Higher salt intake associated with coronary and carotid atherosclerosis
The association between sodium intake and coronary and carotid atherosclerosis in the general Swedish population
Introduction and methods
High dietary sodium intake increases blood pressure [1-2] and the risk of CVD [3-4]. Previous research suggests that there is an association of salt intake with vascular damage [5-6] and the development of peripheral atherosclerosis [7-9]. It remains unclear whether there is an association between salt intake and coronary atherosclerosis.
Aim of the study
The authors investigated whether there is an association between salt intake and coronary or carotid atherosclerosis in the general Swedish population.
Data from the Swedish Cardiopulmonary bioImage Study (SCAPIS) cohort were used in this study. This cohort comprised of 30,154 participants of the general Swedish population aged from 50-64 years, who underwent detailed characterization of atherosclerosis in the coronary and carotid arteries . In this analysis, 10,764 participants (mean age 58 years, 52% woman) from 2 different university hospitals were included, who had additional measurements for urinary sodium and creatine. Sodium intake was determined by calculating an estimated 24h sodium excretion (est24hNA) with the Kawasaki formula. Coronary atherosclerosis was determined with coronary CT angiography (CCTA; n=9623) and coronary artery calcium score (CACS; n=10,289). Carotid atherosclerosis was determined from ultrasound images (n=10,700).
The main outcome was the presence of carotid plaques, coronary artery calcification (CACS) or coronary artery stenosis.
Carotid or coronary atherosclerosis
- There was a significant association between each 1000 mg increase in est24hNa and increased occurrence of carotid plaques (OR: 1.09, 95%CI: 1.06-1.12; P<0.001), higher CACS (OR: 1.16, 95%CI: 1.12-1.19), and coronary artery stenosis (OR: 1.17, 95%CI: 1.13-1.20; P<0.001) when correcting for site.
- Similar associations were obtained when corrections for site + age + sex were included (OR: 1.03; 95%CI: 1.00-1.06; P=0.028 for carotid plaques; OR: 1.04; 95%CI: 1.01-1.07; P=0.016 for CACS; 1.04; 95%CI: 1.01-1.07; P=0.020 for coronary artery stenosis), but these associations were abolished with additional corrections for blood pressure .
- When correcting for site + age + sex + CV risk factors (without blood pressure), the association of est24hNa (per 1000 mg) with carotid plaques remained significant (OR: 1.04; 95%CI: 1.01-1.07; P=0.017). However, the associations between est24hNa and higher CACs and coronary artery stenosis were abolished (both OR: 1.01; 95%CI: 0.98-1.04; P=0.643).
- The association between est24hNa and carotid plaques, CACS, and coronary artery stenosis remained significant when excluding participants with antihypertensive or HF medication (n=2106; OR: 1.08, 1.15, and 1.15, respectively; P<0.001), hypertension (n=3404; OR: 1.07, 1.16, and 1.16, respectively; P<0.001) or known pre-existing ASCVD (n=3404; OR: 1.07, 1.16, and 1.16, respectively; P<0.001).
Higher est24hNa was associated with both coronary and carotid atherosclerosis in the general Swedish population in minimal adjusted models. The association was present in participants with normal blood pressure and without known CVD, but was abolished when correcting for blood pressure. This may suggest that the increase in blood pressure from sodium intake plays an important role in the interplay between salt intake and the atherosclerotic process.
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