Aortic Valvular Stenosis



Aortic stenosis (AS) is a narrowing of the aortic valve area causing obstruction to left ventricular (LV) outflow. The disease has a long asymptomatic latency period, but development of severe obstruction or onset of symptoms such as syncope, angina, and congestive heart failure (CHF) are associated with a high mortality rate without surgical intervention.


AS is the most common primary valve disease leading to surgery or catheter intervention in Europe and North America, with a growing prevalence due to the aging population (1). Cause by age at presentation:

  • <30 years: congenital
  • 30 to 65 years: congenital or rheumatic fever (RF)
  • >65 years: degenerative calcification of aortic valve


  • Affects 1.3% of population 65 to 74 years old, 2.4% 75 to 84 years old, 4% >84 years old
  • Bicuspid aortic valve: 1–2% of population. Bicuspid aortic valve predisposes to development of AS at an earlier age.

Etiology and Pathophysiology

  • Progressive aortic leaflet thickening and calcification results in LV outflow obstruction. Obstruction causes increased afterload and, over time, decreased cardiac output.
  • Increase in LV systolic pressure is required to preserve cardiac output; this leads to development of concentric LV hypertrophy (LVH). The compensatory LVH preserves ejection fraction but adversely affects heart functioning.
    • LVH impairs coronary blood flow during diastole by compression of coronary arteries and reduced capillary ingrowth into hypertrophied muscle.
    • LVH results in diastolic dysfunction by reducing ventricular compliance.
  • Diastolic dysfunction necessitates stronger left atrial (LA) contraction to augment preload and maintain stroke volume. Loss of LA contraction by atrial fibrillation can induce acute deterioration.
  • Diastolic dysfunction may persist after relief of AS due to the presence of interstitial fibrosis.
  • Angina: increased myocardial demand due to higher LV pressure. Myocardial supply is compromised due to LVH.
  • Syncope (exertional): can be multifactorial from inability to augment cardiac output due to the fixed obstruction to LV outflow; arrhythmias; or most commonly, abnormal baroreceptor response resulting in failure to appropriately augment blood pressure
  • Heart failure: Eventually, LVH cannot compensate for increasing afterload resulting in high LV pressure and volume, which are accompanied by an increase in LA and pulmonary pressures.
  • Degenerative calcific changes to aortic valve (2)
    • Mechanism involves mechanical stress to valve leaflets as well as atherosclerotic changes to the valve tissue. Bicuspid valves are at higher risk for mechanical stress.
    • Early lesions: subendothelial accumulation of oxidized LDL and macrophages and T lymphocytes (inflammatory response)
    • Disease progression: Fibroblasts undergo transformation into osteoblasts; protein production of osteopontin, osteocalcin, and bone morphogenic protein-2 (BMP-2), which modulates calcification of leaflets
  • Congenital: unicuspid valve, bicuspid valve, tricuspid valve with fusion of commissures, hypoplastic annulus
  • RF: chronic scarring with fusion of commissures

Risk Factors

  • Congenital unicommissural valve or bicuspid valve
    • Unicommissural valve: Most cases were detected during childhood.
    • Bicuspid valve: predisposes to the development of AS earlier in adulthood (4th to 5th decade) compared to tricuspid valve (6th to 8th decade)
  • RF
    • Prevalence of chronic rheumatic valvular disease has declined significantly in the United States.
    • Most cases are associated with mitral valve disease.
  • Degenerative calcific changes
    • Most common cause of acquired AS in the United States
    • Risk factors are similar to that of coronary artery disease (CAD) and include the following: hypercholesterolemia, hypertension, smoking, male gender, age, and diabetes mellitus.

Commonly Associated Conditions

  • CAD (50% of patients)
  • Hypertension (40% of patients): results in “double-loaded” left ventricle (dual source of increased afterload as a result of obstruction from AS and hypertension)
  • Aortic insufficiency (common in calcified bicuspid valves and rheumatic disease)
  • Mitral valve disease: 95% of patients with AS from RF also have mitral valve disease.
  • LV dysfunction and CHF
  • Acquired von Willebrand disease: Impaired platelet function and decreased vWF results in bleeding (ecchymosis and epistaxis) in 20% of AS patients. Severity of coagulopathy is directly related to severity of AS.
  • Gastrointestinal arteriovenous malformations (AVMs)
  • Cerebral or systemic embolic events due to calcium emboli

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