Aortic Stenosis

Definition: Narrowing of the AV orifice. A high pressure jet can be visualized in the Asc. AO due to the valve narrowing. Observe for post-stenotic dilatation.

Causes (Etiology):

- Degenerative, mean age 65 to 70 (common)
- Congenital (e.x. Bicuspid) Most common in patients <50 yrs
- Rheumatic fever (post-inflammatory process)

Patient History:
- Dyspnea on Exertion
- Heart Failure
- Angina Pectoris
- Effort Syncope
- Right-Sided Heart Failure (e.x. Jugular venous distention, hepatomegaly, peripheral edema, ascites, anasarca. Right-sided Heart Failure paired with AO stenosis is an "ominous sign" for complete heart failure)

- LV pressure overload and hypertrophy
- Increased LV end-diastolic pressure
- Increased LA pressure
- Late course LV systolic dysfunction
- Preterminal PAH

Medical treatment:
- Rheumatic fever prophylaxis (when applicable)
- Digitalis/Diuretics
- ACE inhibitors
- Cardioversion
- Cholesterol lowering drugs

Surgical treatment: 
- AV replacement (high risk when EF <35%)
-Ross procedure (PV transplantation to AV position, reimplantation of coronary arteries, and placement of homo graft in pulmonary position)
Bicuspid AV (AO Stenosis):


- Eccentric diastolic closure of line of AV leaflets
- Normal systolic valve opening may be present

2D Findings:
- Systolic doming of AV valve in PLAX
- Thickened AV leaflets (thickness usually increases with age)
- Elliptical "football" shaped opening in PLAX and PSAX views
- Post-stenotic dilatation of the AO
- Concentric LV hypertophy
- LA & LV dialtation

- If a Bicuspid AO valve is confirmed, make sure to evaluate for Coarctation of the AO (*RDCS test question)
- Anatomic AVA by Planimetry in PSAX
- LV global and segmental systolic function
- Presence and severity of possible coexisting lesions such as AO Regurgitation, AO Coarctation, VSD, PDA, AO Aneurysm, AO Dissection...

Rheumatic/Degenerative (AO Stenosis):

- Increased thickness with decreased systolic excursion of AV leaflets
- Decreased systolic maximal ACS 
(AVA < 0.75 cm2 if maximal ACS is 11mm in PLAX)
- Leaflet edge thickening, commissural fusion, systolic doming, and coexisting MV disease suggest rheumatic etiology
Post stenotic dilatation of the Asc. AO
- LVH (suggests significant AO stenosis, coarctation, and/or systemic hypertension

- Anatomic AVA by planimetry preferably by TEE PSAX
- LV global and segmental systolic function

CW Doppler ranges for significant AO stenosis:
+ Peak AV velocity... 3.92 m/s
+ Max PG... 61.3 mmHg
+ Mean PG... 38.1 mmHg
+ AVA (I,D)... 0.819 cm2 

- Determine AVA- using the continuity equation.
- Velocity ratio (LVOT VTI / AV VTI)
- LV Systolic pressure/evaluate for diastolic dysfunction
Additional notes:
- AS is initially attributed to L. sided heart pressure overload. Predominantly affects males (2:1)
- The main etiology of AS are degenerative changes brought on by the aging process
- LV function is actually preserved by the development of concentric LVH- Dilatation usually does not occur until the contractile state of the myocardium is significantly depressed
- Diseases such as Severe Hypercholesterolemia, Diabetes, Systemic Lupus Erythematosus, Pagets Disease, and Ochronosis can contribute to the onset of AS and it's progression 
- If one AV cusp is seen to move along the periphery in either PSAX or PLAX severe AS is unlikely. Conversely, if AV motion is significantly reduced, severe AS is usually present
- The AV should be examined from several windows (ex. Apical, R. PLAX, Suprasternal, Supraclavicular, Subcoastal, and PLAX) with CW doppler to confirm that the US beam is parallel to flow, this ensures that the highest velocity across the valve can be obtained
- A "Raphe" is an underdeveloped AO cusp and it may give the appearance of three leaflets during diastole
- AS becomes symptomatic around the ages of 20-50, while AS calcification are attributed to the elderly.