Abstract 18941: Association of Urinary Sodium and Adverse Cardiac Mechanics: Findings From the HyperGEN Study
Background: Recent studies have demonstrated a J-shaped relationship between sodium intake, estimated by urinary sodium (UNa), and adverse cardiovascular events. Indices of cardiac mechanics are measures of myocardial function that can provide insight into subclinical cardiac disease, and may provide further insight into the association of UNa and adverse events.
Hypothesis: We hypothesized that UNa would be linearly associated with adverse cardiac mechanics.
Methods: We performed speckle-tracking analysis on echocardiograms from the HyperGEN study with available spot urinary sodium data (N=2111). Global longitudinal strain (GLS) was measured. We evaluated the association between the derived 24-hour UNa excretion and cardiac mechanics using linear mixed effects models (to account for relatedness among subjects) with linear splines (spline 1=UNa<4g/day, spline 2=UNa≥4g/day based upon visual inspection).
Results: Mean age was 51±14 years, 59% were female, 46% were African American, and 58% had hypertension. The mean UNa was 3.57±2.36 g/day. On univariate analysis, increasing UNa was linearly associated with worsening GLS after an apparent threshold of ~4g/day (see LOWESS plot in Figure). After adjusting for age, sex, speckle-tracking analyst, site, image quality, left ventricular mass, wall motion score index, ejection fraction, SBP, BMI, GFR, diuretic use, history of diabetes, and smoking status, UNa was associated with GLS (β=-0.07 [95% CI -0.13, -0.01, P=0.02). Using splines, the association remained for spline 2 (β=-0.10 [95% CI -0.18, -0.03, P=0.01] per 1-gram increase UNa for GLS), but not spline 1 (p=0.26). There were no significant interactions between UNa and sex, race, or history of hypertension.
Conclusions: Higher UNa is linearly associated with a worse cardiac mechanics, most notably after a threshold of 4g/day. These data may provide insight into the mechanistic link between high UNa and adverse cardiovascular events.
Author Disclosures: S. Selvaraj: None. F. Aguilar: None. E. Martinez: None. S. Shah: None.
- © 2016 by American Heart Association, Inc.