The clinical signs of canine and feline heart failure are limited, but they must be distinguished from pulmonary dysfunction
and also systemic problems. Heart disease often results in secondary respiratory signs (e.g., coughing or dyspnea); conversely,
disease of the lung or its vasculature can result in secondary right heart disease (e.g., corpulmonale). It is rare to find
in any individual instance all the signs and other abnormalities that may characterize a specific disease. More commonly,
an animal will manifest only some of these signs, usually in a way that the clinical elements of the disease emerge over time
rather than being grouped at the outset.
The definition of congestive heart failure is the failure of the left and/or right side of the heart to advance blood at a
sufficient rate to meet the metabolic needs of the patient or to prevent blood from pooling within the pulmonary venous circulation.
Asymptomatic Heart Disease
At this level, a cardiac murmur or an ultrasound diagnosis of heart disease has occurred, but clinical signs are absent. Re-evaluation
is the standard, and medication is not required.
Mild to Moderate Heart Failure
Clinical signs of heart failure are evident at rest or with mild exercise and adversely affect the quality of life. Typical
signs of heart failure include exercise intolerance, cough, an increased respiratory rate, dyspnea, and mild to moderate ascites.
Home treatment is often indicated at this stage.
Advanced Heart Failure
Clinical signs of advanced congestive heart failure are immediately obvious. These clinical signs could include respiratory
distress (dyspnea), marked ascites, profound exercise intolerance, or hypoperfusion at rest. In most cases, hospitalization
is mandatory.
Cardiomyopathy
Cardiomyopathy is a disorder of the heart in which the abnormality lies within the muscle tissue (myocardium). A secondary
cardiomyopathy is a disease that affects the myocardium secondary to infectious, toxic, metabolic, or other disease processes.
The majorities of cardiomyopathies diagnosed today are of unknown etiology (primary or idiopathic) and are currently classified
in the literature as representing the hypertrophic or intermediate forms.
Primary cardiomyopathies are classified according to their morphologic appearance:
- Hypertrophic cardiomyopathy (HCM)
- Idiopathic dilated cardiomyopathy (DCM)
- Restrictive cardiomyopathy (RCM)
- Unclassified cardiomyopathies
Secondary causes of cardiomyopathy include:
- Nutritional (taurine deficiency)
- Metabolic (hyperthyroidism, acromegaly)
- Infiltrative (neoplasia, amyloidosis)
- Inflammatory (toxins, immune reactions, infectious agents)
- Genetic (hypertrophic cardiomyopathy is suspected)
- Toxic (doxorubicin)
- Hypertrophic cardiomyopathy (HCM)
Hypertrophic cardiomyopathy (Feline)
Electrocardiography: Left atrial enlargement (p-mitrale – widened P-waves) and left ventricular enlargement (increased R-wave
amplitude and/or increased QRS duration) are present. Arrhythmias are frequent. Most cats with hypertrophic cardiomyopathy
will have a sinus tachycardia. Atrial and ventricular arrhythmias may be present. Interventricular conduction deficits, such
as left anterior fascicular block, are occasionally present.
Radiography: Variable enlargement of the cardiac silhouette is seen. Left atrial enlargement is often most prominent. The
cardiac silhouette may be normal. Cats with congestive heart failure may demonstrate enlargement of the pulmonary veins, variable
pulmonary edema, and pleural effusion.
Echocardiography: Left ventricular hypertrophy involving the left ventricular free wall and, usually to a greater degree,
the interventricular septum is present.
References
Tilley, L.P., and Smith, F.W.K. (Eds): The Five Minute Veterinary Consult-Canine & Feline Medicine 4th
Edition. Ames, Iowa, Wiley Blackwell Publishing, 2008.
Tilley, L.P., Smith, F.W.K., Oyama, M., and Sleeper, M.: Manual of Canine & Feline Cardiology, 4
th
Edition.Elsevier, St. Louis, 2008.
Kittleson, M.D., Kienle, R.D.: Small Animal Cardiovascular Medicine. Philadelphia, Mosby, 1998.
