Difference between revisions of "Aortic Stenosis"

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The three possible areas for aortic stenosis to occur are '''subvalvular or subaortic''' (occurs below the valve), '''valvular or aortic''' (occurs at the valve) and '''supravalvular''' (occurs after the valve). The most common form is subaortic stenosis (SAS), usually as a consequence of fibrous bands that may be circumferential (severe) or may only affect a small area of the LVOTO. The subvalvular fibrous ring may encompass the anterior mitral valve leaflet, causing it to become immobile.  In subaortic stenosis, the lesions may not be present from birth and may develop or progress as the dog matures; but do not generally progress beyond early adulthood. This is in contrast to valvular aortic stenosis, where the valve may become more stenotic as the dog ages.  
 
The three possible areas for aortic stenosis to occur are '''subvalvular or subaortic''' (occurs below the valve), '''valvular or aortic''' (occurs at the valve) and '''supravalvular''' (occurs after the valve). The most common form is subaortic stenosis (SAS), usually as a consequence of fibrous bands that may be circumferential (severe) or may only affect a small area of the LVOTO. The subvalvular fibrous ring may encompass the anterior mitral valve leaflet, causing it to become immobile.  In subaortic stenosis, the lesions may not be present from birth and may develop or progress as the dog matures; but do not generally progress beyond early adulthood. This is in contrast to valvular aortic stenosis, where the valve may become more stenotic as the dog ages.  
  
Aortic stenosis causes an impedence to left ventricular ejection and consequent pressure overload of the left ventricle. The increase in afterload results in a compensatory ''concentric left ventricular hypertrophy'' in attempt to maintain sufficient cardiac output. The severity of stenosis usually determines the extent of hypertrophy. The myocardial hypertrophy results in increased myocardial oxygen demand, beyond the capacity of the coronary capillary vascular bed to supply oxygen. Increased wall stress also compromises coronary perfusion, particularly to the subendocardium. Insufficient oxygen supply to meet the needs of the hypertrophied left ventricle causes myocardial ischaemia and predisposes the animal to ventricular [[:Category:Arrhythmia|arrhythmias]]. There is also an increased risk of bacterial [[Endocarditis|endocarditis]] in animals affected by this condition.
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Aortic stenosis causes an impedence to left ventricular ejection and consequent pressure overload of the left ventricle. The increase in afterload results in a compensatory ''''concentric left ventricular hypertrophy'''' in attempt to maintain sufficient cardiac output. The severity of stenosis usually determines the extent of hypertrophy. The myocardial hypertrophy results in increased myocardial oxygen demand, beyond the capacity of the coronary capillary vascular bed to supply oxygen. Increased wall stress also compromises coronary perfusion, particularly to the subendocardium. Insufficient oxygen supply to meet the needs of the hypertrophied left ventricle causes myocardial ischaemia and predisposes the animal to ventricular [[:Category:Arrhythmia|arrhythmias]]. There is also an increased risk of bacterial [[Endocarditis|endocarditis]] in animals affected by this condition.
  
 
==Signalment==
 
==Signalment==

Revision as of 10:25, 9 June 2016


Introduction

Aortic stenosis is a congenital narrowing of the aortic valve, aorta or left ventricular outflow tract (LVOT).

The three possible areas for aortic stenosis to occur are subvalvular or subaortic (occurs below the valve), valvular or aortic (occurs at the valve) and supravalvular (occurs after the valve). The most common form is subaortic stenosis (SAS), usually as a consequence of fibrous bands that may be circumferential (severe) or may only affect a small area of the LVOTO. The subvalvular fibrous ring may encompass the anterior mitral valve leaflet, causing it to become immobile. In subaortic stenosis, the lesions may not be present from birth and may develop or progress as the dog matures; but do not generally progress beyond early adulthood. This is in contrast to valvular aortic stenosis, where the valve may become more stenotic as the dog ages.

Aortic stenosis causes an impedence to left ventricular ejection and consequent pressure overload of the left ventricle. The increase in afterload results in a compensatory 'concentric left ventricular hypertrophy' in attempt to maintain sufficient cardiac output. The severity of stenosis usually determines the extent of hypertrophy. The myocardial hypertrophy results in increased myocardial oxygen demand, beyond the capacity of the coronary capillary vascular bed to supply oxygen. Increased wall stress also compromises coronary perfusion, particularly to the subendocardium. Insufficient oxygen supply to meet the needs of the hypertrophied left ventricle causes myocardial ischaemia and predisposes the animal to ventricular arrhythmias. There is also an increased risk of bacterial endocarditis in animals affected by this condition.

Signalment

Aortic stenosis is one of the three most common congenital cardiac defects in dogs. Predisposed breeds include the Newfoundland, Boxer, German Shepherd, Golden Retriever and Bull Terrier. Boxers usually have valvular stenosis.

Clinical Signs

Patients may present with exercise intolerance or syncope. However, the disease may be asymptomatic. Lack of clinical signs is not an appropriate reason to delay further investigation of a murmur, as sudden death can be the first indication of aortic stenosis.

Diagnosis

Physical Examination

  • Left sided, systolic murmur with point of maximum intensity at the left base with radiation to the right base and thoracic inlet. The murmur grade usually correlates with the severity of the stenosis for fixed obstructions. The disease has a wide spectrum of severity, and low grade murmurs may be difficult to distinguish from physiological murmurs in puppies.
  • Weak or hypokinetic femoral pulses in severe cases

Thoracic Radiographs

  • May be unremarkable
  • Left ventricular enlargement may be recognised
  • Post-stenotic dilatation of the aorta (bulge) on a dorsoventral view

Electrocardiography (ECG)

  • Often unremarkable
  • Increased R wave amplitude and prolonged QRS duration (indicates left ventricular hypertrophy)
  • Ventricular premature complexes may be present in severe cases, due to myocardial hypoxia and ischaemia.

Echocardiography

  • Left ventricular hypertrophy
  • Structural abnormality of the aortic valve or LVOT with or without a post-stenotic dilatation of the ascending aorta
  • Maximum aortic velocity >2.25m/s, turbulent flow (Doppler)
  • Trans-stenotic pressure gradient: mild <50mmHg, moderate 50-75mmHg, severe >75mmHg (Doppler)

Management

The requirement for treatment is dictated by clinical signs and/or disease severity. Palliative treatment is usually the treatment of choice. It will attempt to alleviate symptoms without curing disease. Methods include exercise restriction and beta-blockers for prevention or control of arrhythmias.

Surgical intervention has been described, but offers no advantage over medical therapy in most cases. Surgery should be considered for dogs with severe stenosis and marked left ventricular hypertrophy. In such cases, surgery should be performed early to minimize ischaemic changes to the myocardium. Surgical options for subaortic stenosis include valve dilation via baloon valvuloplasty or open resection under cardiopulmonary bypass.

Prognosis

The majority of cases are mild, do not require treatment and patients are likely to have a normal lifespan. In severe cases, there is often a poor quality of life. Complications from development of congestive heart failure or cardiac arrhythmias can occur, as can sudden death.


References

Ettinger, S.J, Feldman, E.C. (2005) Textbook of Veterinary Internal Medicine (sixth edition, volume 2), W.B. Saunders Company

Fossum, T. W. et. al. (2013) Small Animal Surgery (fourth edition), Elsevier Mosby

Luis Fuentes, V, Johnson, L.R, Dennis, S. (2010) BSAVA Manual of Canine and Feline Cardiorespiratory Medicine (second edition)



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