The classic concept of a direct pathogenic relationship between high blood pressure and development of left ventricular hypertrophy has been challenged by observations such as the modest correlations between blood pressure and magnitude of left ventricular hypertrophy, its frequent reversal with some antihypertensive medications and its experimental prevention with low doses of an angiotensin-converting enzyme inhibitor that do not modify blood pressure. This evidence has prompted the revision of mechanisms or factors involved in the development of left ventricular hypertrophy. The roles of sympathetic nervous and renin-angiotensin systems, genetic and endothelial factors, are reviewed in this article. It is concluded that blood pressure is not the sole responsible for left ventricular hypertrophy, but an epiphenomenon of one or more local or tissular mechanisms, primary or unchained by an unknown genetic factor.