Canine
cardiomyopathies are a group of aetiologically not well understood diseases
of myocardium (heart muscle). The dilated form, DCM (dilated cardiomyopathy),
is a slowly progressive disease, in which ventricular dilatation and loss
of myocardial contractility are the main features. It is one of the most common
acquired heart diseases in dogs.
Due
to the fact that Dobermanns, for instance, have a very high incidence of heart
disease, a hereditary component is suspected. There is a clear overpresentation
of Dobermanns in all heart disease statistics. Other commonly affected breeds
are Boxers, Irish Wolfhounds, Great Danes, German Shephard, Retrievers and
Spaniels. The breed representations can vary in different countries and different
populations. Moreover, DCM has unique properties in each breed. Besides the
genetic relationship, there is a possibility of nutritional components as
well. For instance, the myocardial concentrations of L-carnitine has been
shown to be low in some Boxers and American Cocker Spaniels and an L-carnitine
responsive cardiomyopathy has been reported in Boxers. Plasma taurine levels
have been associated with DCM in American Cocker Spaniels.
Sex
may also influence the risk in developing DCM. Some statistics show that males
are predominantly affected. This is not universally accepted, however, since
some studies have not confirmed the relationship. Dogs of all ages can be
affected, varying from less than 1 year to more than 10 years of age.
As mentioned, DCM is a slowly progressive, chronic disease causing deterioration
of the heart's function. During the early stages, there are many compensatory
mechanisms which react and the dog will be asymptomatic. When the patient
enteres the decompensatory stage, several hemodynamical and neurohormonal
factors are more highly activated. The change from the compensatory to decompensatory
stage is slowly progressive, occurring during a period of one to several years.
It is thus a common practice today to divide DCM in two stages namely OCCULT
(subclinical or asymptomatic) and END-STAGE culminating in congestive heart
failure. Sudden death can occur during either stage.
During the occult stage, all signs of congestive heart failure are absent. There can be detectable disturbances in the heart rhythm, and sometimes a murmur which are anyway rare in Dobermanns. The abnormalities can be very difficult to observe at the normal auscultation particularly at the early stage of occult DCM. Usually a Holter recording (24 hour EKG) is used for the detection of rhythm abnormalities such as ventricular premature contractions (VPCs), atrial premature contractions and ventricular tachycardia. These rhythm disturbances are typical for Dobermanns and Boxers and can be a cause of a syncope or sudden death without any other indication of DCM. This is especially true for Dobermanns. Normal routine ECG recording is rarely sensitive enough to detect DCM unless VPCs exist.
Echocardiography
is today widely used for the detection of early occult DCM. Significant professional
experience is required to identify the abnormalities and there are variations
between veterinary clinics regarding routine measurements. There is also some
discussion of normal / abnormal findings in the measurements themselves. In
echocardiography, there is evidence of left ventricular dilatation and hypokinesis
(poor contractions).
Clinical signs in dogs with advanced DCM may include exercise intolerance,
depression, weight loss, (cachexia), and sometimes syncope. Other commonly
observed symptoms of chronic heart failure include pulmonary oedema, pleural
effusion and ascites, causing cough and dyspnoea.
Dobermanns more often than other breeds show signs of acute heart failure
or life-threatening arrhythmia. Sudden death can be the first and only sign
of DCM in these dogs.
The
etiology:
The specific aetiology is unknown. It is believed that there may be a mutation
in genes coding the formation of proteins that support the contractile apparatus.
There can be also a mutation in mitochondrial DNA resulting in defects of
the oxidative processes. Due to these unknown genetic defects, the intracellular
energy homeostasis is inpaired and causes the formation of myocardial lesions.
DCM
in Dobermanns was first recognized during the 1970's (1965) when reports of
sudden deaths in Dobermann Pinschers were published in the USA. Later several
publications from all over the world proved that this disease is widely distributed
everywhere. Possibly the origin of affected animals is in Germany dating back
at least to 1940's. There may be two subgroups of affected animals.
There are
dogs that develop congestive heart failure and those that die suddenly.
There is
a wide variation in the age of onset; "puppyhood" to more than 10 years of
age. The disease can occur in both genders. It can also be found in cross-bred
Dobermanns regardless of the Dobermann parent. A lack of information regarding
the occurrence of DCM in other family members usually unknown.
Characteristic
findings:
Cardiac dilatation, arrhythmias, predominantly left sided congestive heart
failure.
Echocardiography
and a Holter recording are useful in the diagnosis of moderate to severe abnormalities
in occult dilated cardiomyopathy of seemingly healthy Dobermanns. There are
however difficulties in the identification of very early abnormalities.
The values
obtained from left ventricular internal dimension during systole and in diastole
(LVIDs and LVIDd) and left ventricular shortening fraction (FS) are considered
important. The e-point septal separation (EPSS) may be less significant. Criteria
for determining "affected"and "unaffected" status are poorly defined in Dobermanns.
The
pathogenesis:
Myocardial failure impairs the systolic function of the left ventricle. Decreased
left ventricular output and incomplete ventricular emptying is followed by
neurohumoral and endocrine changes to support arterial blood pressure. Due
to atrial emptying, decreasing ventricular ejection fraction and residual
ventricular blood in the left ventricle, the end-systolic pressure increases
causing ventricular dilatation. The neurohumoral activation intended to be
beneficial is assoociated with further myoardial damage in the form of an
increased cardiac workload. Ventricular dilatation causes valvular insufficiency
and regurgitation which increase intra-atrial pressure. Also atrial dilatation
develops. At the same time renal sodium and water retention combines with
reduced heart function producing congestive heart failure with its clinical
signs.
Some studies
assume a higher prevalence of hypothyroidism in Dobermanns with DCM
Death
due to:
Congestive heart failure or sudden death due to ventricular tachyarrythmias.
©
Mervi Ihantola
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