Higher sodium intake tied to higher atherosclerotic burden

Audrey Abella
19 Apr 2023
Higher sodium intake tied to higher atherosclerotic burden

Increased sodium intake is associated with increased coronary and carotid atherosclerosis burden in the general Swedish population, even in normotensive individuals and those without known cardiovascular disease (CVD), the SCAPIS* study finds.

Evidence has shown that salt intake is associated with carotid stenosis but not with coronary atherosclerosis. “[Hence, we aimed to study] the association between salt intake and both carotid and coronary atherosclerosis in a contemporary community-based cohort,” said the researchers.

Using the Kawasaki formula, estimated 24-hour sodium excretion (est24hNa) was calculated for SCAPIS participants who underwent a coronary CT angiography (n=9,623) and had measurements of Coronary Artery Calcium Score (CACS; n=10,289). Carotid plaques were detected via carotid ultrasound (n=10,700). [Eur Heart J Open 2023;3:oead024]

In minimally adjusted models, increased est24hNa was significantly associated with increased incidence of carotid plaques (odds ratio [OR], 1.09), higher CACS (OR, 1.16), and coronary artery stenosis (OR, 1.17; p<0.001 for all). However, these associations were not seen when adjusting for blood pressure (BP).

“[O]ur interpretation is that the increase in BP from sodium intake, even below the level that currently defines arterial hypertension, is an important factor that mediates the interplay between salt intake and the atherosclerotic process,” the researchers explained.

Even when excluding participants with hypertension and known pre-existing atherosclerotic disease, the associations remained for carotid plaques (ORs, 1.07 and 1.09), CACS (ORs, 1.16 for both), and coronary artery stenosis (ORs, 1.16 and 1.17; p<0.001 for all).

“As we observed an association in individuals with normal BP, one possible explanation for these findings is that the detrimental pathological processes begin already prior to the development of hypertension. However, due to the observational, cross-sectional design of the study, no causal relationships can be established,” they said.

When adjusting for established cardiovascular risk factors (excluding BP), the association remained for carotid plaques (OR, 1.04; p=0.017). The association for coronary atherosclerosis was abolished (OR, 1.01; p=0.643) which, according to the researchers, indicates “confounding or other pathways [whereby] salt mediates its harmful effects.”

It should be noted that use of the Kawasaki formula could have been a limiting factor as it has not been validated. [J Hypertens 2014;32:1005-1014; Clin Exp Pharmacol Physiol 1993;20:7-14] “In the debate on whether a J-formed curve between sodium intake and CV risk truly exists, the Kawasaki formula has often been blamed for creating biased results,” the researchers noted. “[However,] we did not find any J-formed curve … rendering it unlikely that the formula itself has caused the J-formed associations in previous studies.”

Therefore, the Kawasaki formula may be good enough to approximate salt intake at a population level, but not “accurate enough to conclude ‘safe levels’ of salt intake in milligrams on an individual level,” they continued.


More studies needed

“[F]or the first time, [this study] found a significant link between urinary sodium excretion … and the risk of atherosclerotic lesions in the coronary and carotid arteries, even in participants with normal BP and without known CVD,” said Dr Maciej Banach from the Medical University of Lodz, Lodz, Poland and Stanislaw Surma, academic researcher from the Faculty of Medical Sciences in Katowice, Medical University of Silecia, Katowice, Poland, in an accompanying editorial.

The lowest incidence of both carotid and coronary atherosclerosis was found in the lowest quintiles of sodium excretion, increasing subsequently in a linear fashion. [Eur Heart J Open 2023;3:oead025]

“Therefore, it seems we should look more extensively on the role of dietary salt, as it affects many pathological mechanisms by which, especially with the co-existence of other risk factors, atherosclerosis may progress very fast,” stressed Banach and Surma.

“The results of this study shed new light on the direct relationship between excessive dietary salt intake and the risk of atherosclerotic CVD, indicating that salt intake might be a risk factor for atherosclerosis even prior to the development of hypertension,” they continued.


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