Serum Sodium and Pulse Pressure in SPRINT

Area of Science:

• Cardiovascular Science
• Nephrology
• Endocrinology

Background:

• High dietary sodium intake can elevate serum sodium levels, contributing to increased systolic blood pressure.
• Cellular mechanisms suggest endothelial cell stiffness mediates the link between serum sodium and blood pressure.
• The Systolic Blood Pressure Intervention Trial (SPRINT) provided a cohort to investigate this association.

Purpose of the Study:

• To test the hypothesis that higher serum sodium levels correlate with greater arterial stiffness.
• To examine the association between serum sodium and arterial stiffness measures in SPRINT participants.

Main Methods:

• Multivariable linear regression analysis was employed.
• Baseline serum sodium levels were assessed against pulse pressure (PP), a surrogate for arterial stiffness (n=8,813).
• Carotid-femoral pulse wave velocity (CFPWV), another arterial stiffness measure, was analyzed in an ancillary study (n=591).

Main Results:

• Higher serum sodium levels (tertile 3 [≥141 mmol] vs. tertile 2 [139-140 mmol]) were associated with increased baseline pulse pressure (β = 0.87).
• This association persisted across subgroups, including those with and without chronic kidney disease.
• No significant association was found between higher serum sodium and increased carotid-femoral pulse wave velocity (β = 0.35).

Conclusions:

• In high-risk adults without diabetes, elevated serum sodium is independently linked to arterial stiffness, specifically indicated by pulse pressure.
• The findings suggest serum sodium may serve as a risk marker for increased pulse pressure.
• Arterial stiffness, as measured by CFPWV, did not show a significant association with serum sodium levels in this cohort.