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 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 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 determine the prevalence of ventricular arrhythmias in clinically normal adult Boxers.
Design—Prospective cross-sectional study.
Animals—301 Boxers (181 females and 120 males) > 1 year old with echocardiographically normal systolic function and no history of syncope or congestive heart failure.
Procedures—Physical examination, which included echocardiography, was performed on all dogs. A 24-hour ambulatory ECG was performed on each dog, and results were evaluated to assess ventricular arrhythmias. Statistical evaluation was performed to determine correlations between the total number of ventricular premature complexes (VPCs)/24 h, grade of ventricular arrhythmia, and age of the dogs.
Results—Age of dogs ranged from 1 to 16 years (median, 4 years). Number of VPCs/24 h in each dog ranged from 0 to 62,622 (median, 6 VPCs/24 h). Grade of arrhythmias ranged from 0 to 3 (median, 1). Age was correlated significantly with number of VPCs/24 h (r = 0.43) and with grade of arrhythmia (r = 0.37). Number of VPCs/24 h was significantly correlated with grade of arrhythmia (r = 0.82).
Conclusions and Clinical Relevance—Clinically normal adult Boxers generally had < 91 VPCs/24 h and an arrhythmia grade < 2. Boxers with > 91 VPCs/24 h were uncommon and may have represented dogs with arrhythmogenic right ventricular cardiomyopathy or other disease processes that could have resulted in the development of ventricular arrhythmias.
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 identify cardiac tissue genes and gene pathways differentially expressed between dogs with and without dilated cardiomyopathy (DCM).
ANIMALS 8 dogs with and 5 dogs without DCM.
PROCEDURES Following euthanasia, samples of left ventricular myocardium were collected from each dog. Total RNA was extracted from tissue samples, and RNA sequencing was performed on each sample. Samples from dogs with and without DCM were grouped to identify genes that were differentially regulated between the 2 populations. Overrepresentation analysis was performed on upregulated and downregulated gene sets to identify altered molecular pathways in dogs with DCM.
RESULTS Genes involved in cellular energy metabolism, especially metabolism of carbohydrates and fats, were significantly downregulated in dogs with DCM. Expression of cardiac structural proteins was also altered in affected dogs.
CONCLUSIONS AND CLINICAL RELEVANCE Results suggested that RNA sequencing may provide important insights into the pathogenesis of DCM in dogs and highlight pathways that should be explored to identify causative mutations and develop novel therapeutic interventions.
To evaluate the frequency of variants in the pyruvate kinase dehydrogenase 4 (PDK4) and titin (TTN) genes in a group of Doberman Pinschers with dilated cardiomyopathy (DCM) and to determine whether there were unique clinical attributes to each variant.
48 Doberman Pinschers with DCM.
Doberman Pinschers with recently diagnosed DCM were identified, and genomic DNA from each was genotyped with a PCR assay for detection of PDK4 and TTN genetic variants. Dogs were grouped on the basis of whether they had the TTN variant alone, PDK4 variant alone, both variants, or neither variant. Descriptive statistics were compiled for dog age, body weight, and left ventricular dimensions and fractional shortening and for the presence of ventricular and supraventricular arrhythmias and heart failure. Results were compared across groups.
Of the 48 dogs, 28 had the TTN variant alone, 10 had both variants, 6 had neither variant, and 4 had the PDK4 variant alone. The mean age was younger for dogs with the PDK4 variant alone, compared with other dogs. However, the number of dogs with the PDK4 variant alone was very small, and there was an overlap in age across groups. No other meaningful differences were detected across groups, and independent genotype-phenotype relationships were not identified.
CONCLUSIONS AND CLINICAL RELEVANCE
Although findings indicated that the TTN variant was most common, 6 dogs had neither variant, and this fact supported the concept of ≥ 1 other genetic contributor to DCM in Doberman Pinschers. Future studies are warranted to evaluate genotype-phenotype relationships in Doberman Pinschers with DCM.
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