Am J Hypertens
BACKGROUND: Although higher sodium intake is known to increase blood pressure, its association with cardiovascular mortality is less established. We examined the association of baseline sodium intake in a hypertensive cohort with all-cause and cardiovascular mortality over a mean follow-up of 18.6 years. METHODS: Three thousand five hundred five subjects were participants in a worksite hypertension program. Sodium intake was estimated by 24-hour urine excretion. Mortality data were obtained from the U.S. National Death Index. Unadjusted and multivariable-adjusted associations between sodium quartiles (quartile I (QI) to quartile IV (QIV)) and mortality were assessed using Cox models. RESULTS: Estimated mean +/- SD sodium intake was 130+/-69 mmol overall (55+/-20 mmol in QI; 220+/-56 mmol in QIV). Baseline systolic blood pressure did not vary significantly between groups. Last available mean systolic blood pressure was highest in QI and lowest in QIV (137+/-16 vs. 134+/-14 mm Hg; P = 0.009). Overall there were 1,013 deaths (399 cardiovascular). Unadjusted models exhibited significant inverse relationships between sodium and mortality outcomes. In adjusted models, sodium intake was not significantly associated with cardiovascular mortality (QI vs. QIV: hazard ratio (HR) = 1.00; 95% confidence interval (CI) = 0.71-1.42; P = 0.99). A borderline significant direct association with all-cause mortality was observed (QI vs. QIV: HR = 0.81; 95% CI = 0.66-1.00; P = 0.05) driven partly by noncardiovascular deaths. CONCLUSIONS: Our study found no significant association between sodium intake and cardiovascular outcomes, although a significant association with all-cause mortality was observed. Although these findings suggest that sodium may not have a strong relationship with cardiovascular mortality, the inconsistent results cast doubt on whether a single measurement can reliably predict mortality over a prolonged follow-up period.
Faculty; Northwell Researcher
School of Medicine; Northwell Health