-Etiology
+Secondary to rheumatic inflammation
+Congenital in origin
-Pathophysiology
+The obstruction to LV outflow produces a systolic pressure gradient between the LV and aorta => LV output is maintained by the presence of concentric LV hypertrophy. However, excessive hypertrophy becomes maladaptive, and LV function declines. Although the CO at rest is within normal limits in most patients with severe AS, it usually fails to rise normally during exercise. Late in course, the CO and LV–aortic pressure gradient decline, and the mean LA, PA, and RV pressures rise.
-Symptoms
+Exertional dyspnea, angina pectoris, and syncope are the three cardinal symptoms
-Laboratory Examination
Catheterization:
(1) patients with multivalvular disease,
(2) young, asymptomatic patients with noncalcific congenital AS, to define with precision the severity of obstruction to LV outflow, since operation [which does not usually require aortic valve replacement (AVR)] or PABV may be indicated if severe AS is present, even in the absence of symptoms; balloon valvotomy may follow left heart catheterization immediately.
(3) Patients in whom it is suspected that the obstruction to LV outflow may not be at the aortic valve but rather in the sub- or supravalvular regions.
*Coronary angiography CAD in patients >45 years old with severe AS who are being considered for operative treatment.
-Treatment
+Nonoperative Management: Avoid exercise and physical activity, infective endocarditis prophylaxis is indicated, diuretics, nitrates and other vasodilators
+Surgery: AVR (aortic valve replacement)
Symptomatic patients with Aortic valve area <1.0 cm2
Asymptomatic patients with severe AS should be considered for AVR if LV dilation or decreased systolic function is present or if they have a hypotensive response to exercise.
+Intra-aortic balloon counterpulsation.
+Percutaneous balloon aortic valvuloplasty.