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

• Increase SUA levels preceded the development of hypertension. • The unidirectional relationships from SUA to SBP and DBP were significantly stronger in subjects with incident CVD. • the total association between SUA and subsequent risk of CVD and its subtypes were partially mediated through SBP and DBP. • Interventions on hyperuricemia are needed to reduce the burden of hypertension and CVD. 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. 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. After adjusting for covariates, the cross-lagged path coefficients (β 1) from baseline SUA to follow-up SBP and DBP were significantly greatly than path coefficients (β 2) from baseline SBP and DBP to follow-up SUA (β 1 =0.041 versus β 2 =0.003; P difference <0.0001 for SBP; β 1 =0.040 versus β 2 =0.000; P difference <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 (P difference of β 1 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. Increased SUA levels probably precede elevated BP, and BP partially mediates the pathway from SUA to incident CVD. [ABSTRACT FROM AUTHOR]