24-Hour Urinary Sodium and Potassium Excretion and Cardiovascular Risk.

24-Hour Urinary Sodium and Potassium Excretion and Cardiovascular Risk.
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24小时的尿钠和钾排泄和心血管风险。

DOI:
10.1056/nejmoa2109794
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发表时间:
2022-01-20
期刊:
The New England journal of medicine
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钠摄入量和心血管疾病(CVD)之间的关系仍然存在争议,部分原因是对钠摄入量的评估不准确。24-在多天内每小时尿排泄被认为是最佳方法。我们纳入了来自6个前瞻性队列的一般健康成人的个体参与者数据,其中钠和钾排泄通过至少两次24小时尿液采集进行评估。在10,709名参与者中(54.2%为女性;平均[SD]年龄为51.5 [12.6]岁),在中位8.8年的随访期间确定了571起CVD事件(心肌梗死、冠状动脉血运重建和卒中)(发生率:5.9/1000人-年)。我们使用一致的方法分析每个队列,并使用随机效应荟萃分析合并结果。24小时尿钠中位数(第10 - 90百分位数)为3,270(2,099 - 4,899)mg。在控制混杂因素后,较高的钠、较低的钾排泄和较高的钠钾比均与较高的CVD风险相关(所有P值≤0.005)。钠、钾和钠钾比的风险比[HR]分别为1.60 [95%置信区间[CI]:1.19-2.14]、0.69 [0.51-0.91]和1.62 [1.25-2.10]。钠排泄量每增加1,000 mg/天与CVD风险增加18%相关(95%CI:8%-29%),钾排泄量每增加1,000 mg/天与风险降低18%相关(95%CI:6%-28%)。这些发现可能支持减少目前钠摄入量和增加钾摄入量以降低CVD风险。在多个24小时尿液样本中测量的较高钠和较低钾摄入量与CVD风险较高相关,呈剂量反应方式。
The relation between sodium intake and cardiovascular disease (CVD) remains controversial, partially due to inaccurate assessment of sodium intake. 24-hour urinary excretion over multiple days is considered the optimal method. We included individual participant data from 6 prospective cohorts of generally healthy adults in which sodium and potassium excretion were assessed by at least two 24-hour urine collections. Of 10,709 participants (54.2% women; mean [SD] age, 51.5 [12.6] years), 571 incident CVD events (myocardial infarction, coronary revascularization, and stroke) were ascertained during a median follow-up of 8.8 years (incidence rate: 5.9 per 1000 person-years). We analyzed each cohort using consistent methods and combined results using random-effects meta-analysis. Median 24-hour urinary sodium (10th-90th percentile) was 3,270 (2,099-4,899) mg. Higher sodium, lower potassium excretion and higher sodium-to-potassium ratio were all associated with higher hazard of CVD after controlling for confounding factors (all P-values ≤0.005). The hazard ratio [HR] comparing top with bottom quartiles was 1.60 [95% confidence interval [CI]: 1.19-2.14] for sodium, 0.69 [0.51-0.91] for potassium and 1.62 [1.25-2.10] for sodium-to-potassium ratio. Each 1,000 mg/day increment in sodium excretion was associated with an 18% increase in CVD hazard (95%CI: 8%-29%) and each 1,000 mg/day increment in potassium excretion was associated with 18% lower hazard (95%CI: 6%-28%). These findings may support reducing sodium from current intakes and increasing potassium intakes to lower CVD risk. Higher sodium and lower potassium intakes, measured in multiple 24-hour urine samples, were associated with higher risk of CVD in a dose-response manner.