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)
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 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 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.
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)
To characterize features of myxomatous mitral valve disease (MMVD) in Miniature Schnauzers and Yorkshire Terriers.
69 Miniature Schnauzers and 65 Yorkshire Terriers, each with MMVD.
Medical record data for each dog were collected; the study period was January 2007 through December 2016. If available, radiographic data were evaluated, and a vertebral heart scale score was assigned for each dog. Statistical analysis was performed with Student t and Fisher exact tests.
Compared with Yorkshire Terriers, the prevalence of MMVD was significantly higher in Miniature Schnauzers and affected dogs were significantly younger at the time of diagnosis. Miniature Schnauzers were significantly more likely to have mitral valve prolapse and syncope, compared with Yorkshire Terriers. Yorkshire Terriers were significantly more likely to have coughing and have had previous or current treatment with cardiac medications, compared with Miniature Schnauzers. There was no statistical difference between breeds with regard to abnormally high vertebral heart scale scores or radiographic evidence of congestive heart failure.
CONCLUSIONS AND CLINICAL RELEVANCE
With regard to MMVD, features of the disease among Miniature Schnauzers and Yorkshire Terriers were similar, but there were also a few discernable differences between these 2 breeds and from historical findings for dogs with MMVD of other breeds. Clinical signs at the time of diagnosis differed between the 2 breeds, which may have reflected concurrent breed-specific conditions (sick sinus syndrome or airway disease [eg, tracheal collapse]). Future work should include prospective studies to provide additional information regarding the natural progression of MMVD in these dog breeds.
Objective—To determine aortic ejection velocity in
healthy adult Boxers with soft ejection murmurs without
overt structural evidence of left ventricular outflow
tract obstruction and in healthy Boxers without
Procedure—Dogs were examined independently by
2 individuals for evidence of a cardiac murmur, and a
murmur grade was assigned. Maximal instantaneous
(peak) aortic ejection velocity was measured by
means of continuous-wave Doppler echocardiography
from a subcostal location. Forty-eight dogs were
reexamined approximately 1 year later.
Results—A soft (grade 1, 2, or 3) left-basilar ejection
murmur was detected in 113 (56%) dogs. Overall
median aortic ejection velocity was 1.91 m/s (range,
1.31 to 4.02 m/s). Dogs with murmurs had significantly
higher aortic ejection velocities than did those
without murmurs (median, 2.11 and 1.72 m/s, respectively).
Auscultation of a murmur was 87% sensitive
and 66% specific for the identification of aortic ejection
velocity > 2.0 m/s. An ejection murmur and aortic
ejection velocity > 2.0 m/s were identified in 73
(36%) dogs. For most dogs, observed changes in
murmur grade and aortic ejection velocity during a follow-up examination 1 year later were not clinically
Conclusions and Clinical Relevance—Results
suggested that ejection murmurs were common
among healthy adult Boxers and that Boxers with
murmurs were likely to have high (> 2.0 m/s) aortic
ejection velocities. The cause of the murmurs in
these dogs is unknown. (J Am Vet Med Assoc
Objective—To assess survival time and adverse events related to the administration of pimobendan to cats with congestive heart failure (CHF) secondary to hypertrophic cardiomyopathy (HCM) or hypertrophic obstructive cardiomyopathy (HOCM).
Design—Retrospective case-control study.
Animals—27 cats receiving treatment with pimobendan and 27 cats receiving treatment without pimobendan.
Procedures—Medical records between 2003 and 2013 were reviewed. All cats with HCM or HOCM treated with a regimen that included pimobendan (case cats) were identified. Control cats (cats with CHF treated during the same period with a regimen that did not include pimobendan) were selected by matching to case cats on the basis of age, sex, body weight, type of cardiomyopathy, and manifestation of CHF. Data collected included signalment, physical examination findings, echocardiographic data, serum biochemical values, and survival time from initial diagnosis of CHF. Kaplan-Meier survival curves were constructed and compared by means of a log rank test.
Results—Cats receiving pimobendan had a significant benefit in survival time. Median survival time of case cats receiving pimobendan was 626 days, whereas median survival time for control cats not receiving pimobendan was 103 days. No significant differences were detected for any other variable.
Conclusions and Clinical Relevance—The addition of pimobendan to traditional treatment for CHF may provide a substantial clinical benefit in survival time for HCM-affected cats with CHF and possibly HOCM-affected cats with CHF.
Objective—To identify clinical, echocardiographic,
and electrocardiographic abnormalities in Boxers with
cardiomyopathy and echocardiographic evidence of
left ventricular systolic dysfunction.
Animals—48 mature Boxers.
Procedure—Medical records were reviewed for information
on age; sex; physical examination findings;
and results of electrocardiography, 24-hour ambulatory
electrocardiography, thoracic radiography, and
Results—Mean age of the dogs was 6 years (range, 1
to 11 years). Twenty (42%) dogs had a systolic murmur,
and 9 (19%) had ascites. Congestive heart failure was
diagnosed in 24 (50%) dogs. Seventeen (35%) dogs
had a history of syncope. Mean fractional shortening
was 14.4% (range, 1% to 23%). Mean left ventricular
systolic and diastolic diameters were 4.5 cm (range, 3
to 6.3 cm) and 5.3 cm (range, 3.9 to 7.4 cm), respectively.
Twenty-eight (58%) dogs had a sinus rhythm
with ventricular premature complexes (VPCs), and 20
had supraventricular arrhythmias (15 with atrial fibrillation
and 5 with sinus rhythm and atrial premature complexes).
Sixteen of the dogs with supraventricular
arrhythmias also had occasional VPCs. Morphology of
the VPCs seen on lead II ECGs was consistent with left
bundle branch block in 25 dogs, right bundle branch
block in 8, and both in 11.
Conclusions and Clinical Relevance—Results suggest
that Boxers with cardiomyopathy and left ventricular
dysfunction frequently have arrhythmias of supraventricular
or ventricular origin. Whether ventricular dysfunction
was preceded by electrical disturbances could
not be determined from these data, and the natural history
of myocardial disease in Boxers requires further
study. (J Am Vet Med Assoc 2005;226:1102–1104)
Objective—To evaluate the effect of 4 antiarrhythmic
treatment protocols on number of ventricular premature
complexes (VPC), severity of arrhythmia, heart
rate (HR), and number of syncopal episodes in Boxers
with ventricular tachyarrhythmias.
Design—Randomized controlled clinical trial.
Procedure—Dogs with > 500 VPC/24 h via 24-hour
ambulatory ECG (AECG) were treated with atenolol
(n = 11), procainamide (11), sotalol (16), or mexiletine
and atenolol (11) for 21 to 28 days. Results of pre- and
posttreatment AECG were compared with regard to
number of VPC/24 h; maximum, mean, and minimum
HR; severity of arrhythmia; and occurrence of syncope.
Results—Significant differences between pre- and
posttreatment number of VPC, severity of arrhythmia,
HR variables, or occurrence of syncope were not
observed in dogs treated with atenolol or procainamide.
Significant reductions in number of VPC,
severity of arrythmia, and maximum and mean HR
were observed in dogs treated with mexiletineatenolol
or sotalol; occurrence of syncope was not significantly
different between these 2 treatment groups.
Conclusions and Clinical Relevance—Treatment
with sotalol or mexiletine-atenolol was well tolerated
and efficacious. Treatment with procainamide or
atenolol was not effective. (J Am Vet Med Assoc 2002;221:522–527)