Aortic Stenosis

AS is a progressive valvular disease. The end-stage is characterized by LV outflow obstruction with decreased cardiac output, exercise capacity, heart failure and then death.

No medical therapies prevent or slow the progressive of disease.

Epidemiology

• Prevalence of AS: Age 50-59: 0.2%; Age 75+: 2.8%; Age 80+: 9.8%.

Etiology of AS

• Evidence of a common etiology between atherosclerosis and valvular stenosis:
  • Valve tissue has cellular proliferation, inflammation, lipid accumulation, and increased margination of macrophages and T cells
  • Disruption of endothelium and collagen matrix
  • Deposition of calcium
• Most common causes of aortic stenosis:
  • Calcific tricuspid deterioration (#1)
    • Typically in older patients (>65 yrs)
    • The most common cause in developed countries. Some genetic basis of disease.
    • Similar clinical risk factors to atherosclerosis and CAD
    • Even aortic sclerosis is associated with excess CV death and MI in the elderly.
  • Congenital bicuspid or unicuspid valve (#2)
    • Presents in 1-2% of the American population, typically in younger patients
    • Patients generally need a valve replacement during their lifetime.
      • 60% of valve replacements <70
      • 40% of valve replacements >70
    • Bicuspid AV is the most common congenital valvular defect. Autosomal dominant with incomplete penetrance. Also associated with  ascending aortic aneurysm, aortic coarctation, and other aortopathies. Inherently at risk for aneurysm formation and/or dissection.
  • Rheumatic heart disease (#3)
    • Produces commissural fusion sometimes resulting in a bicuspid-appearing valve. The leaflets are more susceptible to trauma and leads to fibrosis, calcification, stenosis. The valve at presentation is usually a rigid calcified mass
    • 95% of rheumatic AS have coexisting rheumatic mitral disease, and also usually associated with AR
  • Radiation to the mediastinum causes late scarring, fibrosis, and calcific AS.

Pathophysiology of Disease

• Decreased AVA leads to elevation of LV ejection pressures necessary to maintain cardiac output

Natural History of Disease

Clinical History of Disease

• The majority of mild asymptomatic AS will NOT progress to severe or symptomatic disease over 20 years.
• The emergence of symptoms signifies the urgent need for surgical intervention because median survival with symptoms is severely decreased. 50% mortality at 2 years for patients with symptomatic disease unless aortic valve replacement is performed.

Clinical symptoms (presentation prevalence)	Median survival
Asymptomatic/valve replaced	Normal
Angina (35%)	5 years
Syncope (15%)	3 years
Dyspnea (50%)	2 years
A-fib	6 months

After valve replacement surgery, prognosis improves to near normal, especially for patients older than 65 years at the time of valve implantation, presumably because older patients have fewer years at risk for valve-related complications.

Pathophysiologic History of Disease

Progression of valvular involvement:

1. Leaflet disease
2. Aortic sclerosis
3. Valvular obstruction (10-15% of aortic sclerosis will progress to AS)
4. Progressive aortic stenosis (patients who develop some degree of obstruction will progress down this pathway)
   1. +0.1 to 0.3 m/s maximum transvalvular velocity per year
   2. +3 to 10 mmHg mean gradient per year
   3. -0.1 cm2 AVA per year