High Salt Intake Linked to Atherosclerosis Even With Normal Blood Pressure
A large study from Sweden concludes that a high salt intake is an important risk factor for atherosclerosis, even in the absence of hypertension.
The study, including more than 10,000 individuals between the ages of 50 and 64 years from the Swedish Cardiopulmonary bioImage Study, showed a significant link between dietary salt intake and the risk for atherosclerotic lesions in the coronary and carotid arteries, even in participants with normal blood pressure and without known cardiovascular disease.
The finding suggests that salt could be a damaging factor in its own right before the development of hypertension, the authors write. The results were published online March 30 in European Heart Journal Open.
It has been known for a long time that salt is linked to hypertension, but the role that salt plays in atherosclerosis has not been examined, first author, Jonas Wuopio, MD, Karolinska Institutet, Huddinge, and Clinical Research Center, Falun, Uppsala University, both in Sweden, told theheart.org | Medscape Cardiology.
"Hardly anyone looks at changes in the arteries' calcification, the atherosclerotic plaques and the association with salt intake," Wuopio said. "We had this exclusive data from our cohort, so we wanted to use it to close this knowledge gap." The analysis included 10,788 adults ages 50 to 64 years, (average age, 58 years; 52% women) who underwent a coronary computed tomography angiography (CCTA) scan. The estimated 24-hour sodium excretion was used to measure sodium intake.
CCTA was used to obtain 3D images of the coronary arteries to measure the degree of coronary artery calcium as well as detect stenosis in the coronary arteries. Participants also had an ultrasound of the carotid arteries.
After adjusting for age, sex, and study site (the study was done at Uppsala and Malmö), the researchers found that rising salt consumption was linked with increasing atherosclerosis in a linear fashion in both the coronary and carotid arteries.
Each 1000 mg rise in sodium excretion was associated with a 9% increased occurrence of carotid plaque (odds ratio [OR], 1.09; P < .001; confidence interval [CI], 1.06 - 1.12), a higher coronary artery calcium score (OR, 1.16; P < .001; CI, 1.12 - 1.19), and a 17% increased occurrence of coronary artery stenosis (OR, 1.17; P < .001; CI, 1.13 - 1.20).
The association was abolished, though, after adjusting for blood pressure, they note. Their "interpretation is that the increase in blood pressure 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," they write. "As we observed an association in individuals with normal blood pressure, one possible explanation for these findings is that the detrimental pathological processes begin already prior to the development of hypertension," they note, although they caution that no causal relationships can be gleaned from this cross-sectional study.
They also reported no sign of a "J-curve"; participants with the lowest levels of sodium excretion had the lowest occurrence of both coronary and carotid atherosclerosis, which contradicts findings in some studies that found very low sodium linked to increased cardiovascular disease–related events.
"There have been some controversies among researchers regarding very low intake, where some say very low salt intake can increase the risk of cardiovascular disease, but we could not find this in this study," Wuopio said.
"Our study is confirming that excess salt is not a good thing, but the fact that it is linked to atherosclerosis, even in the absence of hypertension, was a bit of a surprise," he said.
"I will be telling my patients to follow the advice given by the World Health Organization and other medical societies, to limit your intake of salt to approximately 1 teaspoon, even if your blood pressure is normal."
Maciej Banach, MD, Medical University of Lodz, and Stanislaw Surma, MD, Faculty of Medical Sciences in Katowice, both in Poland, write that excessive dietary salt intake is a well-documented cardiovascular risk factor, and that the association is explained in most studies by increased blood pressure.
"We should look more extensively on the role of dietary salt, as it affects many pathological mechanisms, by which, especially with the coexistence of other risk factors, atherosclerosis may progress very fast," they write."The results of the study shed new light on the direct relationship between excessive dietary salt intake and the risk of ASCVD [atherosclerotic cardiovascular disease], indicating that salt intake might be a risk factor for atherosclerosis even prior to the development of hypertension," they conclude.