Perspective:

The tremendous success in targeted pharmacologic therapy for hypertension may have blunted our overall enthusiasm in pursuing the mechanisms of the overall causes of hypertension. After all, we have therapies for this common ailment that are proven to decrease overall CV risk, so is it really necessary to know exactly why hypertension happens?

This article by Hundemer et al. is an important reminder that mechanism is important. Subclinical and mild aldosteronism indeed is associated with elevated BP. But even when it is not associated with hypertension, there are CV consequences. Perhaps these consequences are already in play years before patients develop hypertension and that the high BP then only worsens the situation.

In 2006, the TROPHY (Trial of Prevention of Hypertension) group led by Dr. Stevo Julius suggested that treatment of pre-hypertensive patients with an angiotensin receptor blocking agent decreased the percentage of subjects with hypertension years after the pre-treatment was stopped. This was likely attributable to the slowing of vascular remodeling that was already occurring even in the normotensive patients. Similarly, small elevations in plasma aldosterone, as in this study, may be doing their CV harm long before a patient becomes frankly hypertensive.

This study is important in that it should alert us to keep vigilant for mild, subclinical aldosteronism as a potential treatment target. There are therapies in development such as baxdrostat that inhibit aldosterone production and may potentially improve the outcomes in these patients. Naturally, more clinical trials are needed to make that link. Moreover, it should remind us that once a patient develops high BP numbers, a lot of damage may have already occurred. The future treatment of hypertension may go beyond just getting presently high numbers down and include looking at other markers of CV risk in an effort to slow CV damage before frank hypertension develops.