Case Report Rapport de cas

Arrhythmogenic right ventricular cardiomyopathy in a weimaraner

Bryan D. Eason, Stacey B. Leach, Keiichi Kuroki

Abstract — Arrhythmogenic right ventricular cardiomyopathy (ARVC) was diagnosed postmortem in a weimaraner
dog. Syncope, ventricular arrhythmias, and sudden death in this patient combined with the histopathological fatty
tissue infiltration affecting the right ventricular myocardium are consistent with previous reports of ARVC in
non-boxer dogs. Arrhythmogenic right ventricular cardiomyopathy has not been previously reported in weimaraners.

Résumé — Cardiomyopathie ventriculaire droite arythmogène chez un Weimaraner. Une cardiomyopathie

ventriculaire droite arythmogène (CVDA) a été diagnostiquée post-mortem chez un chien Weimaraner. Une
syncope, des arythmies ventriculaires et une mort soudaine chez ce patient, combinées à une infiltration
histopathologique par du tissu adipeux affectant le myocarde droit, correspondent à des rapports antérieurs de
CVDA chez des chiens autres que des Boxers. La cardiomyopathie ventriculaire droite arythmogène n’a pas été
signalée antérieurement chez des Weimaraners.
(Traduit par Isabelle Vallières)
Can Vet J 2015;56:1035–1039

Case description ponin I (cTnI) concentration was analyzed using a point-of-care

A
analyzer (VetScan i-STAT; Abaxis, Union City, California, USA)
40.7 kg, 4-year-old, neutered male weimaraner dog was
on referral presentation and was increased at 3.85 ng/mL (nor-
referred to the cardiology service at the University of
mal canine reference range , 0.05 ng/mL, lower limit of detec-
Missouri Veterinary Medical Teaching Hospital for evaluation
tion 0.02 ng/mL). Thoracic and abdominal radiographs and
of syncope. The first syncopal episode was noted approximately
abdominal ultrasound were unremarkable. Dirofilaria ­immitis
2 mo before referral and a second episode occurred 2 d before
antigen and antibodies to Borrelia burgdorferi, Anaplasma
presentation. The dog was otherwise healthy.
phagocytophilum, and Ehrichia canis were negative by sero-
Physical examination revealed an intermittent arrhythmia
logic testing (SNAP 4Dx; IDEXX Laboratories, Westbrook,
characterized by frequent premature heart beats and pulse
Maine, USA). Serum was also submitted to the Texas Veterinary
deficits, but was otherwise unremarkable. A standard 6-lead
Medical Diagnostic Laboratory (TVMDL) for Trypanosoma
electrocardiogram (ECG) was performed that showed frequent
cruzi immunofluorescent antibody (IFA) testing and revealed
ventricular premature complexes (VPCs) with a right bundle
a titer of 1:20, considered seronegative according to TVMDL
branch block morphology occurring as isolated complexes, cou-
protocol (1). Prophylactic antibiotic therapy with clindamycin
plets, triplets, and periods of ventricular bigeminy and trigeminy
(Watson Pharma Private, Salcette, Goa, India), 14.7 mg/kg body
(repetitive sequence of 2 sinus complexes followed by 1 VPC).
weight (BW), PO, q12h and doxycycline (Teva Pharmaceuticals,
A transthoracic 2-dimensional and Doppler echocardiographic
Sellersville, Pennsylvania, USA), 9.8 mg/kg BW, PO, q12h,
study revealed mild mitral regurgitation, normal chamber
was initiated to treat presumptive protozoal (i.e., Toxoplasma
dimensions, and normal systolic function. A complete blood
gondii, Neospora caninum) and bacterial (i.e., Borrelia burgdoferi,
(cell) count (CBC) and serum biochemistry panel performed
Rickettsia rickettsia, Erlichia canis, Bartonella spp.) causes of
immediately prior to referral were unremarkable. Cardiac tro-
myocarditis, respectively.
A 24-hour ambulatory ECG revealed multiform ventricular
Department of Veterinary Medicine and Surgery (Eason, Leach)
ectopy with periods of ventricular tachycardia and 32 881 ven-
and the Veterinary Medical Diagnostic Laboratory (Kuroki),
tricular ectopic events (total beats were 180 880). Approximately
College of Veterinary Medicine, University of Missouri,
89% of the ventricular ectopic complexes were left bundle
Columbia, Missouri 65211, USA.
branch block morphology and 11% were right bundle branch
Address all correspondence to Dr. Bryan D. Eason; e-mail: block morphology with varying coupling intervals. There were
eason1@purdue.edu periods of ventricular tachycardia composed solely of left bundle
Dr. Eason’s current address is Purdue University Veterinary branch block and of solely right bundle branch block morphol-
Teaching Hospital, West Lafayette, Indiana 47906, USA. ogy, and instances in which the morphology changed abruptly
Use of this article is limited to a single copy for personal study. from one to the other (Figure 1). Oral antiarrhythmic therapy
Anyone interested in obtaining reprints should contact the with sotalol (Qualitest Pharmaceuticals, Huntsville, Alabama,
CVMA office (hbroughton@cvma-acmv.org) for additional USA), 0.98 mg/kg BW, PO, q12h for 3 d, then 1.96 mg/kg BW,
copies or permission to use this material elsewhere. PO, q12h for 3 d was instituted followed by mexiletine (Teva

CVJ / VOL 56 / OCTOBER 2015 1035

R A P P O R T D E CA S
Figure 1. Holter monitor recording showing ventricular ectopy. The narrow arrows indicate a couplet of ventricular premature
complexes with a left bundle branch block morphology. The rhythm then changes to a sustained monomorphic ventricular tachycardia
with a right bundle branch block morphology (thick arrow).
Pharmaceuticals), 6.25 mg/kg BW, PO, q8h. The T. cruzi IFA
test was repeated after 3 wk and remained negative at 1:20. A
repeat 24-hour ambulatory ECG performed 2 mo after initiation
of antiarrhythmic therapy showed marked improvement in both
the frequency and complexity of the arrhythmia as there was a
96% reduction in the frequency of ventricular ectopy and a 99%
reduction of ventricular tachycardic episodes compared with the
baseline ambulatory ECG. Repeat cTnI concentration at that
time was normal at 0.02 ng/mL. Despite a marked decrease
in the frequency and complexity of ventricular ectopy and
strict exercise restriction by the owners, sudden death occurred
approximately 3 mo after initial evaluation.
The heart was collected by the referring veterinarian and
submitted for postmortem examination. Multiple formalin-
fixed myocardial specimens and the remaining fresh heart were
submitted to the University of Missouri Veterinary Medical
Diagnostic Laboratory. On gross examination of the tissue,
no apparent hemorrhagic or necrotic changes were noted.
Externally, the right ventricle was paler than the left. On cut
sections, the right ventricular wall had a pale, greasy appear-
ance that was multifocal and transmural in distribution. The
remainder of the gross examination and the heart dimensions
were unremarkable.
Sections of the interventricular septum and the right ven-
tricular and left ventricular free wall at the level of the papillary
muscles were prepared for histopathologic examination. The
right ventricular myocardium had multifocal, transmural, and
coalescing fatty tissue infiltration covering approximately 60%
of the tissue. The most severe lesions were located near the
epicardium (Figure 2A). Similarly, approximately 30% of the
interventricular septum and approximately 10% of the left ven-
tricle were replaced by fatty infiltrates (Figure 2B). The surviving
myocytes in each section appeared atrophied and occasionally
exhibited vacuolar degeneration. There was minimal interstitial
1036
fibrosis with no inflammatory cells or infectious agents noted.
The myocardial fatty infiltration and replacement of the myo-
cardium, most severe in the right ventricular free wall, and lack
of inflammatory cells or infectious agents was most consistent
with a diagnosis of arrhythmogenic right ventricular cardiomy-
opathy (ARVC).
Discussion
Syncope, defined as sudden but transient loss of consciousness
and postural tone, can be divided into broad categories of car-
diac and non-cardiac causes with the most commonly reported
cause of syncope being cardiac arrhythmias (2). Physical exami-
nation of the dog in the present report was highly suggestive
of a cardiac cause of syncope based on the presence of an
arrhythmia on auscultation; however, a diagnosis of ARVC as
the etiology of heart disease in this patient was only made on
postmortem histopathologic examination. Arrhythmogenic
right ventricular cardiomyopathy is a myocardial disease that is
characterized clinically by syncope, ventricular arrhythmias of
left bundle branch block morphology, and sudden death with
no premonitory clinical signs. Arrhythmogenic right ventricular
cardiomyopathy has been described in humans, cats, and dogs
(3–5). The most common breed of dog affected is the boxer
and a familial pattern of autosomal dominance has been estab-
lished (6). Recently, a causative mutation in the gene encoding
striatin has been identified in a population of boxers, although
other genetic mutations are also suspected (7). Isolated cases of
ARVC without an obvious familial pattern have been reported
in other breeds (8–13). Arrhythmogenic right ventricular car-
diomyopathy has not been previously reported in weimaraner
dogs.
Ante-mortem diagnosis of ARVC presents a unique clini-
cal challenge as sudden death can be the first clinical sign.
In humans, standardized criteria have been proposed for the
CVJ / VOL 56 / OCTOBER 2015
 CA S E R E P O R T
200 mm

Figure 2. Photomicrograph of histopathology of the right (A) and left (B) ventricular free wall. Note that the right ventricular
myocardium is severely infiltrated and replaced by fatty tissue. The most severely affected zone was the epicardium indicated by the
black arrows; however, the fatty infiltration was multifocally and transmurally distributed (A). In the left ventricle (B), cardiomyocytes
are multifocally and occasionally separated and replaced by fatty tissue and sparse connective tissue. Note the predominant pattern
of infiltration in both A and B is fatty tissue without inflammation. Masson’s trichrome stain. A and B are the same magnification.
Bar = 200 mm. 279 3 105 mm (72 3 72 DPI).

diagnosis of ARVC and include a combination of structural,
electrocardiographic, arrhythmic, histopathologic, and familial
features (14). These guidelines have since been modified given
the emergence of advanced diagnostic imaging modalities such
as cardiac magnetic resonance imaging (cMRI) and identifica-
tion of causative genetic mutations (15). In humans, cMRI has
become increasingly utilized for non-invasively evaluating the
function and structure of the right ventricle. It has become the
gold standard for ante-mortem diagnosis of ARVC, with major
criteria consisting of wall motion abnormalities and aneurysmal
dilation of the right ventricle (15). Other less specific findings
include intramyocardial fat deposits seen as an intense signal
compared with surrounding more normal myocardium and
abnormal late gadolinium enhancement suggestive of intramyo-
cardial fibrosis (16,17). In veterinary studies, cMRI was able to
detect fatty infiltrative changes in explanted hearts (18), while
another study failed to show fatty infiltration but did reveal right
ventricular dysfunction (19). This discrepancy may be due to the
difference in ages of dogs in each study, suggesting that cMRI
evidence of fatty infiltration may become more apparent with
chronicity. Although cMRI is becoming increasingly available
in veterinary medicine, it requires general anesthesia and may
be cost-prohibitive. A presumptive diagnosis can be made based
on history/clinical signs, familial history, ECG abnormalities
(ventricular ectopy with a left bundle branch block morphol-
ogy), and the absence of significant structural abnormalities
on echocardiogram to explain abnormal ECG findings (20).
Echocardiographic changes may be present in both humans
and dogs in more severe cases, but specificity and sensitivity are
not high. In humans, right ventricular enlargement or dilation
and hypokinetic regions may be associated with ARVC (16).
In a recent study, there was a positive association between the
development of DCM and a homozygous striatin mutation in
boxer dogs (21). Echocardiographically evident right ventricular
aneurysm has been reported in a case of segmental ARVC in a
non-boxer dog (9).
Syncope is one of the most commonly reported clinical signs
associated with ARVC in boxers and may be the presenting
complaint in up to 68% of cases (22). A 24-hour ambulatory
ECG is often utilized to support an ante-mortem diagnosis as
dogs may have normal ECGs in the hospital. Normal dogs have
a very low incidence of ventricular ectopy. A study of healthy
adult dogs showed a median of 2 VPCs in 24 h when boxers
were excluded from the population (23). Boxers seem to have a
greater tendency toward ventricular ectopy with 75% of healthy
adult boxers reportedly having , 75 VPCs in a 24-hour period
(20), though this population may include dogs with ARVC
not manifesting clinical signs. Recommended guidelines for
interpretation of 24-hour ambulatory ECG recordings in boxers
suggest that . 100 VPCs is suspicious for ARVC and treatment
is generally recommended if . 1000 VPCs are recorded over
a 24-hour period (20). Whether or not these guidelines can
be extrapolated to other breeds has not been established and
warrants further investigation. The decision to use antiarrhyth-
mic therapy in this case was made in light of the dog’s clinical
signs and documentation of frequent sustained ventricular
tachycardia.
Multi-drug anti-arrhythmic therapy was used in this case;
however, monotherapy was considered. When combination
therapy is used, anti-arrhythmic drugs are often added in a
staggered protocol as was done in this case to evaluate for
potential adverse effects. Efficacy of anti-arrhythmic therapy is
optimally evaluated with a repeated 24-hour ambulatory ECG.
This can present additional cost to owners if multiple changes
to medications are required. Because the underlying mecha-
nism of the ventricular arrhythmias in the present case could
not be determined based on ante-mortem diagnostic tests per-
formed, combination therapy was elected in the hope of greater

CVJ / VOL 56 / OCTOBER 2015 1037

 a­ rrhythmia suppression. Mexilitine is a class Ib anti-arrhythmic
drug, inhibiting fast sodium channels, whereas sotalol is a
class III antiarrhythmic with non-selective beta blocking prop-
erties. Sotalol monotherapy and combination therapy with
atenolol-mexiletine have both been shown to be effective at
reducing the frequency and severity of ventricular ectopy in
R A P P O R T D E CA S
boxer dogs with ARVC (24). Combination sotalol-mexilitine
has also been shown to be more effective than sotalol mono-
therapy in reducing the frequency of VPCs in boxer dogs with
ARVC (25). However, in German shepherd dogs with inherited
ventricular arrhythmias, sotalol monotherapy was found to be
proarrhythmic, likely by worsening early afterdepolarization
induced triggered activity, while mexilitine-sotalol combina-
tion was superior to mexilitine monotherapy in reducing the
frequency of VPCs (26). The decision to use multi-drug anti­
arrhythmic therapy in this case was based on clinical judgment
and the owner’s financial concerns regarding cost of repeated
ambulatory ECG for monitoring response to therapy.
The mechanism of the ventricular arrhythmias characteristic
of ARVC is thought to be fatty or fibrofatty replacement of the
normal myocardium generating macro-reentrant electrical cir-
cuits, though associated myocarditis may also play a role (4,16).
Myocyte degeneration, atrophy, and replacement of myocardium
by fatty or fibrofatty tissue can be associated with other diseases
such as dilated cardiomyopathy in dogs (27). In ARVC, however,
these histologic changes are most prominent in the right ventricle
as seen in this case. These findings are similar to the changes noted
in humans affected by this disease (18,28). The disease predomi-
nates in the right ventricle but is also seen in the left ventricle
in both humans and dogs (18,28). Because of the distribution,
ventricular tachycardia tends to be monomorphic. In patients
with multifocal areas of disease involving the interventricular
septum and parts of the left ventricle, the arrhythmias may have
multiple arrhythmogenic foci (4). The presence of myocarditis has
also been postulated as a potential cause or contributory factor
of arrhythmogenesis with multifocal lymphocytic infiltrates and
myocyte death being present in all boxer dogs that died suddenly
in one study (18). Histopathologic lesions suggesting myocarditis
appear to be more commonly associated with the fibrofatty form
of myocyte replacement in both boxers and other breeds with
ARVC, though the exact role of myocarditis in the progression
of this disease remains unclear (8,27). Thinning and aneurysmal
dilation of the right ventricular free wall are more commonly seen
with the fibrofatty form of ARVC in both humans and boxer dogs
(18). The dog in this report had predominantly fatty replacement
of cardiomyocytes, without evidence of myocarditis or right
ventricular thinning or aneurysmal dilations. Whether the fatty
and fibrofatty forms of ARVC represent different stages of the
same disease process remains unknown. Additionally, some of the
reported cases of ARVC in both human and veterinary literature
may actually be cases of Uhl’s anomaly, in which there is partial
or complete loss of the myocardium in the right ventricular free
wall, with only the epicardial and endocardial layers remaining.
It has been previously thought that Uhl’s anomaly was a more
severe form of ARVC, as both may be mediated by unregulated
apoptosis, though a more recent study suggests they may be
distinct entities (29).
1038
The increased cTnI concentrations at initial evaluation sup-
ported the presence of myocarditis clinically, which led to tests
for infectious diseases. Potential infectious causes of myocarditis
in dogs include Rickettsial disease, Lyme disease, leptospirosis,
toxoplasmosis, Chagas’ disease, and bartonellosis and may
potentially increase serum concentration of cardiac troponins
(30). Histopathology combined with clinical abnormalities
may be beneficial in diagnosing the causative agent of myocar-
ditis, but myocardial biopsy is rarely performed in veterinary
medicine as an ante-mortem diagnostic test. Characteristic his-
topathologic findings associated with Chagas’ cardiomyopathy
in humans include myocardial fibrosis resulting from multiple
mechanisms including myocarditis and persistence of parasites
within cardiac tissue (31). Dogs experimentally infected with
T. cruzi similarly showed varying degrees of myocardial fibrosis
on histopathology (32). In one study of naturally occurring
T. cruzi infections in dogs, histopathologic evidence of myo-
carditis was noted in almost 98% of cases (1). Cardiac toxins
and envenomation may also be considered as potential causes of
myocarditis and elevation of cTnI when clinical history indicates
possible exposure (30,33). In the present case, no history of
exposure to toxins was noted by the owners and no microorgan-
isms, inflammatory changes, evidence of toxin exposure such
as necrosis, or ischemic damage was noted on histopathologic
examination and only minimal fibrosis was present, making
infectious and inflammatory diseases or toxins unlikely. The
initial increase in cTnI concentrations may have been second-
ary to ischemia from the frequent tachyarrhythmia or due to
the fatty replacement and atrophy of cardiac myocytes seen
histologically (34,35). It has been previously shown that boxers
with ARVC have significantly greater serum cTnI concentra-
tions compared with both control boxers and non-boxer dogs,
and that there was a significant correlation between serum cTnI
concentrations and both frequency and complexity of ventricular
ectopy (35).
This report presents the diagnosis of ARVC in a breed in
which it has not been previously reported. Unfortunately, sud-
den death remains a common clinical outcome of this disease
despite successful response to anti-arrhythmic therapy. A defini-
tive diagnosis was made postmortem based on the combination
of clinical signs, extensive diagnostic testing and imaging,
and histopathologic findings of fatty myocardial replacement
without myocarditis. Arrhyhmogenic right ventricular car-
diomyopathy should be considered as a differential diagnosis
for syncope and ventricular ectopy in non-boxer dogs without
echocardiographic evidence of structural heart disease. CVJ
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