Left ventricular mass in hereditary human hypertension: glucocorticoid-suppressible hyperaldosteronism

The mineralocorticoid hormone aldosterone may be an important mediator of pathological ventricular hypertrophy and heart failure. Much of the evidence for this arises from experimental work in rat models of mineralocorticoid-dependent hypertension, and a pathological role in humans is still uncertain.

Eleven subjects with glucocorticoid-suppressible hyperaldosteronism, a hereditary form of hyperaldosteronism and hypertension, and 10 age- and sex-matched control subjects were studied.

The subjects with glucocorticoid-suppressible hyperaldosteronism had a higher mean blood pressure and plasma aldosterone concentration, and lower plasma renin concentration, than the control subjects. Left ventricular mass index was not significantly different in the subjects with glucocorticoid-suppressible hyperaldosteronism than in the control subjects. When the subjects with glucocorticoid-suppressible hyperaldosteronism were subdivided into those with and those without hypertension, no difference in left ventricular mass index could be detected between the subgroups or between either subgroup and the control subjects. However, there was a significant correlation between basal plasma aldosterone and left ventricular mass index in the subjects with glucocorticoid-suppressible hyperaldosteronism (r = 0.66, P < 0.03).

Despite marked elevations in plasma aldosterone concentrations from birth in subjects with glucocorticoid-suppressible hyperaldosteronism, left ventricular hypertrophy did not occur. The degree of hyperaldosteronism in the subjects was mild compared with other conditions and, although an effect on left ventricular mass index could be detected, the present results indicate that other factors may be necessary for the development of left ventricular hypertrophy.