Sodium Intake Shows Strong Linear Relationship with Risk of Both Carotid and Coronary Atherosclerosis: Population-based Study

An association between excessive sodium intake and both coronary and carotid atherosclerosis was reported on March 30th by Swedish investigators whose analysis of data from a unique population-based study cohort is thought to be the first of its kind.

Specifically, the researchers found among more than 10 000 participants in the Swedish Cardiopulmonary bioImage Study (SCAPIS) cohort that rising levels of estimated 24-hour sodium excretion were linked to increased occurrence of carotid plaques, coronary artery calcium (CAC) scores, and coronary artery stenosis.

According to lead study investigator Jonas Wuopio, PhD, of the Karolinska Institutet and Uppsala University, the study is the first to examine a potential link between high dietary sodium intake and atherosclerosis in coronary as well as carotid arteries. “The association was linear, meaning that each rise in salt intake was linked with more atherosclerosis,” Wuopio said in a press statement from the European Society of Cardiology (ESC). “The findings applied even at normal blood pressure levels, suggesting that salt could be damaging even before the development of hypertension.”

Wuopio and colleagues cite published evidence of the association between sodium intake and various markers of vascular damage, eg, arterial stiffness, endothelial dysfunction, and inflammation. While some studies have investigated the associations of salt consumption with marked peripheral atherosclerosis, there is no research that reports on an examination of the association between levels of sodium intake and coronary atherosclerosis. Their current study, published in the European Heart Journal Open, was designed to change that.

The Swedish investigators tapped data from SCAPIS, a nationwide, open-access population-based cohort study of cardiovascular and obstructive lung disease among 30 154 Swedish adults aged 50 to 64 years. According to the study, the SCAPIS database includes detailed characterization of both coronary and carotid atherosclerosis, assessed via coronary computed tomography angiography (CCTA). Final data analysis was based on participants from 2 SCAPIS sites (Malmo, Uppsala) where urine sampling was performed.

Using CCTA data, Wuopio and colleagues stratified participants by CAC score into 5 categories: 0, 1-9, 10-99, 100-399, >399, with increasing values indicating increased risk for myocardial infarction. Coronary stenosis was defined using categorical ordinal values of no stenosis, non-significant stenosis (<50%), and significant stenosis (>50%). Based on carotid ultrasound, participants were grouped as having no plaque, plaque in 1 vessel, and plaque in both vessels.

Values for sodium consumption among participants with valid urinary data were calculated using estimated 24-hour sodium excretion.

The final cohort for analysis numbered 10 778; average age was 58 years, and the cohort was 52% women. Among the cohort, 9623 participants underwent CCTA, 10 289 had CAC score data available, and 10 700 had valid results for carotid ultrasound. Odds ratios (ORs) per 1000 mg increase in estimated 24-hour sodium excretion were estimated using ordered logistic regression, according to the study.

FINDINGS

Wuopio et al report that in minimal adjusted models (site, age, sex), increased estimated 24-hour sodium excretion was associated with increased occurrence of carotid plaques (OR 1.09, 95% CI, 1.06–1.12]; P<.001), higher CAC score (OR 1.16, 95% CI, 1.12–1.19; P<.001), and risk for coronary artery stenosis (OR 1.17, [5% CI, 1.13–1.20; P<.001). Specifically, each 1000 mg rise in sodium excretion was associated with a 3%, 4% and 4% higher likelihood of more toxic carotid plaque, CAC, and coronary artery stenosis measurements, respectively.

When investigators adjusted findings for blood pressure (BP), the associations were no longer present, a finding they say suggests that sodium intake-related increase in BP, even below current definitions of arterial hypertension, is a relevant factor mediating between salt intake and the atherosclerotic process.

When investigators adjusted findings for blood pressure (BP), the associations were no longer present, a finding they say suggests that sodium intake-related increase in BP, even below current definitions of arterial hypertension, is a relevant factor mediating between salt intake and the atherosclerotic process.

In the multivariable model, after adjustment for several other established CV risk factors but including BP, the associations with sodium intake remained for carotid plaques but not for coronary atherosclerosis.

Commenting in the ESC press statement, Wuopio reiterated that the greater intake of dietary salt, the greater the burden of both coronary and carotid atherosclerosis.

“The increase in blood pressure due to a high salt intake seems to be an important underlying mechanism for these findings. Interestingly, the results were consistent when we restricted our analyses to participants with normal blood pressure (below 140/90 mmHg) or to those without known cardiovascular disease.” Wuopio cautions that modifying sodium intake may be relevant to the broader population outside of those with hypertension or known cardiovascular disease.

Reference: Wuopio J, Ling YT, Orho-Melander M, Engström G, Ärnlöv J. The association between sodium intake and coronary and carotid atherosclerosis in the general Swedish population. Eur Heart J Open. 2023;3:oead024. Published online March 30, 2023. doi:10.1093/ehjopen/oead024