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The association between cumulative mean arterial blood pressure (MAP) and risks of adverse cardiac and cerebrovascular events (CCVEs) has not been characterized. This prospective cohort study included 53,813 participants, free of prior myocardial infarction or stroke in or before 2010 (baseline) from a community-based cohort including 101,510 participants. Cumulative MAP was defined as the summed average MAP for each pair of consecutive examinations multiplied by the time interval with the data from previous surveys (2006- 2007, 2008 to 2009, 2010-2011). Incident adverse CCVEs were ascertained by both the information collection in biennial follow-up surveys (2012-2013, 2014-2015) and surveying each year's discharge lists from local hospitals and death certificates from state vital statistics offices by three experienced physicians blinded to the study design. The study population were stratified into quartiles based on cumulative MAP (

This study aims to investigate the correlation between the trajectory of systolic blood pressure (SBP) and new renal damage in a nonhypertensive population.This prospective cohort study included a total of 14 382 nonhypertensive individuals, employees of Kailuan Group of Companies, who took part in five healthy examinations in 2006-2007, 2008-2009, 2010-2011, 2012-2013, and 2014-2015, and had complete data. These individuals were divided into four groups according to the different trajectories of SBP: low-low, low-stable, middle-high, and high-high groups. The correlation between the trajectory of SBP and new renal damage in a nonhypertensive population was analyzed using a multivariate Cox's proportional hazard regression model.(a) A total of 14 382 individuals had complete data and the average age of these individuals was 44.6±10.8 years. Among these, 10 888 (75.7%) individuals were men and 3494 (24.3%) individuals were women. (b) These individuals were divided into four groups according to different trajectories of blood pressure: low-low group, accounting for 13.15% (blood pressure was106 mmHg); low-stable group, accounting for 53.91% (blood pressure was between 115 and 116 mmHg); middle-high group, accounting for 28.77% (blood pressure was between 125 and 131 mmHg); and high-high group, accounting for 4.6% (blood pressure was between 126 and 151 mmHg). (c) With the increase in the trajectory of SBP, the detection rate of renal damage increased gradually. From the low-low group to the high-high group, the detection rates of estimated glomerular filtration rate (eGFR) less than 60 ml/min/1.73 m were 2.3, 2.4, 3.6, and 4.3%, respectively; the positive rates of urinary protein were 1.7, 2.9, 3.8, and 5.5%, respectively; and the detection rates of eGFR less than 60 ml/min/1.73 m or positive urinary protein were 4, 5.2, 7.3, and 9.3%, respectively (P0.05). (d) After adjustment for other confounding factors, multivariate Cox's proportional hazard regression analysis showed that compared with the low-low group, the risk of eGFR less than 60 ml/min/1.73 m increased by nearly 1.5 times in the high-high group and in the low-stable, middle-high, and high-high groups, the risks of positive urinary protein, eGFR less than 60 ml/min/1.73 m, or positive urinary protein increased by 1.48-2.34 and 1.20-1.70 times, respectively.In a nonhypertensive population, the high trajectory of SBP is a risk factor for kidney damage.

The aim of this study was to investigate whether clinic, cumulative, and 24h ambulatory systolic blood pressure (SBP) was associated with chronic kidney damage, defind as estimated glomerular filtration rate (eGFR)60 ml/(min·1.73 m2) and/or microalbuminuria ≥30 mg/L, and, if so, which measurement of SBP is more associated with chronic kidney damage in Chinese elderly. A total of 1207 participants older than 60 years old were included in the final analysis. Clinical blood pressure, cumulative blood pressure exposure was calculated and ambulatory 24h blood pressure was assessed. Multiple logistic regression analysis showed that the clinic (p .001), cumulative (p = .033), 24h average (p .001), daytime (p = .001) and nighttime SBP (p = .001) were respectively associated with lower eGFR, and cumulative (p = .008), 24 average (p .001), daytime (p .001), and nighttime SBP (p .001) were the risk factors of microalbuminuria. The degree of correlation were strongest between 24h average SBP and chronic kidney damage (odds ratio, 1.78; 95% confidence interval, 1.46-2.15; p .001), clinic SBP and eGFR (odds ratio, 1.57; 95% confidence interval, 1.13-2.17; p = .007), nighttime SBP and microalbuminuria (odds ratio, 1.45; 95% confidence interval, 1.05-2.00; p = .024). The likelihood ratio test demonstrated that the introduction of 24h average SBP will improve the goodness of fit of the clinic SBP model(p .05), while the introduction of cumulative SBP exposure has no such effect(p .05). Cumulative SBP exposure seems inferior to other measurement in indentifying chronic kidney damage, including decreased GFR and microalbuminuria.

Background and Purpose It remains unclear whether resting heart rate (RHR), particularly cumulative exposure to resting heart rate (cumRHR), is associated with stroke. The aim of our study was to prospectively explore the relationship between cumRHR and stroke morbidity. Materials and Methods The Kailuan study is a prospective longitudinal cohort study on cerebrovascular events and cardiovascular factors. Hazard ratios (HRs) with 95% confidence interval (CI) were calculated using a Cox competing risk model. Results A total of 46,568 participants were included in the final analysis. In the observation population, we identified 851 stroke events and 1012 incident death cases in the 4.98 ± .51 year followed-up. Each 46.74 (beats/min) × year increase in heart rate was associated with a 12% increase in the risk of stroke (HR = 1.12, 95% CI = 1.05-1.20). In the categorical model, the highest quartile had an increased risk of stroke (HR = 1.43, 95% CI = 1.13-1.81), compared with the bottom quartile. Gender and age had no interaction with cumRHR for the risk of stroke. Conclusion Increase of exposure to cumulative heart rate is independently associated with a higher risk of stroke in the general population.

The relationship between cumulative exposure to resting heart rate (cumRHR) and mortality remain unclear in the general population. In the Kailuan cohort study, resting heart rate (RHR) was repeatedly measured at baseline and at years 2 and 4 by electrocardiogram among 47,311 adults aged 48.70 ± 11.68. The cumRHR was defined as the summed average RHR between two consecutive examinations multiplied by the time interval between with two examinations [(beats/min) * year]. A higher RHR was defined as ≥80 beats/min, and the number of visits with a higher RHR was counted. During a median of 4.06 years of follow-up, a total of 1,025 participants died. After adjusting for major traditional cardiovascular risk factors and baseline RHR, the hazard ratio for the highest versus lowest quartile of cumRHR was 1.39 (95% CI: 1.07–1.81) for all-cause mortality. Each 1-SD increment in cumRHR was associated with a 37% (HR: 1.37, 95% CI: 1.23–1.52) increased risk of death and displayed a J-shaped relationship. Compared with no exposure, adults who had a higher RHR at all 3 study visits were associated with a 1.86-fold higher risk (95% CI: 1.33–2.61) of mortality. In summary, cumulative exposure to higher RHR is independently associated with an increased risk of mortality.

Objective To identify long-term fasting blood glucose trajectories and to assess the association between the trajectories and the risk of arterial stiffness in individuals without diabetes. Methods We enrolled 16,454 non-diabetic participants from Kailuan cohort. Fasting blood glucose concentrations were measured in 2006, 2008, and 2010 survey. Brachial-ankle pulse wave velocities were measured during 2011 to 2016. Multivariate regression model was used to estimate the difference of brachial-ankle pulse wave velocity levels and logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (95%CIs) of arterial stiffness risk, according to the fasting blood glucose trajectories. Results We identified five distinct fasting blood glucose trajectories and each of the trajectories was labeled according to its range and change over 2006–2010 survey: elevated-stable pattern (5.0% of participants), elevated-decreasing pattern (6.6%), moderate-increasing pattern (10.9%), moderate-stable pattern (59.3%), and low-stable pattern (18.2%). After adjustment for potential confounders, individuals with elevated-stable pattern had a 42.6 cm/s (95%CI: 24.7 to 60.6 cm/s) higher brachial-ankle pulse wave velocity level and a 37% (OR 1.37, 95%CI: 1.14 to 1.66) higher arterial stiffness risk, and individuals with moderate-increasing pattern had a 19.6 cm/s (95%CI: 6.9 to 32.3 cm/s) higher brachial-ankle pulse wave velocity level and a 17% (OR 1.17, 95%CI: 1.03 to 1.33) higher arterial stiffness risk, related to individuals with moderate-stable pattern. We did not find significant associations of the elevated-decreasing or low-stable patterns with arterial stiffness. Consistently, the cumulative average, variability, and increased rate of fasting blood glucose during 2006–2010 survey were significantly associated with the arterial stiffness risk. Conclusion Discrete fasting blood glucose trajectories were associated with the arterial stiffness risk in non-diabetic individuals.