Singer Pamela, Cohen Hillel, Alderman Michael
Department of Pediatrics, Division of Pediatric Nephrology, Children's Hospital at Montefiore, Albert Einstein College of Medicine, Bronx, New York;
Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, New York.
Am J Hypertens. 2015 Mar;28(3):335-42. doi: 10.1093/ajh/hpu141. Epub 2014 Aug 26.
Although higher sodium intake is known to increase blood pressure, its association with cardiovascular mortality is less established. We examined the association of baseline sodium intake in a hypertensive cohort with all-cause and cardiovascular mortality over a mean follow-up of 18.6 years.
Three thousand five hundred five subjects were participants in a worksite hypertension program. Sodium intake was estimated by 24-hour urine excretion. Mortality data were obtained from the U.S. National Death Index. Unadjusted and multivariable-adjusted associations between sodium quartiles (quartile I (QI) to quartile IV (QIV)) and mortality were assessed using Cox models.
Estimated mean ± SD sodium intake was 130±69 mmol overall (55±20 mmol in QI; 220±56 mmol in QIV). Baseline systolic blood pressure did not vary significantly between groups. Last available mean systolic blood pressure was highest in QI and lowest in QIV (137±16 vs. 134±14 mm Hg; P = 0.009). Overall there were 1,013 deaths (399 cardiovascular). Unadjusted models exhibited significant inverse relationships between sodium and mortality outcomes. In adjusted models, sodium intake was not significantly associated with cardiovascular mortality (QI vs. QIV: hazard ratio (HR) = 1.00; 95% confidence interval (CI) = 0.71-1.42; P = 0.99). A borderline significant direct association with all-cause mortality was observed (QI vs. QIV: HR = 0.81; 95% CI = 0.66-1.00; P = 0.05) driven partly by noncardiovascular deaths.
Our study found no significant association between sodium intake and cardiovascular outcomes, although a significant association with all-cause mortality was observed. Although these findings suggest that sodium may not have a strong relationship with cardiovascular mortality, the inconsistent results cast doubt on whether a single measurement can reliably predict mortality over a prolonged follow-up period.
尽管已知较高的钠摄入量会升高血压,但其与心血管疾病死亡率之间的关联尚不明确。我们在一个高血压队列中研究了基线钠摄入量与平均随访18.6年期间的全因死亡率和心血管疾病死亡率之间的关联。
3505名受试者参与了一项工作场所高血压项目。通过24小时尿排泄量估算钠摄入量。死亡率数据来自美国国家死亡指数。使用Cox模型评估钠四分位数(四分位数I(QI)至四分位数IV(QIV))与死亡率之间的未调整和多变量调整关联。
总体估计平均±标准差钠摄入量为130±69 mmol(QI组为55±20 mmol;QIV组为220±56 mmol)。各组间基线收缩压无显著差异。最后一次可获得的平均收缩压在QI组最高,在QIV组最低(137±16 vs. 134±14 mmHg;P = 0.009)。总体共有1013例死亡(399例心血管疾病死亡)。未调整模型显示钠与死亡率结局之间存在显著的负相关关系。在调整模型中,钠摄入量与心血管疾病死亡率无显著关联(QI组与QIV组:风险比(HR)= 1.00;95%置信区间(CI)= 0.71 - 1.42;P = 0.99)。观察到与全因死亡率存在临界显著的正相关关系(QI组与QIV组:HR = 0.81;95% CI = 0.66 - 1.00;P = 0.05),部分由非心血管疾病死亡导致。
我们的研究发现钠摄入量与心血管疾病结局之间无显著关联,尽管观察到与全因死亡率存在显著关联。尽管这些发现表明钠可能与心血管疾病死亡率没有很强的关系,但结果不一致让人怀疑单次测量能否在长期随访期间可靠地预测死亡率。