Aortic Stenosis


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:

  • Senile calcific

  • Bicuspid aortic valve

  • Rheumatic AS (typically with coexisting mitral stenosis)

  • Congenital/unicuspid AS

  • 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.

Prognosis in severe aortic stenosis (Ross and Braunwald, 1968)
Prognosis in severe aortic stenosis (Ross and Braunwald, 1968)

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

Physical exam

  • Vitals: hypertension in the elderly (risk factor)

  • Peripheral pulses:

    • Carotid artery: pulsus parvus et tardus – slow rising impulse with low amplitude

    • Apical-carotid delay

    • Brachioradial delay

  • Auscultation:

    • 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

JAMA Rational Clinical Exam for AS


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

  • Associated aortopathy

  • Hemodynamic consequences (aortic pressure gradient and velocity)

  • LV size and systolic function

Parameters for mean aortic gradient and peak flow velocity are as follows:


Aortic sclerosis

Mild AS

Moderate AS

Severe AS

Aortic jet velocity (m/s)

< 2.5



> 4.0

Mean gradient (mmHg)


< 20


> 40

Aortic valve area (cm2)


> 1.5


< 1.0

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.

Asymptomatic AS

In asymptomatic AS, serial monitoring with echo is indicated. Timing of follow-up interval is based on severity of AS:

Mild ASModerate ASSevere AS (asymptomatic)
Echo q3-5 yearsEcho q1-2 yearsEcho 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
 The ESC guidelines on valvular heart disease outlines management as follows:
ESC AS algorithm

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


  • Primary Author: Dr. Matthew Church (MD, FRCPC, Cardiology Fellow)
  • Last Updated: February 20, 2021
  • Comments or questions please email
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