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J. Häggström1
1Swedish University of Agricultural Sciences, Department of Clinical Sciences, Uppsala, Sweden
J. Häggström
Professor, DVM, PhD, DECVIM-CA (Cardiology)
Department of Clinical Sciences, Faculty of Veterinary Medicine and Animal Science
Swedish University of Agricultural Sciences, Uppsala, Sweden
Dilated cardiomyopathy is de ned as a primary myocardial disease characterized by cardiac enlargement and impaired systolic function in the absence of other cardiac or non-cardiac causes. Dilated cardiomyopathy is prevalent in certain large to giant sized breeds of dogs and the disease contributes to a large proportion of the overall mortality in these breeds in dogs <10 years of age. Population based European actuarial data showed that out of the 12 breeds with the highest cardiac mortality, 11 were breeds prone to develop DCM (Irish Wolfhound, Great Dane, St. Bernard, Newfoundland, Leonberger, Doberman Pinscher, Finnish Hound, Boxer, Giant Schnauzer, Cocker Spaniels). The impact of DCM on mortality is striking in affected breeds; the mortality ranged from 3.6% per year at risk (Irish Wolfhound). This cause speci c mortality can only be matched by MMVD in CKCS (2.5% per year at risk). Dilated cardiomyopathy is most common in large breed dogs, but not all large breeds are affected. For instance German Shepherds and Labrador Retrievers had cardiac mortality comparable to the ”average breed” in the European actuarial data. Dilated cardiomyopathy is uncommon
in small-bred dogs and  ndings indicative of DCM in such dogs should always be questioned. Because of
the high incidence of DCM in affected breeds, there is a growing interest among breeders and pet owners to take actions to reduce the occurrence of DCM. Screening programs have been initiated in some breeds in several countries. These programs aim to identify affected dogs at an early stage and exclude them from breeding. The prognosis after diagnosis of symptomatic DCM is poor and the median survival time ranges between 27 to 140 days, but there are breed differences. For diagnostic,
prognostic, therapeutic, and breeding purposes it is essential to detect the asymptomatic (preclinical) phase of the disease. For the pet owner with a dog with DCM, it is important that the clinician establish an accurate diagnosis to allow adequate therapy to improve the dogs’ quality of life and improve survival.
Clinical presentation and classi cation of disease
The clinical presentation may be subtle and include
the gradual development of exercise intolerance and weight loss. However, more commonly, these early indications are overlooked and the diagnosis of DCM
is not established until CHF develops and the patient is presented for coughing, dyspnea, tachypnea, wasting, arrhythmia, syncope, and sometimes ascites. Indeed, increasing interest in screening families of dogs where DCM is prevalent has led to an appreciation that there is a very long phase of the disease that is not associated with clinical signs evident to the owner or veterinarian. Indeed, the phase with clinical signs, usually associated with the presence of CHF, is the  nal stage of several years of insidious progression. For the symptomatic patient, it is important for the clinician to rule out other possible causes for the clinical signs, such as pericardial effusion, pneumonia, neoplastic disease, undiscovered congenital heart disease. For the asymptomatic patient, the challenge lies in differentiating normal variation and other cardiac or non-cardiac pathologies from DCM.
Histopathological characterization of dogs with DCM suggests that there are two phenotypes that presumably precipitate different clinical presentations. Most dogs
with DCM present with systolic dysfunction and cardiac dilatation, often accompanied with an arrhythmia, most commonly atrial  brillation. The histopathological  ndings commonly found in these dogs include thin myocytes with a wavy appearance that are separated by a clear space, indicating edematous  uid that is generally free from cellular in ltrates. There may also be diffuse in ltration of subendocardial  brosis. However, a proportion of Boxers and Doberman Pinschers (not all), present with ventricular tachyarrhythmias, causing fainting and weakness, but cardiac dilatation and systolic dysfunction is not apparent. These Doberman Pinschers and Boxers presenting
with ventricular tachyarrhythmias often have myocardial lesions that includes myocytolysis, myo bre degeneration, vacuolization and myocyte atrophy with extensive  brosis and fatty in ltration.
Although DCM is currently considered to be a genetic disease, diagnosis is currently based on phenotypic characterization. Because of the two histopathological phenotypes, dogs of different breeds are screened differently for preclinical disease. Most breeds are screened using echocardiography, whereas Doberman
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