Aldosteronism May Be Driving Far More Cardiovascular Risk Than We Recognize

Aldosterone, a hormone produced by the adrenal glands, regulates sodium and fluid balance — but when produced in excess, it does far more damage than simply raising blood pressure. It promotes cardiac fibrosis, vascular stiffness, inflammation, and metabolic dysfunction, making aldosteronism a potent and underappreciated cardiovascular threat. Despite decades of research, critical questions about its true prevalence and clinical significance remain unresolved.

In this viewpoint piece published in JAMA Cardiology, Messerli, Berzins, and Reichlin from leading Swiss cardiac centers lay out the field's most pressing unanswered questions surrounding aldosteronism and cardiovascular risk. The authors draw attention to gaps in how we define, detect, and treat this hormonal disorder, arguing that the medical community may be systematically underestimating both its frequency and its consequences.

Key questions raised include whether conventional diagnostic cutoffs for primary aldosteronism are set too high, thereby missing a large population with milder but still harmful aldosterone excess. The authors also question whether blood pressure reduction alone accounts for the cardiovascular benefits seen with mineralocorticoid receptor antagonists, or whether blocking aldosterone's direct organ effects provides additional protection. The broader cardiometabolic impact — including links to atrial fibrillation, insulin resistance, and heart failure — is also flagged as insufficiently studied.

The clinical implications are substantial. If aldosteronism is far more prevalent than currently estimated, millions of patients with hypertension or unexplained cardiovascular events may be harboring an undiagnosed and treatable hormonal driver of their disease. Broader screening and lower diagnostic thresholds could open the door to targeted therapies that go well beyond standard antihypertensive treatment.

This is a viewpoint article based on expert opinion and literature synthesis rather than original data, which limits the strength of its conclusions. Nonetheless, it serves as a compelling call for well-powered clinical trials and refined diagnostic criteria to fill these critical knowledge gaps.