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“Senile” calcific: AS often caused by age-related degenerative calcific changes of the valve. Majority of patients diagnosed with AS after age 65 have this form.
Congenital: Calcific changes that progress to AS may also develop in patients with congenitally deformed aortic valves (1-2% population born with bicuspid aortic valve). Majority of young patients with AS have calcification of congenital bicuspid valve.
Three types of congenital:
1/ Congenitally malformed valve
2/ Subvalvular AS
3/ Supravalvular AS – associated with William’s Syndrome and is the rarest form of AS – these babies have
low, wide-set eyes
Rheumatic: AS can result from chronic rheumatic valve disease, although the prevalence of this as a cause in the
US has been greatly decreased. 95% of patients with rheumatic AS also have rheumatic disease of the mitral valve.
Path features of AS derived from etiology…
“Senile” calcific: cumulative wear and tear leads to endothelial and fibrous damage, which results in calcification of an otherwise normal trileaflet valve.
Congenitally deformed valve: years of turbulent flow across the deformed valve disrupt endothelium and collagen matrix of leaflets with result of gradual calcium deposition (like that in the “senile” form, but appearing decades earlier).
Rheumatic: endocardial inflammation leads to organization and fibrosis of the valve, resulting in fusion of the commissures and formation of calcified masses in the aortic cusps.
Regardless of etiology, all AS typified by calcification deep within the fibrosa of the valve cusps, extending toward the surface and resulting in heaped up or nodular deposition extending into sinuses of Valsalva (the pockets that lead to the LCA and the RCA) of the aortic root.
Pathophysiology: oNormal aortic valve area = 3-4 cm2 omild AS = 2 cm2 omoderate AS = 1-1.5 cm2 ocritical AS = 0.8 cm2
In AS, blood flow across aortic valve is obstructed during systole.
This makes large pressure gradients between the LV and the aorta.
AS develops over chronic course, so LV undergoes concentric (pressure) hypertrophy to compensate and overcome the large pressure gradient.
With hypertrophy, stress on wall is relieved, but the LV becomes stiff as a result.
LA contraction, though contributing little to LV stroke volume in normal individuals, contributes 25% of the stroke volume for the LV in AS patients. Thus, LA hypertrophy can be beneficial for AS patients.
Because LA contraction contributes 25% volume to the LV in AS patients, it is dangerous and a poor clinical sign if they develop atrial fibrillation.
Angina occurs because of an imbalance btw myocardial oxygen supply and demand.
Demand is greater because of an increased LV mass and because wall stress is greater due to increased pressure.
Supply is reduced in AS because the elevated LV diastolic pressure reduces the coronary perfusion pressure gradient between the aorta and the myocardium (I think this means that less blood is able to go into the sinuses of Valsalva…leading to the RCA and the LCA).
Syncope during exertion happens because the LV can’t increase its CO during exercise due to the fixed stenotic aortic opening. Also, exercise leads to vasodilatation of the peripheral muscle beds. These two factors lead to decreased cerebral perfusion pressure and a propensity to syncope upon exertion.
Congestive heart failure symptoms happen late in the disease when markedly increased LV end diastolic volume and pressure lead to elevation of the LA and pulmonary venous pressures, which produces pulmonary alveolar congestion and symptoms of congestive heart failure (like dyspnea).