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 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 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)