As the aortic valve area reduces, a systolic pressure gradient develops between the left ventricle (LV) and the aorta. The progressive outflow obstruction requires the LV to contract more forcefully (increased myocardial contractility) to maintain stroke volume, eventually resulting in LV hypertrophy.

As long as the mitral valve is functioning normally, the pulmonary circulation is protected and the patient may be asymptomatic for years.

In severe disease, the ventricle can no longer respond and LV function becomes abnormal. At this stage (i.e. critical aortic stenosis), the balance between cardiac output and myocardial muscle oxygen demand can be easily disrupted causing acute decompensation and severe pump failure.