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Although sleep duration and depression were correlated, their temporal sequence and how the sequence influence on future risk of cardiovascular disease (CVD) remained undetermined. This study aimed to explore the temporal relationship between sleep duration and depression, and its association with future CVD risk. We included 10,629 middle-aged and elderly participants with repeated measurements of sleep duration and depressive symptoms (measured by Center for Epidemiological Studies-Depression scale [CES D]) at the first two visits from the China Health and Retirement Longitudinal Study. Cross-lagged analysis and mediation analysis were used to examine the temporal relationship between sleep duration and depression and its impact on future risk of CVD. The adjusted cross-lagged path coefficient from baseline sleep duration to follow-up CES-D (β 1 = −0.191; 95 % confidence interval [CI], −0.239 to −0.142) was significantly greatly than that from baseline CES-D to follow-up sleep duration (β 2 = −0.031; 95 % CI, −0.031 to −0.024) (P difference < 0.0001). Similarly, the path coefficient from baseline sleep duration to annual changes in CES-D was significantly greater than that from baseline CES-D to annual changes in sleep duration (β 1 = −0.093 versus β 2 = −0.015, P difference < 0.0001). The path coefficient from baseline sleep duration to follow-up CES-D in CVD group was significantly greater than that in those without CVD (P difference of β 1 = 0.0378). Furthermore, 27.93 % of the total association of sleep duration with CVD was mediated by depression symptoms. The findings provide evidence that decrease in sleep duration probably precedes the increased in depressive symptoms, and depression partially mediated the pathway from sleep duration to incident CVD. • Decrease in sleep duration preceded the increase in depressive scores. • The relationship was significantly stronger in subjects with CVD. • 27.93 % of the association of sleep duration with CVD was mediated through depression. [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]

• 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]

Background and Aim: Longitudinal evidence on change in serum (SUA) with risk of cardiovascular disease (CVD) and all-cause mortality is limited, as many prior studies focused on baseline SUA. Further, the optimal threshold range of SUA change is unclear.Methods and Results: A total of 63,127 participants without history of CVD were enrolled. Change in SUA was determined by the difference of SUA levels between 2006 and 2010, which divided by baseline SUA was percent change in SUA. Multivariable Cox proportional hazards models were used to calculated the hazard ratios (HRs) and 95% confidence intervals (CIs). Our analysis also included restricted cubic spline model and three-piecewise Cox proportion hazards model to address the non-linearity between percent change in SUA and outcomes. During a median follow-up of 7.04 years, 3341 CVD and 3238 deaths occurred. We did not observed a significant association between changes in SUA and CVD. However, changes in SUA at extreme were associated with higher risk of all-cause mortality, the HRs (95% CIs) were 1.15 (1.02-1.29) and 1.20 (1.06-1.35) in the first and fifth quintile group, compared with the third quintile group. We further found a U-shaped association between percent change in SUA and all-cause mortality, and the optimal range was within 20%.Conclusions: Changes in SUA at extreme were risk factors for all-cause mortality, but not for CVD in the general population. The findings are relevant for role of SUA in the management of CVD risk and may contribute to improve identification of patients at higher risk. [ABSTRACT FROM AUTHOR]

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]

Previous studies have shown that remnant cholesterol (RC) was associated with cardiovascular disease (CVD) among middle-aged or older adults. However, lack of evidence on long-term exposures to RC and their role in CVD risk among young adults. We thus aimed to explore the association between cumulative RC burden and CVD in young adults. We enrolled participants younger than 45 years free of CVD history in the Kailuan Study who completed the first three health examinations from 2006 to 2010. Cumulative RC burden included cumulative RC burden score, time-weighted cumulative RC, exposure duration of high RC, and time course of RC accumulation. The outcome was the incidence of CVD. Cox proportional hazard models were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) between cumulative RC burden and CVD risk. A total of 15,219 participants were included (73.70% male, median age 39.13 years). During a median follow-up duration of 8.71 years (interquartile range: 8.4–9.15 years), 502 individuals developed CVD. After adjustment for traditional cardiovascular risk factors, highest risk of CVD was observed in participants with the highest cumulative RC burden score (HR, 1.66; 95% CI, 1.29–2.12), the highest quartile time-weighted cumulative RC (HR,1.50; 95% CI, 1.15–1.96), the longest exposure duration of high RC (HR, 1.71; 95% CI, 1.21–2.42), and those with cumulative RC burden and positive slope (HR, 1.79; 95% CI, 1.35–2.36). Cumulative RC burden increased the risk of CVD among young adults, suggesting that maintaining low RC levels throughout young adulthood may minimize CVD risk. • Remnant cholesterol (RC) was associated with cardiovascular disease (CVD) among middle-aged or older adults, but lack of evidence on long-term exposures to RC and their role in CVD risk among young adults. • We explored the association between cumulative RC burden and CVD in younger than 45 years adults. • Cumulative RC burden increased the risk of CVD among young adults, suggesting that maintaining low RC levels throughout young adulthood may minimize CVD risk. [ABSTRACT FROM AUTHOR]