Abstract 13069: Serum Aldosterone is Independently Associated With Subclinical Myocardial Dysfunction: Results From the HyperGEN Study
Background: While prior studies have implicated aldosterone excess in the development of systemic hypertension, experimental studies suggest aldosterone can also directly induce myocardial fibrosis, independent of its effects on blood pressure. We hypothesized that increased aldosterone levels are independently associated with worse cardiac mechanics.
Methods: We investigated the association between serum aldosterone and cardiac mechanics in 1953 participants from the Hypertension Genetic Epidemiology Network (HyperGEN) Study, a population- and family-based study, which included hypertensive and non-hypertensive individuals. Using comprehensive speckle-tracking echocardiography, we measured global longitudinal, circumferential, and radial strain (GLS, GCS, and GRS, respectively); early diastolic (e’) tissue velocities; and early diastolic strain rate. Multivariable-adjusted linear mixed effects models were used to evaluate the independent associations between serum aldosterone and cardiac mechanics.
Results: The mean age was 47±14 years, 45% were black, 47% were hypertensive. Median serum aldosterone was 6.8 ng/dl; 25th-75th percentile 3.9-10.9 ng/dl. Aldosterone was associated with GLS (β = -0.38 [per 1-SD increase in aldosterone], P < 0.001; see Figure), GRS (β = -0.90, P = 0.013), e’ velocity (β = -0.12, P = 0.003), and early diastolic strain rate (β = -0.02, P = 0.002) independent of age, sex, race, and cardiorenal risk factors (blood pressure, diabetes, proteinuria, GFR, urinary sodium to potassium ratio, and albumin). The association between serum aldosterone and cardiac mechanics persisted in subgroup analyses of (1) normotensives, (2) normal LV geometry, (3) normal renal function, and (4) non-diabetics (P<0.05 for all associations).
Conclusions: Increased aldosterone is independently associated with subclinical systolic and diastolic dysfunction independent of its effect on blood pressure.
- © 2013 by American Heart Association, Inc.