Page 285 - Clinical Small Animal Internal Medicine

253

VetBooks.ir

26

Canine Myocardial Disease
M. Lynne O’Sullivan, DVM, DVSc, DACVIM (Cardiology)

Department of Companion Animals, Atlantic Veterinary College, University of Prince Edward Island, Charlottetown, Prince Edward Island, Canada

Canine myocardial diseases are those that affect the heart 30–50% of cases of DCM are familial or inherited, and
muscle, as opposed to valvular, endocardial, or pericar- mutations involving over 50 cardiac genes have been
dial diseases. Cardiomyopathies are the most common described to date. Mutations in two genes (PDK4 and
myocardial diseases in dogs, and are a “heterogenous titin) have been associated with DCM in Doberman pin-
group of diseases of the myocardium associated with schers in North America, but do not account for all
mechanical and/or electrical dysfunction” according to cases. The PDK4 mutation was not significantly associ-
the American Heart Association. They may be classified ated with DCM in a group of European Dobermans in
clinically according to structural and functional pheno- which DCM was linked to a different chromosome
type: dilated, hypertrophic, restrictive, and arrhythmo- (candidate genes yet unidentified). This highlights the
genic right ventricular. Dilated cardiomyopathy (DCM) complex nature of the role that genetics play in this dis-
is by far the most common cardiomyopathy in dogs. ease and that multiple genetic factors are involved, even
Arrhythmogenic right ventricular cardiomyopathy within one breed. Juvenile DCM in the Portuguese water
(ARVC) is seen most commonly in the boxer, and hyper- dog has been linked to chromosome 8 and candidate
trophic cardiomyopathy (HCM) is reported in dogs but is gene identification is ongoing.
rare. Restrictive cardiomyopathy is not recognized in Additional well‐recognized etiologies in dogs include
dogs. Other forms of canine myocardial disease include nutritional deficiencies (taurine, carnitine) and tachycar-
myocarditis (infectious, inflammatory, toxic, traumatic), dia induced (secondary to sustained tachyarrhythmia).
infiltrative disease (neoplastic, storage diseases), ischemic Infectious and toxic causes of myocarditis, characterized
disease, myocardial disease secondary to systemic hyper- by myocardial inflammation and necrosis, can produce a
tension, and muscular dystrophies affecting the heart. DCM‐like phenotype (ventricular dilation, systolic dys-
The focus of this chapter is the cardiomyopathies. function, arrhythmias) in the chronic phase, and may be
worth considering as the underlying “insult” in certain
clinical presentations or geographic areas. Examples
Dilated Cardiomyopathy include bacterial (e.g. Borrelia burgdorferi, Bartonella),
viral (e.g., parvovirus, West Nile virus), protozoal (e.g.,
Trypanosoma cruzi [Chagas disease], Toxoplasma gon-
Etiology/Pathophysiology
dii), fungal (e.g., Aspergillus, Blastomyces, Coccidioides),
Dilated cardiomyopathy is a primary myocardial disease and toxic (e.g., anthracyclines) agents. The above‐
characterized by dilation and systolic dysfunction of the mentioned nonfamilial, nonidiopathic causes make up a
left or both ventricles, in the absence of valvular, pericar- very small percentage of the total DCM caseload, as
dial, congenital, coronary artery, or hypertensive heart idiopathic or familial cases are most common.
disease. The DCM phenotype may be the result of vari- On a whole‐heart level, the primary abnormality is a
ous myocardial insults, which are often not identified, reduction in contractility. This results in a reduction in
rendering many cases idiopathic. In dogs, those “insults” stroke volume (the volume ejected) and an increase
are in many cases genetic mutations leading to altered in end‐systolic volume (the volume remaining in the
cardiac protein structure and function, particularly in heart after ejection), in turn resulting in progressive
the pure breeds predisposed to DCM. In humans, increases in end‐diastolic volume. A reduction in

Clinical Small Animal Internal Medicine Volume I, First Edition. Edited by David S. Bruyette.
© 2020 John Wiley & Sons, Inc. Published 2020 by John Wiley & Sons, Inc.
Companion website: www.wiley.com/go/bruyette/clinical