• Causes-
    • Bicuspid aortic valve
    • Calcific AS
    • Rheumatic
    • Congenital
    • Atherosclerotic eg type II hypercholesterolemia
    • Rheumatoid
    • Ochronosis (alkaptonuria)


  • Congenital- Unicuspid valves cause severe AS in infancy.
  • Bicuspid aortic valve
    • More in males (3 times more)
    • Some cases are inherited as autosomal dominant
    • NOTCH1 gene mutation in some cases
    • Complications-
      • AR- 20% develop severe AR needing surgery between 10 and 40 years of age
      • AS- Severe AS occurs after 50 years of age. Due to calcification due to turbulence.
      • Infective endocarditis
      • Ascending aortic dilation- Unrelated to stenosis severity. Due to medial degeneration.
      • Aortic dissection- Risk is increased 5 to 9 times
  • Calcific AS-
    • Also called senile or degenerative AS
    • Proliferative and inflammatory changes present. Not simple wear and tear.
    • Calcification of commissures causes AS.
    • Pathogenesis may be similar to atherosclerosis.
    • Risk factors for development- dyslipidemia, diabetes, hypertension, smoking
    • Higher prevalence in Paget disease and ESRD.
    • There may be coexisting mitral annular calcification.
    • Even if there is no AS, calcific aortic sclerosis increases cardiovascular death and MI by 50%
    • Rosuvastatin has been shown to decrease progression of less severe AS to severe AS.
  • Rheumatic-
    • Commissural fusion and cusp stiffening. Central small opening. So usually AS + AR.






Peak velocity (m/s)

< 3



Mean gradient (mm Hg)




Valve area (cm2)




Valve area index (cm2/m2)




  • Mechanisms of myocardial ischemia-
  • Increased myocardial oxygen consumption due to-
    • Increased LV systolic pressure
    • Increased LV ejection time
    • LVH
  • Decreased myocardial oxygen supply due to-
    • Increased LV diastolic pressure
    • Decreased diastolic time
    • Decreased aortic pressure
  • Wall stress- There are two types of response. In one type, wall stress is not allowed to rise by development of concentric LVH- this is more likely in females. Males are more likely to have ventricular dilation, eccentric hypertrophy, rise in wall stress and systolic dysfunction.
  • Diastolic dysfunction (rise in diastolic pressure) occurs due to myocardial hypertrophy and interstitial fibrosis.
  • LV pressure tracing-
    • Increased systolic pressure
    • Rounded top (not normal flat top)
    • Increased end-diastolic pressure
  • LA pressure tracing-
    • Large a waves
  • Atrial contraction in AS- Very important booster pump function as it ensures filling of LV and prevents increase in LA pressure.
  • PAH in AS-
    • Due to increased LV diastolic pressure
    • Mild PAH in one-third cases
    • Severe PAH in 15% cases
  • Exercise in AS-
    • Cardiac output is normal at rest, but does not rise with exercise.


  • Time of onset of symptoms-
    • BAV- 50 to 70 yrs
    • Calcific AS- > 70 yrs
  • Exercise intolerance-
    • Most common initial presentation
    • Dyspnea or fatigue with exertion
    • Dyspnea with exertion is due to diastolic dysfunction
    • Fatigue with exertion is due to inadequate rise of cardiac output
  • Angina-
    • Causes-
      • Mismatch in myocardial oxygen demand-supply ratio
      • Coexistent CAD- in half cases
      • Calcium embolism- very rare
    • Features- typical exertional angina
  • Syncope (or presyncope)-
    • Causes-
      • Exertional syncope-
        • Systemic vasodilation with fixed cardiac output
        • Baroreceptor malfunction
        • Vasodepressor response to increased LV systolic pressure
      • Syncope at rest-
        • Transient VF
        • Transient AF
        • Transient AV block (calcium extending to conduction system)
  • Heart failure-
    • Orthopnea, PND
    • Late feature
  • GI bleeding
    • Angiodysplasia of right colon
    • Mechanisms- High shear stress causes
      • Platelet aggregation
      • Reduction in high molecular weight multimers of von Willebrand factor and
      • Increase in proteolytic subunits
  • Infective endocarditis-
    • More in non-calcified AS than in calcified AS
  • Embolism-
    • Sources-
      • Microthrombi from valve
      • Calcium

Physical examination-

  • Pulse-
    • Parvus and tardus pulse-
      • Slow rising, late peaking, low amplitude
      • Specific for severe AS
    • Normal pulse- AR, HT
  • BP-
    • Low systolic and pulse pressures
    • Normal- AR, inelastic arterial bed in elderly
  • Carotid shudder-
    • Thrill in carotids due to radiation of AS murmur to carotids
  • Heaving LV type apex
  • Palpable and audible LV S4
  • Systolic thrill in aortic area, suprasternal notch and carotids- specific for severe AS
  • Mid systolic murmur-
    • Late peaking
    • Best in base of heart
    • Radiation to carotids
    • In calcific AS, high frequency components radiate to apex- Gallavardin phenomenon
    • Grade 3 or more intensity indicates severe AS- specific, but not sensitive
    • With LV failure, murmur intensity decreases and murmur may disappear.
    • Dynamic auscultation-
      • Increases after long pause in AF and after VPC- helps to differentiate from MR
      • Increased with squatting
      • Decreased with Valsalva
      • Decreased with standing
  • S1- normal or soft
  • LV S4
  • S2-
    • Single S2 due to-
      • Prolonged LV ejection time or
      • Absent A2 due to immobility
    • Normally split S2 makes severe AS unlikely in older adults
    • Normally split S2 is possible in severe AS in young adults as valve mobility is preserved.
  • Aortic ejection sound-
    • Due to halting of upward movement of aortic valve
    • Depends on valve mobility- heard in children and young adults with congenital AS; not heard in older adults with calcific AS


  • Evaluation of AS severity may be inaccurate in-
    • HT- reevaluate after BP control
    • LV dysfunction- do dobutamine echo


  • LVH- correlation between QRS voltage and AS severity is good in children (not good in adults)
  • LAE
  • AF- in 10 to 15%
  • AV conduction defects and IVCD- in 5% of calcific AS- due to extension of calcium to conduction system

Chest radiography-

  • Rounding of apex due to concentric LVH
  • Dilation of ascending aorta- more prominent if bicuspid aortic valve

Natural history-

  • Asymptomatic AS- chance of symptoms at 2 years-
    • Mild AS- 16%
    • Severe AS- 79%
    • Asymptomatic severe AS -chance of sudden death- 1% per year
  • Time of death with symptoms-
    • Angina- 5 yrs
    • Syncope- 3 yrs
    • Heart failure- 2 yrs
  • Hemodynamic progression- annual change-
    • Valve area- 0.12 cm2
    • Peak velocity- 0.32 m/s
    • Mean gradient- 7 mmHg
  • Rapid hemodynamic progression is seen with-
    • Severe calcification
    • Old age
    • Smoking
    • HT
    • Hyperlipidemia and
    • Renal insufficiency
  • Evaluation of patients with absent or equivocal symptoms-
    • TMT- symptoms or BP fall (Note- avoid TMT in symptomatic patients)
    • BNP elevation


Medical treatment

  • Severe AS- avoid vigorous physical activity
  • Diuretics decrease dyspnoea but may decrease cardiac output
  • ACE inhibitors- give only if LV failure- use with caution
  • Beta blockers- avoid- causes LV failure
  • Vasodilators for other purposes like angina- be careful in titration as there will be no compensatory increase in cardiac output
  • Atrial fibrillation- try to cardiovert

Surgical treatment

  • Child, adolescent or young adult with congenital severe AS
    • Procedure-
      • First choice is balloon valvotomy
      • Second choice is surgical valvotomy
    • Indications- (any one of the following)
      • Symptoms
      • Gradient more than 60 mmHg
      • ST changes at rest or with exercise
  • Adults with severe AS-
    • Procedure-
      • AVR (after coronary angiography)
      • Balloon valvotomy- if patient cannot tolerate surgery
      • Percutaneous aortic valve replacement if patient cannot tolerate surgery – not widely available
    • Indications- (any one of the following)
      • Class I-
        • Symptoms
        • EF less than 50%
        • Undergoing cardiac surgery including CABG
      • Class IIb-
        • TMT causes symptoms or BP fall
        • Rapid disease progression
        • Very severe AS, severe valve calcification
  • AS with LV dysfunction
    • Surgical risk is high if EF is less than 35%
    • AVR should still be done as survival is improved
    • Nitroprusside is used as bridge to surgery
    • AVR may not be beneficial in advanced HF (high operative risk) and in patients with HF due to past MI (in whom AVR may not improve LV function)
  • AS with low gradient and low cardiac output
    • DDs-
      • Severe AS with LV dysfunction
      • Mild AS with LV dysfunction due to dilated cardiomyopathy
    • Dobutamine stress echo-
      • Severe AS- Increase in gradient. No change in valve area.
      • Mild AS- Increase in valve area.
      • Also assesses contractile reserve- predicts improvement in LV function after surgery
  • Results of AVR-
    • Operative mortality-
      • 4% (note- that of MVR is 6%)
      • 1% if age is less than 70 years
      • 7% if associated CABG
    • 10 year survival-
      • 85%
    • Higher surgical risk in-
      • Old age
      • Associated CAD
      • LV dysfunction
      • Females