Changes in left ventricular remodeling due to antihypertensive therapy have been demonstrated in experimental animal studies although no quantitative relationship has been shown between correction of blood pressure and regression of myocardial mass. As regards the qualitative aspects of regression, only the ACE inhibitors have been shown to prevent the development and induce regression of the excess collagen content of the myocardium submitted to chronic pressure overload. The problems posed by remodeling in clinical practice are more complex: should regression of myocardial mass itself be the therapeutic objective in the absence of a practical method of analysing the interstitial factor of hypertensive disease or should we concentrate on the satellite problems of hypertrophy which are correction of ischemia, left ventricular filing abnormalities and arrhythmias. For each of these clinical problems, the benefits attributed to changes in remodeling, though probable, are to a large degree hypothetical. The benefits offered by these drugs which reduce ventricular hypertrophy are, however, considerable.