Definition: incomplete opening of the AV. Under some circumstances, the AV becomes narrower than normal, impeding the flow.
Epidemiology: prevalence of AS in population = 2% >65yo, 3% >75yo, 4% >85yo.
Clinical presentation: “SAD” triad. Syncope, angina, dyspnoea.
In heydes syndrome = AS and angiodysplasia of the colon causing CRC.
Risk factors: Rheumatic fever, bicuspid aortic valve (seen in 40-50s), calcification (seen in 70-80s), Fabrys, SLE.
Pathophysiology: stenosis = increased pressure gradient between LV and aorta, increased pumping pressure of LV to overcome increased afterload = myocyte hypertrophy ( = LVH)
Investigations: clinical findings: a slow or sustained upstroke of the arterial pulse and low volume pulse (pulsus parvus et tardus). Delay between S1 and carotid pulse. Brachio-radial delay.
Murmur: systolic crescendo-decrescendo ejection murmur, loudest at upper right sternal border, radiating to carotids bilaterally. Louder during expiration.
Diagnostic tests: ECG = LVH, heart catheterisation, echo.
Treatment: replacement of diseased valve, in neonates/children can consider using a balloon valvuloplasty. Can give supportive diuretics, ACEi
Prognosis: if replaced >80% survive 5 years (good outcome), if no replacement and SAD symptoms present = >50 die in 2 years.