[29] The development of left ventricular hypertrophy (LVH) and fibrosis results in poor outcome in patients with AS, and the persistence of hypertrophy and diastolic dysfunction after surgical valve replacement increases mortality.[30, 31] The renin-angiotensin system is activated at an early stage in AS, promoting development of LVH, diastolic dysfunction, myocardial fibrosis and myocardial contractile failure. This evidence concerns the gene REN and aortic stenosis.