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Incorporation both the magnitude and duration of exposure to elevated fasting blood glucose (FBG) into a single risk parameter (cumulative FBG load) for future diseases is intuitively appealing, although a data-based demonstration of the utility of this metric is not available. This study aimed to investigate the associations with cumulative FBG load with the risk of cardiovascular diseases (CVD) and all-cause mortality in the general population. This prospective cohort study included 41,728 participants who were free of CVD and underwent four health examinations from 2006 to 2012. Cumulative FBG load during 2006–2012 was calculated as the area under curve for FBG values ≥ 5.6 mmol/L divided by the total area curve. We also compared the predicting value cumulative FBG load with other FBG metrics. During a median follow-up of 6.75 years, we identified 2323 cases of CVD and 1724 cases of all-cause mortality. Per 1-standard deviation increase in cumulative FBG load was associated with a 16 % higher risk of CVD (hazard ratio [HR]: 1.16; 95 % confidence interval [CI], 1.13–1.20) and 20 % higher risk of all-cause mortality (HR, 1.20; 95 % CI, 1.16–1.25). For the prediction of cardiovascular outcomes and all-cause mortality, cumulative FBG load outperformed FBG time-in-target, visit-to-visit FBG variability, and mean FBG in terms of C-statistics and reclassification indexes. Cumulative FBG load may provide a better prediction of cardiovascular outcomes compared with other FBG metrics in the general population. These findings emphasized the important role of cumulative FBG load in assessing cardiovascular and mortality risk. • A higher cumulative FBG load was independently associated with cardiovascular outcomes and all-cause morality. • Cumulative FBG load was superior than FBG TITRE in predicting cardiovascular outcomes and all-cause mortality. • Cumulative FBG load was superior than FBG SD in predicting cardiovascular outcomes and all-cause mortality. • Cumulative FBG load was superior than mean FBG in predicting cardiovascular outcomes and all-cause mortality. • Cumulative FBG load could be used in conjunction in future cardiovascular risk prediction algorithms. [ABSTRACT FROM AUTHOR]

• 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]

• A large SUA variation was associated with a higher risk of CVD and its subtypes. • Both a large rise or fall in SUA was associated with a higher risk of CVD. • The harmful effect of a large variation of SUA on CVD was more pronounced in older adults than that in young adults. • The hazardous effect of SUA variation on CVD was mainly induced by excessive inflammation and elevated blood pressure. The association of serum uric acid (SUA) with cardiovascular disease (CVD) is inconsistent and limited by a single measurement of SUA. This study aimed to investigate the association of SUA variation, considering its magnitude and direction, with the risk of CVD. This study included 41,578 participants with four biennial measurements of SUA during 2006–2012 from the Kailuan study. SUA variation was measured using the coefficient of variation (primary index), standard deviation, average real variability, and variability independent of mean, and the direction of variation was also assessed. Multivariate-adjusted Cox regressions were used to assess the associations, and Bayesian network was utilized to find the most important pathway from SUA variation to CVD. During a median follow-up of 6.74 (interquartile range: 6.45–7.03) years, we identified 1,852 (4.45%) cases of incident CVD. A large SUA variation (top vs. bottom tertiles) was associated with a higher risk of CVD (hazard ratio [HR], 1.24; 95% confidence interval [CI], 1.11–1.40), especially in older adults than that in young adults (P int =0.0137). The higher risk of CVD was observed with both large rises (HR, 1.24; 95% CI, 1.10–1.39) and falls (HR, 1.19; 95% CI, 1.03–1.38) in SUA variation. The hazardous effect of SUA variation on CVD was mainly induced by excessive inflammation and elevated blood pressure. Similar results were observed for CVD subtypes. Elevated SUA variation was associated with a higher risk of CVD, irrespective of the direction of SUA variation, and inflammation played an important role in the pathway. [ABSTRACT FROM AUTHOR]