Lower 24-hour urinary sodium excretion was associated with higher cardiovascular mortality (HR 1.56; 95% CI 1.02-2.36; P=0.04) and did not translate into a higher risk of incident hypertension.
Cohort (n=3,681)
Sí
Does 24-hour urinary sodium excretion predict blood pressure changes, incident hypertension, and cardiovascular outcomes in a population without baseline cardiovascular disease?
In a population without baseline CVD, lower sodium excretion was paradoxically associated with higher cardiovascular mortality, and changes in sodium excretion did not translate to a higher risk of hypertension or CVD complications.
Estimación del efecto: HR 1.56 (95% CI 1.02-2.36)
Tasa de eventos absoluta: 4.1% vs 0.8%
valor p: p=0.04
CONTEXT: Extrapolations from observational studies and short-term intervention trials suggest that population-wide moderation of salt intake might reduce cardiovascular events. OBJECTIVE: To assess whether 24-hour urinary sodium excretion predicts blood pressure (BP) and health outcomes. DESIGN, SETTING, AND PARTICIPANTS: Prospective population study, involving 3681 participants without cardiovascular disease (CVD) who are members of families that were randomly enrolled in the Flemish Study on Genes, Environment, and Health Outcomes (1985-2004) or in the European Project on Genes in Hypertension (1999-2001). Of 3681 participants without CVD, 2096 were normotensive at baseline and 1499 had BP and sodium excretion measured at baseline and last follow-up (2005-2008). MAIN OUTCOME MEASURES: Incidence of mortality and morbidity and association between changes in BP and sodium excretion. Multivariable-adjusted hazard ratios (HRs) express the risk in tertiles of sodium excretion relative to average risk in the whole study population. RESULTS: Among 3681 participants followed up for a median 7.9 years, CVD deaths decreased across increasing tertiles of 24-hour sodium excretion, from 50 deaths in the low (mean, 107 mmol), 24 in the medium (mean, 168 mmol), and 10 in the high excretion group (mean, 260 mmol; P < .001), resulting in respective death rates of 4.1% (95% confidence interval CI, 3.5%-4.7%), 1.9% (95% CI, 1.5%-2.3%), and 0.8% (95% CI, 0.5%-1.1%). In multivariable-adjusted analyses, this inverse association retained significance (P = .02): the HR in the low tertile was 1.56 (95% CI, 1.02-2.36; P = .04). Baseline sodium excretion predicted neither total mortality (P = .10) nor fatal combined with nonfatal CVD events (P = .55). Among 2096 participants followed up for 6.5 years, the risk of hypertension did not increase across increasing tertiles (P = .93). Incident hypertension was 187 (27.0%; HR, 1.00; 95% CI, 0.87-1.16) in the low, 190 (26.6%; HR, 1.02; 95% CI, 0.89-1.16) in the medium, and 175 (25.4%; HR, 0.98; 95% CI, 0.86-1.12) in the high sodium excretion group. In 1499 participants followed up for 6.1 years, systolic blood pressure increased by 0.37 mm Hg per year (P < .001), whereas sodium excretion did not change (-0.45 mmol per year, P = .15). However, in multivariable-adjusted analyses, a 100-mmol increase in sodium excretion was associated with 1.71 mm Hg increase in systolic blood pressure (P.<001) but no change in diastolic BP. CONCLUSIONS: In this population-based cohort, systolic blood pressure, but not diastolic pressure, changes over time aligned with change in sodium excretion, but this association did not translate into a higher risk of hypertension or CVD complications. Lower sodium excretion was associated with higher CVD mortality.
Katarzyna Stolarz‐Skrzypek (Tue,) conducted a cohort in Without cardiovascular disease (n=3,681). 24-hour urinary sodium excretion vs. Average risk in the whole study population was evaluated on Cardiovascular mortality (HR 1.56, 95% CI 1.02-2.36, p=0.04). Lower 24-hour urinary sodium excretion was associated with higher cardiovascular mortality (HR 1.56; 95% CI 1.02-2.36; P=0.04) and did not translate into a higher risk of incident hypertension.