Introduction and Context
Primary aldosteronism (PA) was once considered a rare cause of hypertension, thought to affect fewer than 1% of patients with high blood pressure. However, over the last decade, a paradigm shift has occurred. We now recognize that PA is the most common specifically treatable and potentially curable cause of hypertension, appearing in up to 20% of patients with resistant hypertension. More importantly, recent evidence, including the landmark findings from the Atherosclerosis Risk in Communities (ARIC) study, suggests that aldosteronism exists not as a binary ‘present or absent’ disease, but as a continuous spectrum of renin-independent aldosterone production.
This evolving consensus matters because excess aldosterone is toxic to the cardiovascular system, independent of its effect on blood pressure. It promotes fibrosis, inflammation, and oxidative stress in the heart and blood vessels. The latest research indicates that many individuals who do not meet the classic diagnostic criteria for PA still suffer from ‘subclinical’ aldosteronism, which places them at a heightened risk for devastating events like stroke and atrial fibrillation (AF).
