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An analysis of data from more than 10,000 individuals in Europe sheds new light on risk of arterial stiffness associated with excess sodium intake.
In what investigators suggest is the first study of its kind, new research indicates excessive sodium intake was associated with both coronary and carotid atherosclerosis.
Results of the study, which included data from individuals at a pair of sites involved in the Swedish Cardiopulmonary bioImage Study, suggest greater levels of estimated 24-hour sodium excretion were associated with increased occurrence of carotid plaques, higher coronary artery calcium scores (CACs), and coronary artery stenosis.1
“This was the first study to examine the association between a high salt intake and atherosclerosis in both the heart and neck arteries,” said lead investigator Jonas Wuopio, PhD, of the Karolinska Institutet and Uppsala University.2 “The association was linear, meaning that each rise in salt intake was linked with more atherosclerosis. The findings applied even at normal blood pressure levels, suggesting that salt could be damaging even before the development of hypertension.”
A leading cause of death in the US and abroad, atherosclerotic cardiovascular disease represents one of the most prominent public health issues across the globe. To build on previous research between salt intake and carotid stenosis, Wuopio and a team of colleagues designed the current study as an analysis of data from the Swedish Cardiopulmonary bioImage Study (SCAPIS). Billed as the world’s largest general population study assessing coronary computed tomography angiography (CCTA), SCAPIS provided investigators with information related to a cohort of 10,778 adults aged 50-64 years of age for inclusion in the current study.1
For the purpose of analysis, 24-hour urinary sodium excretion was measured to estimate salt consumption. Using CCTA data, investigators created 5 groups to stratify CACs, with these groups defined as 0, 1-9, 10-99, 100-399, and greater than 399. with a higher value indicating a greater risk of myocardial infarction. Investigators classified stenosis as no stenosis, non-significant stenosis, and significant stenosis, with 50% representing the threshold for significant stenosis.1
Of the 10,778 identified for inclusion, 9623 underwent CCTA, 10,289 had CAC score data available, and 10,700 had undergone carotid ultrasound. Investigators pointed out ordered logistic regression was used to estimate odds ratios (ORs) per 1000 mg increase in estimated 24-hour sodium excretion.1
Upon analysis, results indicated increased levels of 24-hour sodium excretion was associated with increased occurrence of carotid plaques (OR, 1.09 [Confidence interval [CI], 1.06–1.12]; P <.001), higher CACs (OR, 1.16 [95% CI, 1.12–1.19]; P <.001), and coronary artery stenosis (OR, 1.17 [95% CI, 1.13–1.20]; P <.001) in minimally adjusted models. Further analysis demonstrated these associations were no longer present when adjusting for blood pressure and, when accounting for other established cardiovascular risk factors and not blood pressure, associations remained for carotid plaques but not for coronary atherosclerosis.1
“The results show that the more salt people eat, the higher the burden of atherosclerotic plaques in the arteries of the heart and neck. The increase in blood pressure due to a high salt intake seems to be an important underlying mechanism for these findings,” Wuopio added.2 “Interestingly, the results were consistent when we restricted our analyses to participants with normal blood pressure or to those without known cardiovascular disease. This means that it’s not just patients with hypertension or heart disease who need to watch their salt intake.