A 74-year-old man with severe aortic stenosis and oxygen-dependent lung disease was referred for treatment of aortic valve disease. His past medical history was significant for diabetes mellitus, hypertension, hyperlipidemia, coronary artery disease, peripheral vascular disease, and interstitial lung disease. Pulmonary function testing 6 months earlier showed moderate restrictive lung disease (total lung capacity 58% predicted) and severely reduced diffusion capacity (31% predicted). Over the preceding few months, he had experienced rapidly worsening dyspnea and oxygen desaturations at rest, requiring initiation of supplement oxygen. Computed tomography scan of the lungs showed end-stage interstitial fibrotic lung disease, and echocardiogram showed mildly depressed left ventricular function (ejection fraction 45%-50%) with severe aortic stenosis (peak velocity 5.0 m/s, mean gradient 60 mm Hg, valve area 0.77 cm²). He was referred for consideration of aortic valve replacement.

This patient had multiple conditions that could be contributing to his dyspnea. The degree of dyspnea and desaturation seemed out of proportion to his valve disease, especially in the absence of obvious volume overload on exam or imaging. As such, upon discussion with the patient’s pulmonologist, it was decided to pursue balloon aortic valvuloplasty to allow time to complete his pulmonary workup and to help determine how much benefit he might derive from valve replacement.

AORTIC STENOSIS (AS)

• 
  

  Most common causes are calcification of a normal trileaflet valve and a congenital bicuspid valve.^1,2

  
  
• 
  

  Calcific AS is the most common acquired valvular disorder in the developed world.²

  
  
• 
  

  Calcification restricts leaflet motion and decreases the effective orifice area.

  
  
• 
  

  Classification is determined by velocity, gradient, and valve area (Table 20-1).

  
  
• 
  

  Rate of progression is highly variable.³

  
  
  
  
  • 
    

    Annual decrease in aortic valve area = 0.12 cm²/yr

    
    
  • 
    

    Annual increase in aortic jet velocity = 0.32 m/s/yr

    
    
  • 
    

    Annual increase in mean aortic valve gradient = 7 mm Hg/yr

  
  
• 
  

  Severity of obstruction usually increases gradually over 10 to 15 years, resulting in a latent period before symptoms develop.⁴

  
  
• 
  

  Symptoms are related to increased workload on the left ventricle.

  
  
• 
  

  In the absence of treatment, severe AS is associated with significant morbidity and mortality once symptoms develop.^5,6

  
  
  
  
  • 
    

    Mean survival is 3 years after onset of angina or syncope.

    
    
  • 
    

    Mean survival is 2 years after onset of heart failure.

AS is best treated with aortic valve replacement (AVR)⁷ using either a surgical (SAVR) or transcatheter (TAVR) technique, both of which are associated with improved symptoms and survival.^6,8 In patients who are not considered candidates for SAVR or TAVR, balloon aortic valvuloplasty (BAV) can be considered.

AMERICAN COLLEGE OF CARDIOLOGY/AMERICAN HEART ASSOCIATION GUIDELINES

• 
  

  Class IIb: BAV may be considered as a bridge to surgery in hemodynamically unstable patients who are at high risk for AVR.⁷

  
  
• 
  

  Class IIb: BAV may be considered as palliation in adult patients in whom AVR cannot be performed because of serious comorbid conditions.