Aortic stenosis can occur at three levels: (1) subvalvular; (2) valvular; and (3) supravalvular. Subvalvular aortic stenosis is the most common form in dogs; in severe cases a distinct fibrous band forms below the valve. Valvular lesions are relatively rare in the dog. Supra valvular stenosis is more common in the cat and is always associated with malformation of the aortic valve.
Aortic stenosis results in left ventricular outflow obstruction and pressure overload. The clinical presentation of aortic stenosis, as with pulmonic stenosis, relates to the severity of die outflow obstruction, the pressure gradient which develops across the aortic valve and the degree of compensatory left ventricular hypertrophy. A progressive increase in left ventricular workload leads to myocardial isehaemia which predisposes to arrhythmias and left ventricular failure. In severe cases, symmetrical concentric hypertrophy of the left ventricle and outflow tract contributes to the outflow obstruction and results in impaired diastolic filling (decreased myocardial compliance). Turbulence of blood through the stenotic region results in post-stenotic dilatation of the ascending aorta. Damage to the aortic valve leaflets and left ventricular pressure overload may result in the concur rent regurgitation of blood through aortic and mitral valves, respectively.
The highest incidence of aortic stenosis occurs in boxers, golden retrievers. German short-haired pointers and German shepherds. A genetic trait has been identified in the Newfoundland breed. The high incidence in golden retrievers suggests a mode of inheritance similar to that of Newfoundlands.
Dogs with mild defects often show no clinical signs and may have normal life expectancy. More severe stenosis is associated with exercise intolerance, muscular weakness and syncopal episodes. The onset of clinical signs often occurs between 6 and 10 months of age. Left-sided heart failure is uncommon in dogs with aortic stenosis; most animals die suddenly and unexpectedly probably as a result of severe ventricular arrhythmias.
Aortic stenosis is characterized by the presence of a low-grade systolic ejection-type crescendo-decrescendo murmur with a point of maximal intensity over the aortic valve region; occasionally there is a diastolic component due to aortic insufficiency- The intensity of the murmur tends to correlate with the magnitude of the outflow obstruction. The murmur may radiate up the carotid arteries and severe murmurs can occasionally be auscultated over the cranium and may be associated with a palpable precordial thrill. The murmur may also be audible over the right third or fourth intercostal spaces. The femoral pulse becomes attenuated as cardiac output falls.
Mild aortic stenosis is unlikely to cause significant electrocardiographs abnormalities. More severe lesions may result in increases in R wave amplitude and QRS duration (left ventricular enlargement), depression of the ST segment (myocardial hypoxia) and ventricular or supraventricular arrhythmias.
Radiographs are often unremarkable. Post-stenotic dilatation of the ascending aorta may result in an enlarged aortic arch on the dorsoventral view, although this ‘knuckle’ may be hidden within the mediastinum, and filling of the cardiac waist on the lateral projection. Signs of left atrial and left ventricular enlargement and left-sided failure may be present with more severe lesions or if the aortic stenosis is complicated by mitral regurgitation.
Echocardiography may reveal a ring of fibrous tissue befow the level of the aortic valve and is useful for confirming the presence of post-stenotic dilatation and left ventricular hypertrophy. Premature closure of the aortic valve during mid-systole may be evident in severe cases. Other echocardiographic features include systolic fluttering of the aortic valve, and systolic anterior motion and diastolic fluttering of the mitral valve. Left ventricular fractional shortening may be normal or increased. The severity of the lesion can be assessed by Doppler echocardiography. The flow velocity and pressure
gradient across the aortic valve can be measured non-invasively using the Bernoulli equation (pressure = 4 x flow velocity) and the results correlate well with those obtained via imraeardiac catheterization. Flow velocities less than 5 m s-1 by the time the dog reaches maturity may not significantly reduce longevity or quality of life; normal maximum aortic flow velocity is 1.5 m s-1. Doppler echocardiography may also demonstrate retrograde flow of blood through the aortic valve due to aortic regurgitation. An unusual form of subaortic stenosis in combination with mitral valve dysplasia has been reported in golden retrievers.
Angiocardiography and pressure studies
Maximum pressure gradient across the aortic valve should not exceed 9 mm Hg. Moderately severe lesions have pressure gradients greater than 40 mm Hg; a pressure gradient greater than SO mmHg is consistent with severe stenosis and surgery is indicated.
A selective injection of contrast material into the left ventricle can be used to demonstrate left ventricular hypertrophy, subvalvular stenosis and post-stenotic dilatation.
Whereas the long-term survival of dogs with untreated mild to moderate subaortic stenosis is favourable (30-50 months) most dogs with pressure gradients greater than 80 mm Hg die before three years of age (median survival 19 months).
Aortic stenosis: Treatment
The administration of beta-adrenergic blockers as prophylactic antiarrhythmic agents and their effect on myocardial compliance has not been fully investigated in dogs with aortic stenosis. It has been suggested, on the basis of favourable clinical reports, that beta blockers may improve diastolic filling and, by decreasing heart rate, decrease myocardial oxygen demand.