The challenge of co-existent moderate aortic stenosis and left ventricular systolic impairment

Aortic stenosis (AS) is the commonest cause of valvular heart disease in the western world with an estimated prevalence of up to 7% in patients aged 65 years or over (1). Characterised predominantly by progressive valve fibrosis and calcification, leading to restriction of the aortic valve cusps, the severity of AS has traditionally been defined by haemodynamic parameters assessed either invasively, or more commonly using echocardiography. In the setting of clinically significant AS, reactive hypertrophy of the left ventricle (LV) occurs in response to the associated LV pressure overload, maintaining wall stress and cardiac performance for many years if not decades. Ultimately, however, this process decompensates and patients transit from hypertrophy to symptomatic heart failure with poor clinical outcomes unless the valve is replaced.