Abstract

The increasing evidence that identifies left ventricular hypertrophy (LVH) as a powerful prognostic factor leads to the question whether or not reduction of LVH is a desirable goal of antihypertensive therapy and, moreover, whether a decrease in arterial pressure per se is the only or the main determinant for reduction of LVH. An analysis of the underlying pathogenic mechanisms suggests the presence of multiple interacting pathogenic factors in the development of LVH. Conversely, disparate rates of reduction of LVH with various antihypertensive drugs as well as conflicting results in different hypertensive patients point to the existence of blood pressure-independent factors influencing reduction of LVH.

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