Key result
Subclinical primary aldosteronism linked to elevated MACE, incident hypertension, and structural cardiac changes.
Why the study?
Whether subclinical primary aldosteronism is associated with major adverse cardiovascular events prior to overt hypertension remains incompletely characterized.
Subclinical primary aldosteronism represents an early cardiometabolic state associated with elevated risk of MACE, suggesting a continuum of renin-independent aldosterone excess that warrants further investigation for early detection and intervention.
Elevated MACE risk in subclinical primary aldosteronism warrants vigilance; leaves open whether early intervention improves outcomes.
Background: Primary aldosteronism (PA), a renin-independent state of aldosterone excess, is associated with excess risk of stroke, myocardial infarction, atrial fibrillation, heart failure, and chronic kidney disease compared with essential hypertension. Emerging evidence suggests that renin-independent aldosterone excess exists on a continuum rather than as a dichotomous disease state, including subclinical primary aldosteronism (sPA), even in normotensive individuals. Whether sPA is associated with major adverse cardiovascular events (MACE) prior to overt hypertension remains incompletely characterized. Objective: To synthesize available evidence linking renin suppression and mild aldosterone excess to cardiovascular outcomes. Methods: A narrative review of the literature was conducted using PubMed/MEDLINE, the Cochrane Library, and Web of Science from inception through May 2025, to identify cohort studies evaluating renin phenotype, aldosterone levels, and cardiovascular outcomes. Results: Suppressed renin and higher aldosterone levels, even within conventionally normal ranges, are associated with incident hypertension, left ventricular hypertrophy (LVH), atrial fibrillation, and cardiovascular events. In overt PA, significantly higher rates of cardiovascular diseases have been observed compared with blood pressure-matched essential hypertension. Emerging population-based data suggest a graded cardiovascular risk extending below traditional diagnostic thresholds. Conclusion: Biochemical phenotypes consistent with sPA may represent an early cardiometabolic state associated with elevated risk of MACE, even before overt PA criteria are met. The absence of standardized diagnostic thresholds and randomized interventional data currently limits clinical translation. Prospective trials evaluating renin-guided screening and early mineralocorticoid receptor antagonism are needed to determine whether intervention at the subclinical stage reduces long-term cardiovascular harm.
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Akoum et al. (2026) conducted a review in Subclinical primary aldosteronism. Subclinical primary aldosteronism (renin-independent aldosterone excess) vs. Normal aldosterone and renin levels was evaluated on Cardiovascular outcomes including incident hypertension, left ventricular hypertrophy, atrial fibrillation, and major adverse cardiovascular events (MACE). Subclinical primary aldosteronism is associated with an elevated risk of major adverse cardiovascular events, incident hypertension, and structural cardiac changes even before overt primary aldosteronism criteria are met.
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