Most common valvular heart disease; prevalence only 0.2% among adults aged 50-59 y, but increases to almost 10% after age 80 y.

Calcific aortic stenosis: Major risk factors are increasing age, LDL, diabetes mellitus, smoking, hypertension, and bicuspid valve anatomy. Less common risk factors include disorders of calcium metabolism, renal failure, and history of mediastinal radiation.

Bicuspid aortic valve is present in 1-2% of USA population and accounts for 60% of AVRs in pts under age 70 y and 40% over 70 y.

Rheumatic aortic stenosis: Late sequela of streptococcal infection, more common in developing countries and often involves other valves.

Hypovolemia and/or vasodilation from anesthetic drugs lead to hypotension due to lack of preload reserve necessary to overcome systolic pressure gradient in pts with severe AS

Risk of myocardial ischemia is elevated due to increase in LVED pressure (reducing coronary perfusion gradient) and LVH (associated with structural coronary abnormalities)

Bicuspid valve associated with ascending aortic aneurysm and dissection, with a lifetime risk of about 6%

Hypovolemia and/or vasodilation from anesthetic drugs lead to hypotension due to lack of preload reserve necessary to overcome systolic pressure gradient in pts with severe AS

Risk of myocardial ischemia is elevated due to increase in LVED pressure (reducing coronary perfusion gradient) and LVH (associated with structural coronary abnormalities)

Bicuspid valve associated with ascending aortic aneurysm and dissection, with a lifetime risk of about 6%

Drop in SVR and preload leads to reduced stroke volume through stenotic valve.

Reduced SVR and stroke volume leads to hypotension, which reduces coronary perfusion and may lead to myocardial ischemia.

Tachycardia poorly tolerated.

Diastolic dysfunction very common.

Atrial fibrillation; atrial kick provides up to 40% of LVED volume in AS pts, and its loss can lead to profound hypotension.

Normal valve area (AVA) 2.6-3.5 cm ² ; AS classified as mild (AVA >1.5 cm ² ), moderate (AVA 1-1.5 cm ² ), and severe (AVA <1 cm ² ).

Stenosis at the aortic valve leads to development of pressure gradient from LV to aorta.

Increase in LV systolic pressure increases wall tension, producing LV hypertrophy.

LV hypertrophy and augmented preload are primary means of maintaining adequate stroke volume and cardiac output in severe AS.

Hypertrophy decreases LV compliance and diastolic dysfunction may ensue, making atrial contraction critical for maintaining adequate LV filling and stroke volume.

Preload reserve generally exhausted in severe AS, so hypovolemia and reduced SVR are poorly tolerated.

Elevated LVED pressure and alterations in coronary microcirculation associated with LV hypertrophy reduce coronary perfusion.

Angina, dyspnea, and syncope are common presenting symptoms.

Diagnosis of AS is made using ECHO or in the cath lab by assessing pressure gradient and valve area.

Mean and peak pressure gradients across the valve also are used to classify severity.

Pressure gradients may be low despite severe AS in pts with reduced EF (low-flow/low-gradient AS) or small ventricular volumes (low-flow/low-gradient AS with preserved EF).