It is well known that, in patients with essential hypertension, left ventricular hypertrophy (LVH) is an independent risk factor for cardiovascular disease. However, it has been demonstrated that normalisation of arterial pressure, by therapy with antihypertensive drugs, is associated with regression of LVH, although the extent and time-course of this phenomenon depend on the antihypertensive drug used. In particular, angiotensin converting enzyme (ACE) inhibitors seem capable of inducing a faster and more complete reversal of LVH in patients with essential hypertension than other antihypertensive drugs. The mechanisms underlying this property of ACE inhibitors remain unclear, although 2 features of ACE inhibitors may be particularly relevant. The first is their ability to improve large artery compliance, this being a major determinant of LVH. Arterial compliance is reduced in essential hypertension, resulting in increased left ventricular end-systolic stress, which then contributes to the development of LVH. The second possible mechanism by which ACE inhibitors reverse LVH to a greater degree than other antihypertensive drugs may relate to their ability to interfere with the cardiopulmonary receptor control of the circulation. Thus, ACE inhibitors may counteract the neural and hormonal abnormalities that contribute to the maintenance of LVH in hypertensive patients.