The association between sodium intake and coronary and carotid atherosclerosis in the general Swedish population

Author:

Wuopio Jonas12ORCID,Lin Yi-Ting13ORCID,Orho-Melander Marju4ORCID,Engström Gunnar4ORCID,Ärnlöv Johan125ORCID

Affiliation:

1. Department of Neurobiology, Care Sciences and Society (NVS), Division of Family Medicine and Primary Care, Karolinska Institute , Alfred Nobels Allé 23, 141 52, Huddinge , Sweden

2. Center for Clinical Research Dalarna , Nissers väg 3, 791 82 Falun, Uppsala University , Sweden

3. Department of Family Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University , No 100, Tzou 1st Road Kaohsiung, Sanmin District, Kaoshiung City, 807 , Taiwan

4. Department of Clinical Sciences, Lund University, Clinical Research Centre , Box 50332, 202 13 Malmö , Sweden

5. School of Health and Social Studies, Dalarna University , 79188 Falun , Sweden

Abstract

Abstract Aims A high intake of salt raises blood pressure and the risk of cardiovascular disease. Previous studies have reported on the association between salt intake and carotid stenosis, but the association with coronary atherosclerosis has not been reported. Therefore, this project aimed at studying the association between salt intake and both carotid and coronary atherosclerosis in a contemporary community-based cohort. Methods and results Estimated 24-h sodium excretion (est24hNa) was calculated by the Kawasaki formula for participants of two sites (Uppsala and Malmö) of the Swedish Cardiopulmonary bioImage Study, who underwent a coronary computed tomography (n = 9623) and measurement of coronary artery calcium score (CACS, n = 10 289). Carotid ultrasound was used to detect carotid plaques (n = 10 700). Ordered logistic regression was used to calculate odds ratios (OR) per 1000 mg increase in est24hNa. We also investigated potential J-formed associations using quintiles of est24hNa. Increased est24hNa was associated with increased occurrence of carotid plaques [OR: 1.09, P < 0.001, confidence interval (CI): 1.06–1.12], higher CACS (OR: 1.16, P < 0.001, CI: 1.12–1.19), and coronary artery stenosis (OR: 1.17, P < 0.001, CI: 1.13–1.20) in minimal adjusted models. Associations were abolished when adjusting for blood pressure. When adjusting for established cardiovascular risk factors (not including blood pressure), associations remained for carotid plaques but not for coronary atherosclerosis. There was no evidence of J-formed associations. Conclusion Higher est24hNa was associated with both coronary and carotid atherosclerosis in minimal adjusted models. The association seemed mainly mediated by blood pressure but to some degree also influenced by other established cardiovascular risk factors.

Publisher

Oxford University Press (OUP)

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