Central systolic augmentation indexes and urinary sodium in a white population

The association between cardiovascular health and salt intake remains controversial. The objective of our study was to assess the association between arterial stiffness and urinary sodium, both cross-sectionally and prospectively.

In 630 participants (mean age 40.6 years; 51% women), randomly recruited from a Flemish population, we measured sodium and creatinine in 24-hour urine samples at baseline and follow-up (median, 9.7 years) and the carotid and aortic augmentation indexes (AIs) standardized to heart rate at follow-up only.

From baseline to follow-up, the urinary sodium concentration decreased (117.1 vs. 105.2 mmol/L; P < 0.0001), whereas 24-hour urinary sodium did not change significantly (166.5 vs. 171.5 mmol/L; P = 0.12). In multivariable-adjusted longitudinal analyses, a 40 mmol/L (~1 SD) increase in the urinary sodium concentration was independently and inversely associated with the carotid AI (effect size, -1.38 ± 0.66%; P = 0.04) and aortic AI (-1.54 ± 0.72%; P = 0.02). In cross-sectional analyses of follow-up data, these estimates were -1.26 ± 0.70% (P = 0.07) and -1.52 ± 0.76% (P = 0.04), respectively. In the longitudinal and cross-sectional analyses, the carotid and aortic AIs were unrelated to the 24-hour urinary excretion of sodium.

Our study showed an inverse association between the central arterial AIs and the urinary sodium concentration. Further research is required to consolidate our findings, to unravel the underlying mechanism, and to establish the role of renal vasodilatation in the maintenance of sodium balance.