Rationale: Previous studies on the relationship between diabetes and arterial stiffness were mostly cross-sectional. A few longitudinal studies focused on one single direction. Whether the association between arterial stiffness and diabetes is bidirectional remains unclear to date. Objective: To explore the temporal relationship between arterial stiffness and fasting blood glucose (FBG) status. Methods and Results: Included were 14,159 participants of the Kailuan study with assessment of brachial-ankle pulse wave velocity (baPWV) from 2010 to 2015, and free of diabetes, cardiovascular and cerebrovascular diseases and chronic kidney disease at baseline. FBG and baPWV were repeatedly measured at baseline and follow-ups. Cox proportional hazard regression model was used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) of incident diabetes across baseline baPWV groups: <1,400 cm/s (ref), 1,400 {less than or equal to} baPWV < 1,800 cm/s, and {greater than or equal to}1,800cm/s. Path analysis was used to analyze the possible temporal causal relationship between baPWV and FBG, among 8,956 participants with repeated assessment of baPWV and FBG twice in 2010-2017. The mean baseline age of the observed population was 48.3{plus minus}12.0 years. During mean 3.72 years of follow-up, 979 incident diabetes cases were identified. After adjusting for potential confounders, the HR (95% CI) for risk of diabetes was 1.59 (1.34, 1.88) for the borderline arterial stiffness group and 2.11 (1.71, 2.61) for the elevated arterial stiffness group, compared with the normal ideal arterial stiffness group. In the path analysis, baseline baPWV was associated with follow-up FBG (the standard regression coefficient was 0.09; 95% CI: 0.05 to 0.10). In contrast, the standard regression coefficient of baseline FBG for follow-up baPWV (β = 0.00, 95% CI: -0.02 to 0.02) was not significant. Conclusions: Arterial stiffness, as measured by baPWV, was associated with risk of developing diabetes. Arterial stiffness appeared to precede the increase in FBG.

BACKGROUND: Data are lacking regarding cardiovascular health (CVH) with Life’s Essential 8 approach and future stroke risk. We sought to elucidate whether the CVH score constructed by the Life’s Essential 8 metrics predicted stroke risk in 2 Chinese ongoing cohorts. METHODS: This included 41 043 participants of the Kailuan I study and 27 842 participants of the Kailuan II study who were free of cardiovascular disease or cancer in 2014. CVH score (ranged from 0 to 100) was assessed using the Life’s Essential 8 metrics (body mass index, cigarette smoking, diet quality, physical activity, sleep health, lipid, blood glucose, and blood pressure). A composite of incident stroke events (ischemic stroke and hemorrhagic stroke) was identified via review of medical records. The follow-up period was calculated from the finishing date of the 2014 survey to either the date of stroke occurrence, death, loss to follow-up, or the end of follow-up (December 31, 2020). We also examined the longitudinal association between the CVH score and arterial stiffness status, as assessed by brachial-ankle pulse wave velocity, in 25 922 participants free of cardiovascular disease during the follow-up. We performed a meta-analysis to assess the association between CVH, based on the 2010 American Heart Association recommendation, and stroke integrating the results of current study and previous studies. RESULTS: During a median follow-up of 5.65 years (interquartile range, 5.20–6.09), a total of 1750 incident stroke events were identified in the pooled Kailuan study. The pooled hazard ratios were 0.33 (95% CI, 0.20–0.54) for ideal versus poor health category of CVH ( P _trend <0.0001). Higher CVH scores were also associated with lower brachial-ankle pulse wave velocity values at baseline and slower increments of brachial-ankle pulse wave velocity during follow-up ( P _trend ≤0.001 for both). Arterial stiffness mediated 9.07% (95% CI, 5.83%–15.0%) of the total association between CVH and incident stroke. The pooled hazard ratio comparing 2 extreme CVH categories for stroke was 0.45 (95% CI, 0.35–0.59) when including 10 published studies and the current study. CONCLUSIONS: The CVH score as assessed by the Life’s Essential 8 metrics significantly predicted future stroke risk and arterial stiffness status.

Background: Whether the combination of different blood pressure and arterial stiffness (AS) status is independently associated with diabetes has not been fully investigated so far. This study aimed at investigating the status of hypertension and AS in determining diabetes. Methods: This prospective cohort study included 11 156 participants from the Kailuan study. AS was measured by brachial-ankle pulse wave velocity. We compared the risk of diabetes between individuals with ideal vascular function (defined as normotension with normal AS), normotension with elevated AS, hypertension with normal AS, and hypertension with elevated AS. Results: After a median follow-up of 6.16 years, diabetes occurred in 768 participants. Compared with ideal vascular function group, the highest risk of diabetes was observed in hypertension with elevated AS group (hazard ratio, 2.42 [95% CI, 1.93–3.03]), followed by normotension with elevated AS group (hazard ratio, 2.11 [95% CI, 1.68–2.66]), hypertension with normal AS group exhibited the lowest risk of diabetes (hazard ratio, 1.48 [95% CI, 1.08–2.02]). Multiple sensitivity and subgroup analyses yielded similar results. Furthermore, the additional of AS to a conventional model including traditional risk factors had a higher incremental effect on the predictive value for diabetes than the addition of hypertension (the C statistics was 0.707 versus 0.695; the integrated discrimination improvement was 0.65% versus 0.28%; net reclassification improvement was 40.48% versus 34.59%). Conclusions: Diabetes is associated with not only hypertension but also AS. Additionally, AS shows a better predictive ability than hypertension in predicting diabetes.

Background: The serum uric acid/serum creatinine ratio (SUA/SCr), which represents renal function‐normalized SUA, is associated with diverse adverse outcomes. The aim of this study was to investigate the association between SUA/SCr and cardiovascular disease (CVD), and determine whether and to what extent this association is mediated by cardiometabolic factors. Methods and Results: This prospective study enrolled 96 378 participants from the Kailuan study without stroke and myocardial infarction at baseline (2006). Cox proportional hazard models were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs). Mediation analyses were conducted to separately explore the mediating effects of cardiometabolic factors on the association between SUA/SCr and CVD. During median follow up of 11.01 years, 6315 (6.55%) individuals developed incident CVD. After adjustment for potential confounders, the highest quartile of SUA/SCr was associated with the highest risk of CVD (HR, 1.15; 95% CI, 1.07–1.23), stroke (HR, 1.16; 95% CI, 1.07–1.26), ischemic stroke (HR, 1.12; 95% CI, 1.02–1.22), and hemorrhagic stroke (HR, 1.36; 95% CI, 1.11–1.65), but not with myocardial infarction (HR, 1.07; 95% CI, 0.92–1.25). The association was consistent across different degrees of kidney function and glucose tolerance statuses. Additionally, the association between high SUA/SCr and CVD was partially mediated by triglycerides (30.74%), body mass index (BMI) (19.52%), total cholesterol (15.06%), hs‐CRP (high‐sensitivity C‐reactive protein) (13.06%), diastolic blood pressure (11.75%), and blood glucose (−16.38%). Conclusions: SUA/SCr and CVD were positively associated. Furthermore, this association was partially mediated through blood lipids, BMI, blood pressure, hs‐CRP, and blood glucose.

Background: Serum uric acid (SUA) has been demonstrated as a risk factor for myocardial infarction (MI) and all‐cause mortality; however, the impact of cumulative SUA (cumSUA) remains unclear. We aimed to investigate the association of cumSUA with MI risk and all‐cause mortality, and to further explore the effects of SUA accumulation time course. Methods and Results: The study enrolled 53 463 participants without a history of MI, and these participants underwent 3 examinations during 2006 to 2010. cumSUA from baseline to the third examination was calculated, multiplying mean values between consecutive examinations by time intervals between visits. Cox models estimated hazard ratios (HRs) and 95% CIs of MI and all‐cause mortality for cumSUA quartiles, hyperuricemia exposure duration, and SUA accumulation time course. During a median follow‐up of 7.04 years, 476 incident MIs and 2692 deaths occurred. In the fully adjusted model, a higher MI risk was observed in the highest cumSUA quartile (HR, 1.48; 95% CI, 1.10–1.99), in participants with longer hyperuricemia exposure duration (HR, 1.71; 95% CI, 1.06–2.73), and in participants with cumSUA≥median and a negative slope (HR, 1.58; 95% CI, 1.18–2.11). Similar associations persisted for all‐cause mortality. Conclusions: The risk of MI and all‐cause mortality increased with higher cumSUA and was affected by the SUA accumulation time course. Early SUA accumulation contributed more to MI risk and all‐cause mortality than later SUA accumulation with the same overall cumulative exposure, emphasizing the importance of optimal SUA control early in life.

BACKGROUND: Hypertension and enlarged perivascular spaces (EPVS) are thought to be associated with cognitive impairment. However, the correlations among hypertension, EPVS, and cognitive impairment have not been studied yet. We aimed to investigate the relationships between cumulative blood pressure (cBP) exposure with EPVS and cognitive impairment and whether EPVS may mediate the relationship between cBP and cognitive impairment. METHODS: A total of 1507 subjects from the Kailuan prospective cohort study were enrolled. cBP was calculated from 2006 to 2022. The effects of cBP, EPVS scores, and cognitive impairment were evaluated using a logistic regression model. The relationships among cBP, EPVS score, and cognitive impairment were analyzed using a mediation model. RESULTS: An increase in cBP was positively correlated with an increase in EPVS score. For every SD increase in cBP, the odds ratios (95% CI) of increased EPVS score of the centrum semiovale were 1.67 (1.43–1.95), 1.63 (1.4–1.9), and 1.35 (1.17–1.56), respectively; the odds ratios (95% CI) of increased EPVS score of the basal ganglia were 1.83 (1.56–2.15), 2.01 (1.7–2.36), and 1.31 (1.13–1.52), respectively; and the odds ratios (95% CI) of developing cognitive impairment were 1.28 (1.06–1.53), 1.13 (0.95–1.34), and 1.28 (1.07–1.5), respectively. Basal ganglia-EPVS score accounted for 10.46% to 18.32% of the mediating effects on the relationships of cBP/SD with cognitive impairment. CONCLUSIONS: High cBP exposure was an independent risk factor for EPVS, and basal ganglia-EPVS score mediated the effects of cBP on cognitive impairment. REGISTRATION: URL: https://www.clinicaltrials.gov ; Unique identifier: ChiCTR-TNRC-11001489.