Aortic stenosis impedes normal left ventricular emptying and is caused by a narrowing at one of three locations:
The most common form of aortic stenosis in dogs is subaortic stenosis (SAS), caused by fibrous nodules or a ridge or ring of fibrous tissue within the left ventricular outflow tract just below the aortic valve. Subaortic stenosis is generally seen in large-breed dogs. Predisposed breeds include Boxers, Golden Retrievers, Rottweilers, German Shepherds, and Newfoundlands.
Aortic stenosis induces left ventricular concentric hypertrophy, the degree of which depends on the severity of the stenosis. In severe cases, left ventricular output may be decreased, especially notable during exercise. The major ramification of left ventricular concentric hypertrophy is the risk of myocardial ischemia secondary to inadequate perfusion. Myocardial ischemia is a major factor in the development of life-threatening ventricular arrhythmias.
Clinical signs do not consistently parallel the severity of stenosis. Inadequate output can result in lethargy, exercise intolerance, and syncope. Animals with no history of illness may die suddenly, with the defect first detected at necropsy.
Affected animals have an ejection-type systolic murmur heard best at the aortic valve area. The intensity of the murmur correlates fairly well with the degree of stenosis and may increase as animals mature, reflecting progressive stenosis. Puppies without detectable murmurs should not be considered free of disease until they reach maturity (~1 year of age). In more severe cases, femoral pulse strength is diminished. Electrocardiography may show left ventricular enlargement (tall R waves in lead II) and ventricular premature complexes that may increase in frequency with exercise. Holter monitoring is indicated in syncopal animals or in animals with severe disease to define the presence of any arrhythmias, assess arrhythmia severity, and help determine the risk of sudden death. A recheck Holter monitor may be considered after initiation of antiarrhythmic therapy to assess efficacy.
Radiographically, there is variable left ventricular enlargement and poststenotic dilatation of the aorta. Two-dimensional and Doppler echocardiography can generally provide a definitive diagnosis of aortic stenosis and exclude other cardiac abnormalities. A subaortic ridge or ring may be visible, and the velocity of systolic blood flow through the defect determines the severity of the stenosis. Dogs with more significant stenosis may show left ventricular concentric hypertrophy and hyperechoic areas within the myocardium consistent with myocardial ischemia and fibrosis.
Medical management generally consists of the use of a beta-blocker (eg, atenolol) for its potential to decrease myocardial oxygen demand, prolong diastole, and reduce left ventricular wall stress. Antiarrhythmic therapy is indicated in dogs with significant ventricular ectopy. Balloon valvuloplasty, although potentially effective short term, is unlikely to offer consistent longterm benefits. Open surgical resection is costly, limited to facilities offering cardiopulmonary bypass, and associated with higher morbidity/mortality. Mildly affected animals commonly require no treatment, and the prognosis can be fair to good in animals very mildly affected. Affected animals should not be bred. Affected dogs are at higher risk of aortic valve infection (infective endocarditis); precautions that may reduce risk include perioperative antibiotic therapy and prompt treatment of infections (ie, urinary, skin, ear, etc.).
Subaortic stenosis occurs most commonly in large-breed (Boxer, German Shepherd, Golden Retriever, Newfoundland and Rottweiler) dogs.
A loud, systolic ejection murmur is typically heard over the left base of the heart and may radiate to the right base; pulse quality may be weak.
Definitive diagnosis can be achieved by echocardiography and treatment recommendations, and risks vary with severity of disease.
Affected dogs are at higher risk of infective endocarditis.