Aortic stenosis was once considered a pure isolated valve obstacle challenging left ventricle driving force of contraction and flow generation. Left ventricular (LV) adaptation was merely interpreted as a uniform hypertrophic response to increased afterload. However, in these last 2 decades cardiac imaging research and some histopathology correlation studies brought insight towards the complex interaction between the vasculature, the valve and the myocardium. Verily, LV remodeling in this setting is a complex multidetermined process that goes further beyond myocardial hypertrophy. Ultrastructural changes involving both diffuse and replacement fibrosis of the myocardium take part and might explain the transition of clinical phenotypes with distinct prognosis, from compensated hypertrophy to LV maladaptive dysfunction and heart failure. Presently, the combined appropriate use of echocardiography and cardiac magnetic resonance may better assess the global LV afterload, hypertrophy and geometric remodeling, global and regional LV function, beyond ejection fraction, and structural changes that include the fibrotic burden of the myocardium. As a whole these may not only better stratify individual risk of disease progression but also identify patients benefiting from earlier valve intervention. In this paper, we review the maladaptive response of the LV to chronic pressure overload, describing the different signaling pathways and mechanisms that underly both hypertrophy and remodeling. Histomorphology changes in this setting are described and we try to make sense of the use of new imaging tools for LV characterization.