Q. Please review dilated cardiomyopathy in the dog.
A. Dr. Keith N. Strickland at the 77th Western Veterinary Conference in Las Vegas gave a lecture on canine dilated cardiomyopathy. Some relevant points in this
lecture are provided below.
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Dilated cardiomyopathy (DCM) is an idiopathic disease of the myocardium that is characterized by progressive myo-cardial failure
(pathologic decreases in contractility). The progressive myocardial failure results in enlargement of the cardiac chambers
(sometimes one side worse than the other) in association with the compensatory mechanisms (renin-angiotensin-aldosterone system,
sympathetic nervous system, and eccentric ventricular hypertrophy) that become activated in response to sustained cardiac
dysfunction. This disease scenario is likely to be multiple diseases that are lumped into a group of idiopathic diseases that
result in progressive myocardial failure, congestive heart failure (CHF), and occasionally, sudden death.
Although heartworm disease may be the second most common cardiac disease in some U.S. regions, DCM is the second most commonly
encountered cardiac disease in dogs.
In general, DCM is seen in middle-age and older (median age is between 4-8 years) large- and giant-breed dogs. Males seem
to be affected more commonly than females. Breeds that are predisposed for this condition include Doberman Pinscher, Irish
Wolfhound, Great Dane, Newfoundland, German Shepherd, Old English Sheepdog, Boxer, St. Bernard and Afghan Hound. Medium-size
breeds may also be affected and include the Portuguese Water Dog, American and English Cocker Spaniel and Dalmatian. Geographic
variations in the prevalence of this disease may suggest genetic and/or environmental factors that may significantly increase
the risk of developing this condition. Recently, a potential abnormality in the protein titin has been identified as a potential
cause of DCM in Doberman Pinschers. DCM is uncommon in small-breed dogs. DCM occasionally is recognized in puppies as young
has 6 weeks of age.
Marked dilation of the cardiac chambers is the most common finding at necropsy. The cause of this progressive myocardial failure
is not known. In general, microscopic evaluation of the myo-cardium reveals moderate changes that are nonspecific. There are
areas of myo-cyte degeneration, necrosis and fibrosis most pronounced in the subendocardial regions of the left ventricular
free wall and papillary muscles. The cause of DCM in dogs is not known. There are many potential causes ranging from specific
genetic mutations, biochemical abnormalities and nutritional deficiencies to immune-mediated causes.
The progression of the disease can be described as having three phases:
- Phase 1: Initiation of injury or defect,
- Phase 2: Physiologic and genetic response to myocardial dysfunction,
- Phase 3: Hemodynamic and clinical syndrome of congestive heart failure.
During Phase 2, cytokines (e.g., tumor necrosis factor-alpha and interleukins) and other neurohumoral substances (e.g., renin-angiotensin-aldosterone
system, endothelin, antidiuretic hormone and the sympathetic nervous system) promote pathologic myocardial hypertrophy and
ongoing loss of contractile mass.
Chamber dilatation results in secondary atrioventricular valvular regurgitation that further volume-overloads the failing
ventricle. Dogs with symptomatic myocardial failure have elevated diastolic pressures resulting in venous congestion and edema
formation. This clinical scenario is further complicated by the presence of arrhythmias. Atrial fibrillation is a common cause
of decompensation in dogs with DCM. Atrial fibrillation results in a significant decrease in cardiac output and an increase
in ventricular filling pressures. Ventricular arrhythmias may cause syncope in some dogs and sudden cardiac death in up to
25-30 percent. Ventricular arrhythmias can be particularly problematic in Boxers and Doberman Pinschers.
The clinical evaluation of DCM starts with the signalment. It is uncommon to diagnose DCM in small-breed dogs. A history of
syncope, exercise intolerance, coughing or tachypnea/dyspnea may be noted. Physical examination may reveal weak femoral pulses,
cardiac arrhythmias with pulse deficits, soft cardiac murmurs and gallop rhythms. Gallop rhythms are best heard at the left
apex with the low frequency part of the stethoscope with light pressure on the body wall. An S3 gallop rhythm suggests severe
volume overload and elevated ventricular filling pressures. Presence of jugular pulses and ascites are suggestive of right-sided