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Aortic valve stenosis



Calcific aortic valve stenosis is characterized by a progressive fibro-calcific remodeling and thickening of the aortic valve cusps, which subsequently leads to valve obstruction. The underlying pathophysiology is complex and involves endothelial dysfunction, immune cell infiltration, myofibroblastic and osteoblastic differentiation, and, subsequently, calcification.

Among symptomatic patients with medically treated moderate-to-severe aortic stenosis, mortality from the onset of symptoms is approximately 25% at 1 year and 50% at 2 years. Symptoms of aortic stenosis usually develop gradually after an asymptomatic latent period of 10-20 years.

Systolic hypertension can coexist with aortic stenosis. The carotid arterial pulse typically has a delayed and plateaued peak, decreased amplitude, and gradual downslope (pulsus parvus et tardus).

Other symptoms of aortic stenosis include the following:

  • Pulsus alternans: Can occur in the presence of left ventricular systolic dysfunction
  • Hyperdynamic left ventricle: Unusual; suggests concomitant aortic regurgitation or mitral regurgitation
  • Soft or normal S1
  • Diminished or absent A2: The presence of a normal or accentuated A2 speaks against the existence of severe aortic stenosis
  • Paradoxical splitting of the S2: Resulting from late closure of the aortic valve with delayed A2
  • Accentuated P2: In the presence of secondary pulmonary hypertension
  • Ejection click: Common in children and young adults with congenital aortic stenosis and mobile valve leaflets
  • Prominent S4: Resulting from forceful atrial contraction into a hypertrophied left ventricle
  • Systolic murmur: The classic crescendo-decrescendo systolic murmur of aortic stenosis begins shortly after the first heart sound; the intensity increases toward mid systole and then decreases, with the murmur ending just before the second heart sound.

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