Reversal of left ventricular (LV) hypertrophy has definitely been proved to follow effective blood pressure control in hypertensive patients. This reduction in cardiac mass does not depend solely on blood pressure levels as measured in routine follow-up; it varies markedly with the type of drug used and even among patients treated with the same antihypertensive agent. The factors influencing the degree of regression of hypertrophy include stability of blood pressure control (entailing diurnal variations and response to stress), neurohumoral disturbances or fluid retention induced by the antihypertensive drug, and the presence of associated cardiac disease, as well as individual variations such as genetic background and possibly age. LV performance at rest was not depressed by the reduction in cardiac mass but remained normal in relation to changes in LV end-systolic stress.