Urinary Sodium and Cardiac Mechanics
What is the relationship between estimated sodium intake (ESI) and indices of cardiac mechanics?
The investigators performed speckle-tracking analysis on HyperGEN (Hypertension Genetic Epidemiology Network) study echocardiograms with available urinary sodium data (N = 2,996). They evaluated the association between ESI and longitudinal strain (LS), circumferential strain (CS), and e’ velocity using multivariable-adjusted linear mixed-effects models (to account for relatedness among subjects) with linear splines (spline 1: ESI ≤3.7 g/day, spline 2: ESI >3.7 g/day based on visual inspection of fractional polynomial plots of the association between ESI and indices of strain and e’ velocity). The authors performed mediation analysis to understand the indirect effects of systolic blood pressure (SBP) and serum aldosterone on the relationship between ESI and strain and e’ velocity.
The mean age was 49 ± 14 years, 57% were female, 50% were African American, and 54% had hypertension. The median (25th-75th percentile) ESI was 3.73 (3.24-4.25) g/day. ESI >3.7 g/day was associated with larger left atrial and left ventricular (LV) dimensions (p < 0.05). After adjusting for speckle-tracking analyst, image quality, study site, age, sex, smoking status, alcohol use, daily blocks walked, diuretic use, estimated glomerular filtration rate, LV mass, ejection fraction, and wall motion score index, ESI >3.7 g/day was associated with all strain parameters and e’ velocity in (p < 0.05 for all comparisons), but ESI ≤3.7 g/day was not (p > 0.05 for all comparisons). There were significant interactions by potassium excretion for CS. Mediation analysis suggested that SBP explained 14% and 20% of the indirect effects between ESI and LS and e’ velocity, respectively, while serum aldosterone explained 19% of the indirect effects between ESI and LS.
The authors concluded that ESI >3.7 g/day is associated with adverse cardiac remodeling and worse systolic strain and diastolic e’ velocity.
This study reports that ESI above 3.7 g/day was associated with reduced strain. Furthermore, increased ESI was also associated with adverse left atrial and LV remodeling. Mediation analysis showed that SBP and serum aldosterone explained a significant proportion of the indirect effects between ESI and several indices of strain and e’ velocity; however, adjustment for blood pressure or serum aldosterone did not eliminate these associations. Overall, these data provide support for the adverse cardiovascular effects of high sodium intake. Additional studies are indicated to assess the mechanism by which dietary sodium impairs myocardial function and to investigate therapeutic interventions that may improve clinical outcomes.
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