The usual concept of ventricular hypertrophy is simple and logical: increased systolic wall stress induces a hypertrophic reaction which is 1) symmetrical affecting all ventricular walls harmoniously, 2) concentric, developing at the expense of cavity size, increasing the thickness to radius ratio, and, 3) appropriate allowing normalisation of wall stress. This hypertrophy appears initially to be useful as it contributes to the maintenance of systolic function in the face of increasing load. However, it is accompanied by abnormalities of ventricular filling, of coronary circulation and myocardial excitability which may have undesirable consequences on the prognosis. In fact this simplistic and didactic view is inadequate for describing the complexity of left ventricular remodeling in hypertension. This is apparent at three levels at least: the stimuli responsible; if increased wall stress is a necessary and sometimes in itself enough to induce hypertrophy, other mechanisms may effect the degree and nature of this reaction; the protein, cellular and tissular expression; this is particularly true with respect to the connective (collagen) tissue which seems to develop in response to distinct stimuli and which could have an important influence on the functional properties of the myocardium; the morphological expression; this is the only parameter which can be analysed directly by the clinician by echocardiography. This investigation enables assessment of the frequency of eccentric and asymmetric forms of hypertrophy, the significance of which remains unclear.