Dilated cardiomyopathy is the most significant
acquired cardiac disease of large to giant breed dogs.
Although no sex predilection has been proven, the disease has a
strong breed predilection. These breeds include but are not limited to the Doberman
pinscher, Great Dane, Labrador retriever, Golden retriever, Saint
Bernard, Boxer, Newfoundland, Irish wolfhound, and one medium size
breed, the Cocker Spaniel. DCM
is most commonly seen in dogs between the ages of 4 and 10 years of age
on the average.
The most common etiology is still idiopathic.
Other causes include hypothyroidism, which may be reversible if
thyroxine supplementation is administered in a timely manner,
doxorubicin toxicity, taurine deficiency (more commonly in cats but is
seen on rare occasions in Cocker Spaniels and Golden retrievers), L-carnitine
deficiency, untreated rapid ventricular pacing such as supraventricular
tachycardia, neoplasia where neoplastic cells infiltrate the myocardium
and disrupt it’s normal function, parvovirus and Lyme disease.
DCM is primarily a systolic dysfunction caused by a
progressive decrease in myocardial contractility.
As contractility worsens, the chambers of the heart progressively
dilate and the walls become increasingly less compliant, which in return
causes an increase in intracardiac pressure.
Pathophysiologically, the result is depressed cardiac output
leading to decreased muscle perfusion with oxygen-rich RBC’s while
clinically the result may be exercise intolerance and syncope.
As the disease progresses, the ventricles continue to enlarge
leading to the widening of the mitral valve annulus which further
decreases the cardiac output via mitral regurgitation.
Clinically, it is at this stage of the disease that most animals
will develop pulmonary edema. Additionally,
decreased cardiac output also leads to myocardial ischemia, which is the
most common cause of atrial and ventricular arrhythmia at this stage of
the disease. Arrhythmias in and of themselves cause a decrease in cardiac
output, further worsening the animal’s condition.
Most animals present with clinical signs related to
poor cardiac output. These
signs include weakness, lethargy, exercise intolerance, coughing,
anorexia, ascites, syncope, tachypnea, and dyspnea. On physical examination, mucous membranes may be pale with a
decrease capillary refill time. Pulses
are often weak and rapid with the presents of pulse deficits.
Respiratory rate may be increased and labored with pulmonary
crackles. Jugular
distention and muffled heart sounds may also be present.
Diagnostically, baseline radiographs and an ECG should
be preformed to assess for cardiomegaly and the presence of arrhythmias.
Some animals may have no radiographic evidence of cardiomegaly
and in these echocardiography is the only way to definitively diagnose
these patients. Echocardiography
allows for a complete hemodynamic assessment of the heart including
fractional shortening (a measure of myocardial contractility), wall
motion, atrial and ventricular size, and mitral valve status.
More importantly, the echocardiogram can be used as a baseline
for monitoring the progression of disease and response to treatment.
With a few exceptions, acquired dilated cardiomyopathy
is a progressive, irreversibly fatal disease.
Even under the ideal circumstances, prognosis is guarded to poor
at best. Dogs with pleural
effusion and pulmonary edema have the shortest survival rate.
On average most dogs succumb to the disease within 3 months with
less then 30% surviving greater than 2 years.
