瑞典普通人群钠摄入量与冠状动脉和颈动脉粥样硬化之间的关系。

European Heart Journal Open Pub Date : 2023-03-30 eCollection Date: 2023-03-01 DOI:10.1093/ehjopen/oead024
Jonas Wuopio, Yi-Ting Ling, Marju Orho-Melander, Gunnar Engström, Johan Ärnlöv
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引用次数: 4

摘要

目的:高盐摄入会增加血压和患心血管疾病的风险。以前的研究报道了盐摄入与颈动脉狭窄之间的关系,但与冠状动脉粥样硬化的关系尚未报道。因此,本项目旨在研究当代社区队列中盐摄入量与颈动脉和冠状动脉粥样硬化之间的关系。方法和结果:瑞典心肺生物图像研究的两个地点(Uppsala和Malmö)的参与者接受了冠状动脉计算机断层扫描(n = 9623)和冠状动脉钙评分(CACS, n = 10 289),通过川asaki公式计算估计24小时钠排泄(est24hNa)。应用颈动脉超声检测颈动脉斑块(n = 10 700)。使用有序逻辑回归计算est24hNa每增加1000 mg的优势比(OR)。我们还利用est24hNa的五分位数研究了潜在的j型关联。在最小校正模型中,est24hNa升高与颈动脉斑块发生率升高相关[OR: 1.09, P < 0.001,可信区间(CI): 1.06-1.12]、CACS升高(OR: 1.16, P < 0.001, CI: 1.12-1.19)和冠状动脉狭窄(OR: 1.17, P < 0.001, CI: 1.13-1.20)。当对血压进行调整时,这些关联就被消除了。当调整已确定的心血管危险因素(不包括血压)时,颈动脉斑块的相关性仍然存在,但与冠状动脉粥样硬化无关。没有证据表明存在j形关联。结论:在最小校正模型中,较高的est24hNa与冠状动脉和颈动脉粥样硬化相关。这种关联似乎主要由血压介导,但在某种程度上也受到其他已知心血管危险因素的影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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

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

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

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

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.

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