Left ventricular hypertrophy (LVH) is a fundamental component of cardiac adaptation to disorders which alter left ventricular pressure, volume or contractility on a chronic basis. In pressure and volume overload, the LVH response is, initially, quantitatively matched to the increase in hemodynamic load, so that each unit of myocardium performs under normal mechanical loading conditions [1]. As a result, cardiac compensation can be maintained without reliance on either preload reserve or increased contractility. This phase of compensated hypertrophy in turn permits the long asymptomatic phases observed in subjects with aortic stenosis, hypertensive heart disease, aortic regurgitation and mitral regurgitation. When decompensation occurs, it can be due in part to failure of compensatory hypertrophy to keep up with the hemodynamic burden, as well as to depression of contractile state [2]. Furthermore, successful therapeutic interventions, such as aortic valve replacement for aortic stenosis or aortic regurgitation, are often characterized by reversal of LVH and failure of such reversal may be a poor prognostic sign [3].