Aortic stenosis (AS) is a common valvular condition that can have major hemodynamic consequences from the progressively stenotic aortic valve.
The etiology of a patient’s aortic stenosis often dictates the age of onset of severe AS and symptoms. The causes of AS are grouped into:
Bicuspid aortic valve
Rheumatic AS (typically with coexisting mitral stenosis)
Prosthetic valve AS (not discussed in this summary)
Subvalvular and supravalvular AS (not discussed in this summary)
Determination of the optimal approach to management of symptomatic severe AS is evolving, with surgical and interventional approaches possible.
The aortic valve can be prone to progressive calcification and stenosis, with similar risk factors as atherosclerosis such as age and hypertension.
Some conditions, such as a bicuspid aortic valve, predispose a patient to earlier development of stenosis.
Aortic stenosis results in a pressure-overload state in the left ventricle, resulting in LVH and diastolic dysfunction.
A famous postmortem review of patients with AS found that symptom onset is a marker for increased mortality, after a long latent period.
History & Physical
The classical symptoms of severe aortic stenosis are:
Angina: average survival 5 years
Syncope: average survival 3 years
Heart failure: average survival 2 years
Other clinical features:
Dyspnea due to diastolic dysfunction or eventual heart failure
GI bleeding due to angiodysplasia (Heyde’s syndrome)
High-velocity flow across the stenotic aortic valve leads to increased shear stress of blood cells, with resultant acquired von Willebrand factor deficiency
Vitals: hypertension in the elderly (risk factor)
Carotid artery: pulsus parvus et tardus – slow rising impulse with low amplitude
Single or inaudible S2 (loss of A2 component)
S4 may suggest LVH
Systolic crescendo-descrendo murmur: later peaking suggests more severe AS
Radiation to carotids in severe AS
Radiation to apex (“Gallavardin” phenomenon of high-pitched murmur)
Note that a later peaking murmur suggests more severe AS; intensity of murmur does not correlate with severity of AS
Systolic ejection click may suggest bicuspid aortic valve
ECG will often show LVH, as a result of adaptation to LV pressure overload.
CXR may show a calcified aortic valve and aorta, along with features of heart failure (cardiomegaly, pulmonary edema, etc).
Echocardiography (TTE) is the preferred test for diagnosis and is recommended in any patient with signs or symptoms suggestive of aortic stenosis or bicuspid aortic valve.
TTE allows for the determination of:
Aortic valve anatomy
Etiology of AS
Hemodynamic consequences (aortic pressure gradient and velocity)
LV size and systolic function
Parameters for mean aortic gradient and peak flow velocity are as follows:
Low flow low gradient severe AS
- There is a subset of patients with severe AS who have reduced flow across the aortic valve (i.e. reduced LVEF), along with a low gradient that would not otherwise suggest severe AS.
- For these patients, dobutamine stress echo (or invasive hemodynamic assessment) is reasonable to assess severity and contractile reserve.
In asymptomatic AS, serial monitoring with echo is indicated. Timing of follow-up interval is based on severity of AS:
|Mild AS||Moderate AS||Severe AS (asymptomatic)|
|Echo q3-5 years||Echo q1-2 years||Echo q6months – 1 year|
Symptomatic severe AS
For severe symptomatic aortic stenosis, management is surgical or interventional. Medical management only temporizes symptoms from the inevitable progression of stenosis.
Diuretics can help with symptomatic pulmonary edema. Avoid or use extreme caution with afterload-reducing agents such as ACE inhibitors, ARBs, and nitrates.
The class 1 indications for valve replacement are the following:
- Severe AS with symptoms
- Severe AS with LV dysfunction (defined as LVEF < 50%)
- Moderate or severe AS and going for other cardiac surgery
Choice of aortic valve prosthesis
Choice of bioprosthetic versus mechanical should consider valve durability, potential need for anticoagulation, and patient preferences.
In general, mechanical valves are very long-lasting but come with the need for lifelong anticoagulation with warfarin. Bioprosthetic valves do not generally require anticoagulation but come with a high risk for early valve deterioration.
The current guidelines suggest that patients < age 50 should favour mechanical AVR, unless anticoagulation is contraindicated or undesired. Patients over age 65 can typically favour bioprosthetic AVR, as the valve is likely to outlive them.
Note that all TAVI valves are bioprosthetic.
Choice of aortic valve procedure
Determination of the optimal strategy primarily depends on a patient’s operative risk and should involve a consensus with the multidisciplinary cardiac team (cardiologist and cardiac surgeon).
Current guidelines suggest the following:
Age <65 years or life expectancy >20 years: SAVR preferred
Age 65-80: either SAVR or transfemoral TAVI, with shared decision-making to balance patient longevity and valve durability
Age >80: transfemoral TAVI preferred
Percutaneous balloon valvuloplasty/dilation is a high-risk interventional procedure that in very limited settings can act as a bridge to SAVR or TAVI.
If patient survival is predicted to be <12 months despite SAVR/TAVI, then neither procedure should be performed