Department of Internal Medicine, Section on Hospital Medicine, Wake Forest School of Medicine, Winston-Salem, North Carolina.
Department of Internal Medicine, Section on Hospital Medicine, Wake Forest School of Medicine, Winston-Salem, North Carolina.
Am J Cardiol. 2019 Mar 15;123(6):882-888. doi: 10.1016/j.amjcard.2018.12.016. Epub 2018 Dec 19.
Whether elevated uric acid (UA) is associated with silent myocardial infarction (SMI) or whether their joint association predicts an increased risk of mortality has not been explored. This analysis included 6,323 participants (58.4 ± 13.1 years, 53.9% women, and 49.7% Non-Hispanic whites) without clinical cardiovascular disease (CVD) from third National Health and Nutrition Examination Survey. SMI was defined as electrocardiographic evidence of myocardial infarction (MI) without a history of MI. Multivariable logistic regression model was used to examine the cross-sectional association between baseline UA and SMI. Cox-proportional hazard analysis was used to calculate hazard ratio (HR) with 95% confidence interval (CI) for the risk of all-cause and CVD mortality with UA in the absence and presence of SMI. The higher baseline level of UA was associated with higher odds of baseline SMI. The prevalence of SMI was 0.79%, 1.18%, 1.59%, and 2.27% across the UA quartiles respectively; multivariable-adjusted odds ratio (95% CI): 2.37 (1.11 to 5.08) comparing the upper with lower quartile. During a median follow up of 14 years, there were 1916 all-cause death of whom 774 were CVD deaths. Compared with participants with the lowest UA quartile values and without SMI, those with highest UA had a 29% increased the risk of all-cause mortality (multivariable-adjusted HR: [95% CI]: 1.29 [1.10 to 1.51]). This risk increased by 107% in the presence of SMI (multivariable-adjusted HR (95% CI): 2.07 (1.38 to 3.10)). Similar results were observed for CVD mortality. SMI carried an increased risk of all-cause and CVD mortality only in higher quartiles of UA. In conclusion, the strong association of UA with SMI and the additive effect of UA and SMI on mortality further support the potential role of UA as a marker of poor outcomes.
高尿酸（UA）是否与无症状性心肌梗死（SMI）有关，或者它们的联合是否预示着死亡率的增加，这些问题尚未得到探讨。本分析纳入了来自第三次全国健康和营养调查的 6323 名无临床心血管疾病（CVD）的参与者（58.4±13.1 岁，53.9%为女性，49.7%为非西班牙裔白人）。SMI 的定义为心电图有心肌梗死（MI）证据但无 MI 病史。采用多变量逻辑回归模型来检验基线 UA 与 SMI 的横断面关系。使用 Cox 比例风险分析来计算 UA 与 SMI 存在和不存在时全因和 CVD 死亡率的风险比（HR）及其 95%置信区间（CI）。较高的基线 UA 水平与较高的基线 SMI 发生几率相关。UA 四分位间距分别为 0.79%、1.18%、1.59%和 2.27%，经多变量校正的优势比（95%CI）为：与 UA 四分位间距最低者相比，四分位间距最高者分别为 2.37（1.11 至 5.08）。在中位随访 14 年期间，共发生了 1916 例全因死亡，其中 774 例为 CVD 死亡。与 UA 四分位间距最低且无 SMI 的参与者相比，UA 四分位间距最高者的全因死亡率风险增加了 29%（多变量校正 HR：[95%CI]：1.29[1.10 至 1.51]）。若存在 SMI，则风险增加了 107%（多变量校正 HR（95%CI）：2.07（1.38 至 3.10））。CVD 死亡率也有类似的结果。仅在 UA 四分位间距较高者中，SMI 与全因和 CVD 死亡率的增加相关。结论：UA 与 SMI 之间的强关联以及 UA 和 SMI 对死亡率的累加效应进一步支持了 UA 作为不良结局标志物的潜在作用。
