Page 297 - Clinical Small Animal Internal Medicine

26 Canine Myocardial Disease 265

A genetic test for the striatin mutation in boxers is study of boxers, the median survival time after identifi-
VetBooks.ir available through the Veterinary Genetics laboratory at cation of >300 VPC/24h was just over four years, and in
North Carolina State University (https://cvm.ncsu.edu/
fact overall survival of the affected group was not sig-
nc-state-vet-hospital/small-animal/genetics/).
vival to 10–11 years of age), whereas a retrospective
Interpretation and breeding recommendations are as for nificantly different from the control boxer group (sur-
the DCM genetic tests outlined above, and genetic study of boxers with more advanced disease suggested a
screening cannot replace clinical screening. median survival time of 365 days (range 7–1971 days).
The probability of death within a year was almost five
times greater with a history of syncope, just over five
Therapy
times greater with >10 000 VPCs/24h, and 20 times
While AAs have been shown to reduce VA frequency and greater with >200 runs VT/24h. In a case series of
syncope, it is uncertain whether they decrease risk of SD English bulldogs, a median survival time of 8.3 months
because studies are lacking. Nevertheless, AA therapy was reported, but whether the prognosis is truly worse
remains the mainstay of ARVC treatment. A consensus in that breed is not known, as it is likely that these dogs
on arrhythmia threshold necessitating treatment is lack- had more advanced disease at the time of diagnosis than
ing, and each patient must be approached on a case‐by‐ other boxer studies.
case basis. Even asymptomatic dogs may be at risk of SD,
but this must be balanced with proarrhythmic risk of AA
drugs and owner factors including commitment to long‐ Hypertrophic Cardiomyopathy
term therapy. Suggested candidates for AA therapy
include dogs with a history of syncope, those with VT Hypertrophic cardiomyopathy is a primary myocardial
regardless of total VPC number, those with >300 VPC/24h disease characterized by symmetric or asymmetric con-
and increased complexity including couplets, triplets, or centric hypertrophy (thickening) of the LV in the
R‐on‐T (rapid VPCs), or those with >1000 VPC/24h. absence of a stimulus for hypertrophy (e.g., stenosis or
For immediate treatment of VT or VA causing weak- hypertension), leading to diastolic dysfunction and
ness or collapse, intravenous lidocaine is recommended. arrhythmias that may result in CHF or SD. In humans,
The most common and effective oral AAs are sotalol, 50% or more of cases are related to familial genetic
mexiletine, or a combination of the two in more refrac- mutations. While common in the cat, HCM is very rare
tory cases (see Table 26.2). Note that therapy may be in dogs. Like in the cat, dynamic LV outflow tract
indicated prior to Holter recording, as in instances where obstruction (LVOTO) caused by systolic anterior
there is a history of syncope and VT is identified on ECG. motion of the mitral valve (SAM) is described in some
Therapy should be monitored by Holter examination cases.
within 1–2 weeks of AA initiation, and periodically Many cases of canine HCM appear to be in young
thereafter (every six months). Therapeutic efficacy is dogs, with males overrepresented. This has raised the
supported by a >80% reduction in arrhythmia number question as to whether the disease may be congenital
and complexity. An increase in syncope post treatment and furthermore, whether LVOTO may represent a form
may suggest a proarrhythmic effect and should be evalu- of mitral valve dysplasia predisposing to SAM and sec-
ated with Holter promptly. ondary hypertrophy. Many affected breeds have been
There is some evidence that oral supplementation with reported and include the pointer, golden retriever,
omega‐3 fatty acids may also be beneficial (see Table 26.2). Rottweiler, German shepherd, and shih tzu, amongst
For the minority that experience CHF (left, right, or others. Cases are frequently evaluated for the presence
biventricular), therapy with ACEI, pimobendan, and of an incidental murmur which may be dynamic.
diuretics is indicated as described above for DCM, in Echocardiography is necessary for diagnosis. Treatment
addition to AA therapy. L‐carnitine may also be added is targeted at reducing dynamic LVOTO with beta‐
given positive response in a small family of boxers. blockade (atenolol), and treating CHF or arrhythmias in
severe cases. A number of cases in young dogs have been
noted to resolve with maturity, while others have
Prognosis
persisted and resulted in CHF or SD. It is difficult to
While all dogs with ARVC are at risk of SD, many estimate prognosis based on the sparse reports of this
remain symptom free for years. In one prospective disease in dogs.