Primary aldosteronism screen positivity was associated with significantly higher 24-h and nighttime systolic blood pressure compared to normal RAAS among patients on single-agent therapy.
Cohort
Do primary aldosteronism and subclinical PA phenotypes increase 24-h and nighttime ambulatory blood pressure compared to normal RAAS in hypertensive patients?
Primary aldosteronism screening positivity is associated with higher ambulatory blood pressure in hypertensive patients on single-agent therapy, highlighting the utility of early RAAS biomarker phenotyping.
Objective: Primary aldosteronism (PA) and milder autonomous aldosterone excess may contribute to adverse ambulatory blood pressure (BP) phenotypes. Whether these BP differences persist after accounting for antihypertensive treatment intensity in real-world screening cohorts remains unclear. Design and method: In a hypertensive cohort with clinic BP, ambulatory BP monitoring (ABPM), and mass-spectrometry hormone measurements, participants were classified into three phenotypes: PA screen-positive (aldosterone >10, plasma renin activity PRA 20), subclinical PA (aldosterone 5–10, PRA = 3 drugs), adjusting for age, sex, BMI, creatinine, and potassium. Associations of log-transformed hormones (lnPAC, lnPRA, lnARR) with ABPM BP were also examined within drug strata. Results: PA and subclinical PA showed the expected higher PAC and ARR, lower PRA compared with normal RAAS. Differences in ABPM were modest overall but became evident after stratifying by treatment intensity. In the 1-drug stratum, PA screen-positive participants had higher BP than normal RAAS, including higher 24-h SBP and nighttime SBP (both statistically significant), with smaller but significant increases in 24-h DBP and nighttime DBP. In contrast, phenotype differences were not consistently observed in drug-naïve, 2-drug, or >=3 drug strata. In hormone-BP models, within the 1-drug stratum, lnPRA was inversely and lnARR positively associated with 24-h and nighttime BP, whereas lnPAC showed weaker and less consistent associations. Dipping-related phenotypes (non-dipping, reverse dipping, isolated nocturnal hypertension) did not materially differ across phenotypes. Conclusions: After accounting for antihypertensive treatment intensity, RAAS phenotypes—particularly PA screen positivity—are associated with higher 24-h and nighttime BP most clearly among patients receiving single-agent therapy. Renin suppression and elevated ARR appear more informative correlates of ambulatory BP than aldosterone alone in this setting. These findings support incorporating RAAS biomarker phenotyping into early hypertension evaluation and treatment stratification.
Zhou et al. (Fri,) conducted a cohort in Hypertension. Primary aldosteronism (PA) screen-positive phenotype vs. Normal RAAS phenotype was evaluated on 24-h and nighttime systolic/diastolic BP. Primary aldosteronism screen positivity was associated with significantly higher 24-h and nighttime systolic blood pressure compared to normal RAAS among patients on single-agent therapy.