Temporal relationship between hyperuricemia and hypertension and its impact on future risk of cardiovascular disease

医学 高尿酸血症 血压 疾病 调解 心肌梗塞 内科学 冲程(发动机) 心脏病学 舒张期 内分泌学 尿酸 政治学 机械工程 工程类 法学
作者
Xue Tian,Shuohua Chen,Penglian Wang,Qin Xu,Yijun Zhang,Xiaoli Zhang,Shouling Wu,Yanxia Luo,Anxin Wang
出处
期刊:European Journal of Internal Medicine [Elsevier BV]
卷期号:111: 82-89 被引量:16
标识
DOI:10.1016/j.ejim.2023.02.023
摘要

Background Although hyperuricemia and hypertension are significantly correlated, their temporal relationship and whether this relationship is associated with risk of cardiovascular disease (CVD) are largely unknown. This study aimed to examine temporal relationship between hyperuricemia and hypertension, and its association with future risk of CVD. Methods This study included 60,285 participants from the Kailuan study. Measurement of serum uric acid (SUA), systolic and diastolic blood pressure (SBP and DBP) were obtained twice at 2006 (baseline) and 2010. Cross-lagged and mediation analysis were used to examine the temporal relationship between hyperuricemia and hypertension, and the association of this temporal relationship with CVD events risk after 2010. Results After adjusting for covariates, the cross-lagged path coefficients (β1) from baseline SUA to follow-up SBP and DBP were significantly greatly than path coefficients (β2) from baseline SBP and DBP to follow-up SUA (β1=0.041 versus β2=0.003; Pdifference<0.0001 for SBP; β1=0.040 versus β2=0.000; Pdifference<0.0001 for DBP). The path coefficients from baseline SUA to follow-up SBP and DBP in group with incident CVD were significantly greatly than that in group without incident CVD (Pdifference of β1 in the two groups was 0.0018 for SBP and 0.0340 for DBP). Furthermore, SBP and DBP partially mediated the effect of SUA on incident CVD, the mediation effect was 57.64% for SBP and 46.27% for DBP. Similar mediated results were observed for stroke and myocardial infarction. Conclusion Increased SUA levels probably precede elevated BP, and BP partially mediates the pathway from SUA to incident CVD.
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