Dilated cardiomyopathy (DM) is an autosomal-dominant (variable penetrance) polygenetic heart disease of dogs characterized by left ventricular dilatation and impaired systolic contraction leading to congestive heart failure or sudden death due to ventricular tachyarrhythmia.
This disease is common in large and giant pure-bred dogs such as the Doberman, Irish Wolfhound, Newfoundland, Portuguese Water Dog, Boxer, Huntaway, German Shepherd, Labrador Retriever, Cocker Spaniel, Estrella Mountain Dog and Great Dane.
Although canine DCM is usually a disease of genetic origin, taurine-deficient DCM has been diagnosed in the Golden Retriever, which resolved with taurine supplementation. Similarly, Portuguese Water Dog DCM is associated with abnormal taurine metabolism.
In most breeds, DCM is a missense mutation resulting in a 16-base pair deletion in the pyruvate dehydrogenase kinase 4 (PDK4) gene on chromosome 5, resulting in calcium-handling abnormalities and increased rates of cardiac myocyte apoptosis. In other breeds, such as the Portuguese Water Dog, the abnormality is located on chromosome 8.
A number of progressive pathological changes occur in the heart associated with DCM including reduced catecholamine and nitrous oxide production, myocardial insulin resistance, increases in myocardial O2 consumption, increased coronary blood flow requirements and decreased myocardial mechanical efficiency. These collectively contribute to cardiac decompensation.
Unlike human DCM, where loss of temporal synchrony of myocardial contraction results in disease progression, impairment of longitudinal fibre synchrony does not appear to be significantly associated with clinical status with canine DCM.
Clinical symptoms may be vague or absent in many dogs, and sudden death may be the only observation. Male dogs appear more predisposed and, in many affected patients (from 1 - 8 years of age), clinical symptoms may be occult, with only intermittent dyspnea, tachycardia, coughing, syncope, reduced exercise tolerance and weakness, which invariably progresses to congestive heart failure.
Although a tentative diagnosis can be established through thoracic radiographs which may show pleural effusion or pulmonary edema, most cases necessitate electrocardiography, 24-hour ambulatory electrocardiographic (Holter) monitoring, echocardiography and Doppler echocardiography.
Echocardiography allows the earliest detection of DCM, beginning 1–4 weeks before the onset of clinical signs, and occult dogs have characteristic slowing of conduction velocities, reduced systolic and diastolic pulmonary venous flow, pseudonormal transmitral flow and reduced flow propagation velocities.
Blood tests are usually unrewarding, although elevated cardiac troponin levels may be noted. Plasma insulin-like growth factors (IGF-I) and growth hormone levels are usually normal.
Ventricular arrhythmias are commonly noted and can occur with or even before morphological changes of the heart.
A definitive diagnosis can be established using M-mode echocardiography, histopathology analysis of affected heart muscle and PCR-based genetic testing.
Histological examination of canine DCM hearts usually shows varying degrees of fatty infiltration, fibrosis and attenuated wavy fibers in both ventricles and interventricular septum.
A poor prognosis is associated with presence of cardiogenic pulmonary edema and ventricular premature complexes, shorter transmitral flow on echocardiography, elevated levels of NT-pro-BNP ≥ 4865 pmol/L , cardiotropin ≥ 0.63 ng/ml (normal <0.11 ng/mL), vasovagal tone ≥ 7.59 and QRS durations ≥60 ms.
A differential diagnosis would include nemaline myopathy, hyperthyroidism, other cardiomyopathies, Duchenne muscular dystrophy, endocarditis, mitral valve endocardiosis, ventricular septal defect, other causes of congestive heart failure and infections with Dirofilaria spp.
Treatment revolves around medical alleviation of congestive heart failure, with drugs such as furosemide and/or enalapril/benazepril for relief of pulmonary edema and pulmonary venous hypertension, pimobendan and/or digoxin for reducing preload.
Pimobendan, which has both inotropic and vasodilatory properties, prolongs the time to the onset of clinical signs and extends survival in dogs with preclinical DCM
Nutritional supplementation with n-3 fatty acids, taurine, L-Carnitine and Coenzyme Q-10 may be beneficial, however the effects of these supplements on canine DCM have not been proven.
- Dog Nutrition Advice
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