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.

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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 (<354.62 mmHg, n = 13,454; 354.62 to 392.82 mmHg, n = 13,452; 392.82 to 438.04 mmHg, n = 13 453; ≥ 438.04 mmHg, n = 13,454). We documented 1055 incident adverse CCVEs, including 271 myocardial infarction and 794 stroke (10 comorbid with myocardial infarction), which consisted of 673 ischemic stroke and 134 hemorrhagic stroke (13 comorbid with ischemic stroke). The incidence of adverse CCVEs increased with the increase of cumulative MAP with significant difference (p < 0.001). Cox proportional hazards regression models revealed the elevated cumulative MAP as an independent risk factor for adverse CCVEs, especially hemorrhagic stroke, after adjusting potential confounders. A J-shaped relationship between cumulative MAP and hemorrhagic stroke was also observed.

ObjectiveTo 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.MethodsWe 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.ResultsWe 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.ConclusionDiscrete fasting blood glucose trajectories were associated with the arterial stiffness risk in non-diabetic individuals.