Aortic Stenosis and Sclerosis

Obstruction of blood flow across the aortic valve.

Background and Epidemiology

  • Most common valve disease
    • About 25% of people >65 have aortic sclerosis and about 3% over 75 have severe stenosis.
  • Serious cause of anaesthetic complications

Aetiology

  • There are several common causes of aortic stenosis
  • In younger (<70) patients:
    • Congenital abnormality (unicuspid or bicuspid aortic valve) accounts for ~50% of cases
    • Postinflammatory changes (e.g. rheumatic heart disease) (~25% of cases)
  • In older patients (>70)
    • Degenerative changes (~50%)
      • This is usually fibrosis/calcification (similar process to atherosclerosis- with similar risk factors including hyperlipidaemia, hypertension, male, age etc)
    • Bicuspid and postinflammatory causes account for a similar amount of the remainder (~25%)

Pathophysiology

  • Resistance to blood outflow from the heart causes an increase in left ventricular pressure, which causes LV hypertrophy and dilation
    • In most patients, this will preserve LV function and cardiac output for years.
    • However, as this process continues, the LV becomes thickened such that compliance is reduced and the ability of the ventricle to fully dilate is limited
      • This increases the work load needed of the heart
      • Eventually, if the changes progress, the pressure gradient across the aortic valve grows.  When the LV can no longer manage to force blood out to maintain CO, back flow and pulmonary oedema ensues

Presentation

  • Many patients are diagnosed asymptomatically
  • Classic symptoms are a triad of angina, breathless and syncope.
    • Angina due to increased demand of the hypertrophied LV working against the stenotic valve
      • Mismatch between oxygen supply and demand
      • May be worsened/precipated by co-existent coronary artery disease (particularly in older patients)
    • Breathless can be due to cardiac failure (both as a direct consequence of decreased cardiac output and of pulmonary oedema)
      • Usually exertional
    • Syncope is also usually exertional (as cardiac output cannot raise in response to exertion- causing decreased oxygenation to the brain)
  • On examination
    • Examination of the pulse
      • ‘Slow-rising’ pulse- the only way I can describe this is like the pulse beat builds up more slowly.
      • Pulse may also feel decreased in volume
      • NOTE- this is feature exclusive to aortic stenosis (i.e. not sclerosis)
    • Examination of BP
      • May reveal a narrow pulse pressure i.e. SBP and DBP are close together
    • Murmur
      • ‘Ejection systolic murmur’- crescendo-decrescendo murmur starts shortly after the first heart sound that ends just before the second heart sound
      • A2 is diminished in stenotic disease but can be loud in sclerotic disease
      • Similarly, the murmur can radiate to the carotids in aortic stenosis- this is rarer in sclerosis
      • Splitting of the second heart sound may also be heard

Investigation

  • ECG
    • May show signs of LVH
      • ‘Voltage criteria’ (not diagnostic)
        • Limb leads
          • R wave in lead I plus S wave in lead III >25mm
          • R wave in aVL >11mm
          • R wave in aVF >20mm
          • S wave in aVR >14mm
        • Chest leads
          • R wave in V4, V5, V6 >26mm
          • R wave in V5 or V6 + S wave in V1 >35mm
          • Largest R wave plus largest S wave >45mm
      • ‘Strain pattern’
        • ST segment depression and T wave inversion in the left sided leads (aVL; V5-6)
  • CXR (may show heart enlargement or pulmonary oedema)
  • Echocardiography
  • Exercise testing
    • NB ONLY for asymptomatic patients (looking for LV strain)
    • Contraindicated in symptomatic patients

Management

  • Symptomatic patients should be offered valve replacement (balloon valvuloplasty or transcatheter Aortic valve implantation)
    • If patients are unsuitable for surgery, treat symptoms of heart failure as per heart failure
    • If the patient receives mechanical valve replacement, long term anticoagulation (warfarin or new-generation oral anticoagulants) is required
  • Other medical management includes reducing cardiovascular risk factors e.g. statins (if hyperlipidaemic); if hypertensive- control BP with ACE inhibitors/diuretics
    • NB Avoid hypotension
  • Asymptomatic patients should be monitored with Echo +/- exercise tolerance testing, every 6 months (if severe on echo); 12 months (if mild-moderate with calcification) or 24-36 months (if mild, no calcification)
    • Note that these patients do NOT require surgery, despite severity

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