Left ventricular hypertrophy (LVH), despite its adaptive nature, is associated with an increased risk of cardiovascular morbidity and mortality. Achievement of LVH regression is thus considered a principal therapeutic aim. However, regression of LVH induced by various therapeutic means may exhibit differing patterns, with variable biological implications. Inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase (statins) have been shown to induce prevention or regression of LVH in different models of pathological myocardial growth. In addition to reduction of LV mass, statins were shown to reduce myocardial fibrosis, increase capillary density network and attenuate electrical instability of the hypertrophied heart. Most importantly, statins improved systolic and diastolic LV function and even decreased mortality. The inhibition of hypertrophic growth was only partly achieved by reduction of haemodynamic overload. Direct mechanisms, such as inhibition of neurohumoral activation in the myocardial tissue, attenuated production of growth factors and markers of inflammation and reduction of oxidative stress also seem to participate. The protective effect of statins was associated with the inhibition of expression and activation of small guanosintriphosphate-binding proteins such as Ras and Rho, which control the intensity of oxidative stress, the production and availability of nitric oxide, and the expression of genes involved in myocardial growth. In addition to reduction of LV mass, statins may also improve the prognosis of LVH independently of their lipid-lowering effect.