Aortic stenosis is the obstruction of blood flow across the aortic valve. It can be caused by congenital abnormalities such as unicuspid or bicuspid valve, rheumatic fever and age-related calcific changes. When the valve becomes stenotic, resistance to systolic ejection develops. A pressure gradient develops between the left ventricle and the aorta. Left ventricular pressure increases and left ventricular hypertrophy occurs in response. In most patients, LV systolic function is preserved and cardiac output is maintained despite increased systolic pressure. Although cardiac output is normal during rest, it fails to increase during exercise and exercise-related symptoms may be seen.
Diastolic dysfunction occurs as a result of LV relaxation impairment, decreased LV compliance, increased afterload or LV hypertrophy. LV hypertrophy can reverse following relief of valvular obstruction. Atrial filling plays an important role in diastolic filling of the left ventricle. Development of atrial fibrillation in aortic stenosis can lead to heart failure due to the inability to maintain cardiac output.
Symptoms of aortic stenosis are dyspnea on exertion, syncope and anginal chest pain. A slow upstroke of the arterial pulse and low pulse volume, known as pulsus parvus etc tardus, is also noted. Systolic crescendo-decrescendo murmur is heard at the 2nd intercostal space.
Indications for surgery
Indications for intervention are expanded from previous to include patients with very severe AS (above) and low surgical risk (Class IIa); asymptomatic severe AS and decreased exercise tolerance or exercise-related decrease in blood pressure (Class IIa); and symptomatic patients with LFLG severe AS and normal LVEF if clinical, hemodynamic, and anatomic data support valve obstruction as the likely cause of symptoms (Class IIa).