas and alpacas are similar to those of other
ruminants. Changes in the morphology of the QRS
complexes and mean electrical axis are unlikely to be
sensitive indicators of ventricular enlargement in llamas
and alpacas. (Am J Vet Res 2004;65:1719–1723)