Calcific aortic stenosis represents the most frequent valvular heart disease and one of the major cause of morbidity and mortality in the elderly. Aortic stenosis results from active biological events, characterized by lipid infiltration, inflammation, neoangiogenesis, endothelial dysfunction and bone deposition. The reduced mobility of aortic valve leaflets produces a fixed obstruction at the outflow, with a consequent remodelling of the left ventricle. The degree of left ventricle hypertrophy and fibrosis results in different degree of diastolic dysfunction and heart failure. Thus, the response of the left ventricle to the pressure overload guides the clinical status and the prognosis of patients with aortic stenosis. After aortic valve replacement hypertrophy and fibrosis partially regress, however the maladaptive LV remodelling strongly impacts the prognosis even after surgery. This review outlines the importance in the evaluation of the left ventricle in patients with severe aortic stenosis, exploring the pathophysiology of the transition from adaptive to maladaptive remodelling.