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7 Cards in this Set

  • Front
  • Back

etiologies of aortic stenosis (AS)

calcific: predominant cause in >70y, risk factors incl HTN, high cholesterol, ESRD



congenital: i.e. bicuspid valve w/ premature calcification (cause in 50% of AS <70y)



rheumatic heart disease (AS usually + AI and MV dz)

"mimickers" of AS

subvalvular (e.g. hypertrophic CM, subaortic membrane) or supravalvular stenosis

clinical manifestations of AS

angina (incr O2 requirement 2/2 hypertrophy + decr O2 supply 2/2 decr coronary perfusion, +/- CAD)



syncope, exertional (cannot increase CO when needed)



heart failure (outflow obstr + diastolic dysfxn = pulm edema, worsened with tachycardia and AF)

hematologic complication of severe AS?

acquired vWF disease (~20% of severe AS): destruction of vWF + GI angiodysplasia/bleeding (Heyde's syndrome)

murmur of AS

midsystolic, crescendo-decrescendo murmur at RUSB



harsh, high pitch; radiates to carotids, apex (holo-systolic = Gallavardin effect)

how does the murmur of AS change with passive leg raise, standing, and Valsalva?

increased with passive leg raise, decreased with standing and Valsalva



this is in contrast to the dynamic outflow obstruction of HCM, which decreases with leg raise and increases with standing, Valsalva

physical exam signs of severe AS

late-peaking murmur, paradoxically split S2 or inaudible A2, small and delayed carotid pulse (parvus et tardus), LV heave, +S4 (occ palpable)