The classic concept of a direct pathogenic relationship between high b
lood pressure and development of left ventricular hypertrophy has been
challenged by observations such as the modest correlations between bl
ood pressure and magnitude of left ventricular hypertrophy, its freque
nter reversal with some antihypertensive medications and its experimen
tal prevention with low doses of an angiotensin-converting enzyme inhi
bitor that do not modify blood pressure. This evidence has prompted th
e revision of mechanisms or factors involved in the development of /ef
t 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 resp
onsible for left ventricular hypertrophy, but an epiphenomenon of one
or more local or tissular mechanisms, primary or unchained by an unkno
wn genetic factor.