Left ventricular anatomy and function in primary aldosteronism and renovascular hypertension

Abstract

Left ventricular hypertrophy (LVH) is a common finding in hypertension and represents a detrimental outcome since it is associated with increased morbidity and mortality. For similar elevation of blood pressure the severity and type of LVH vary considerably in relation to several factors. Compelling evidence suggests that both the renin-angiotensin system (RAS) and the aldosterone excess play an important role in the pathogenesis of LVH, since experimentally angiotensin II has been found to cause myocardial cells hypertrophy and/or hyperplasia and excess aldosterone has been related to extracellular matrix and collagen deposition and therefore to myocardial fibrosis. Secondary forms of hypertension offer models for investigating the relative role of the RAS and aldosterone on the heart in humans. Being rare in the population of hypertensive patients, they furnish an example of the so called Bateson's approach to the understanding of diseases "Treasure your exceptions." In this paper, we review the data concerning the LV changes in primary aldosteronism and renovascular hypertension and discuss the insight that they have provided into the pathogenesis of LVH.