Key result
Higher dietary sodium in females links to ~73% fewer femoral plaques but greater arterial stiffness.
Why the study?
Recent evidence suggests a J-shaped association between sodium intake and CV disease, with animal studies showing accelerated atheromatosis on low-salt diets, but human data are scarce.
Does moderate dietary sodium intake compared to very low intake affect the prevalence of atheromatosis and arterial stiffness in individuals at increased CV risk?
Cohort (n=901)
Does moderate dietary sodium intake compared to very low intake affect the prevalence of atheromatosis and arterial stiffness in individuals at increased CV risk?
Effect estimate: OR 0.274 (95% CI 0.118-0.638)
p-value: p=0.003
Very low dietary sodium intake is associated with accelerated atheromatosis but lower arterial stiffness, suggesting diverging effects of sodium restriction on different arterial pathologies.
Higher sodium intake associated with fewer plaques yet more stiffness in females; leaves open optimal targets pending prospective data.
BACKGROUND: Recent epidemiological evidence suggests a J-shaped, rather than the classical linear, association between dietary sodium (Na) intake and cardiovascular (CV) disease. Numerous animal studies have shown the acceleration of atheromatosis in a low-salt diet but data in humans are scarce. Our aim was to test the hypothesis that in a cohort of patients who are CV-free, yet at increased CV risk, moderate Na intake is associated with lower prevalence of atheromatosis and arterial stiffening than those at very low Na intake. METHODS: Two 24-h dietary recalls were conducted to estimate Na intake. Atheromatosis (carotid and femoral plaques) was assessed by B-mode ultrasonography and arterial stiffness through tonometry (carotid-to-femoral pulse wave velocity, cf-PWV). RESULTS: In 901 individuals (age: 52.4 ± 13.8 years, 45.2% males), only females at 3rd and 4th quartile of total Na intake (derived from food and discretionary salt) had significantly lower probability to present femoral plaques than those at 1st quartile (751.0 ± 215.5 mg/day), even in the full-adjusted model [0.462(0.229-0.935) and p = 0.032 3rd quartile; 0.274(0.118-0.638) and p = 0.003 4th quartile]. On the contrary, male and female individuals at 3rd quartile had significantly higher probability to present arterial stiffness (PWV >10 m/s) than those at 1st quartile [1.991(1.047-3.785) and p = 0.036]. CONCLUSIONS: Overall, the present data suggest that very low Na intake is associated with: a) accelerated atheromatosis, verifying findings from animal models, and providing a possible explanation of the modern epidemiology and b) lower arterial stiffness, which is in line with previous human findings, therefore suggesting a diverging effect of Na in the two major arterial pathologies.
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Tsirimiagkou et al. (2021) conducted a cohort in Cardiovascular-free patients at increased cardiovascular risk (n=901). Dietary sodium intake vs. Very low sodium intake (1st quartile, 751.0 ± 215.5 mg/day) was evaluated on Atheromatosis (femoral plaques) and arterial stiffness (OR 0.274, 95% CI 0.118-0.638, p=0.003). Higher dietary sodium intake in females was associated with lower probability of femoral plaques (OR 0.274; 95% CI 0.118-0.638; p=0.003) but higher arterial stiffness compared to very low intake.
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