Objective: To evaluate the difference of plasma myeloperoxidase (MPO) level in different types of acute coronary syndrome (ACS) patients, and the value of baseline MPO level in predicting short-term and long-term outcomes in patients with ACS. Methods: The study cohort was derived from "the 12th Five-Year" National Science and Technology Support Program Project "Study on Comprehensive Intervention and Prognosis of Acute Coronary Syndrome" . We enrolled all hospitalized ACS patients who were enrolled in "the 12th Five-Year" cohort from January 1, 2011 to December 31, 2013. A total of 630 patients from 20 centers were enrolled. According to the diagnosis, the patients were divided into two groups: ST-segment elevation myocardial infarction (STEMI) group and non-ST-elevation acute coronary syndrome (NSTE-ACS) group. Plasma levels of MPO were measured by ELISA method. Cardiovascular events in the hospital were recorded. All patients were followed-up by telephone, follow-up ended December 31, 2015. The occurrence of major adverse cardiovascular events (MACE, defined as cardiac death, recurrent myocardial infarction, unscheduled coronary revascularization procedure and stroke) and all-cause death were recorded. Logistic regression analysis and Cox regression analysis were used to evaluate the predictive value of baseline MPO levels obtained during hospitalization and the long-term outcomes of ACS patients. Results: A total of 597 ACS patients were enrolled in final analysis. Level of plasma MPO in STEMI patients was significantly higher than that of NSTE-ACS patients (34.02(19.31, 67.87) μg/L vs. 27.25(16.69, 52.92) μg/L, P=0.028) . MPO was not related to the in-hospital cardiovascular events (OR=0.797, 95%CI 0.366-1.737, P=0.569). Follow up was completed in 476 patients, median follow-up time was 796 (32, 1 816) days. There were 23 all-cause deaths and 51 MACE. Plasma MPO level was not an independent predictor for all-cause death (HR=1.434, 95%CI 0.502-4.100, P=0.501) and MACE (HR=1.271, 95%CI 0.662-2.442, P=0.471). Conclusion In hospitalized ACS patients, level of plasma MPO was significantly higher in STEMI patients than in NSTE-ACS patients, but MPO could not predict the short-term or long-term outcomes in patients with ACS.

Objective:To investigate the effects of exposure to ambient fine particulate matter-bound polycyclic aromatic hydrocarbons on blood coagulation in adults.Methods:A total of 73 adult volunteers were recruited in a cohort study and had four clinical visits from November 2014 to January 2016. Blood samples were obtained and used to measure biomarkers of blood thrombogenicity, including soluble CD40 Ligand (sCD40L), soluble P-selection (sCD62P) and Fibrinogen (FIB). White blood cell (WBC), 8-Hydroxy-2′-Deoxyguanosine (8-OHdG), matrix metalloproteinase-2 (MMP-2) and HDL cholesterol efflux capacity (HDL-CEC) were also determined. Daily concentrations of ambient fine particulate matter-bound polycyclic aromatic hydrocarbons (PAHs) were measured throughout the study period, and positive matrix factorization (PMF) approach was used to identity PAHs sources. Linear mixed-effect models including single-pollutant model, two-pollutant model and stratification analysis were constructed to estimate the effects of exposure to ambient fine particulate matter-bound PAHs on blood thrombogenicity in adults after adjusting for potential confounders.Results:The mean age of participants was (23.3±5.4) years. During the study period, the median level of PM 2.5-bound PAHs was (55.29±74.99) ng/m 3. Six sources of PM 2.5-bound PAHs were identified by PMF, with traffic sources contributing more than 50%. The linear mixed-effect model showed that PAHs exposure had a significant effect on elevated blood thrombogenicity. Significant elevations in sCD40L, sCD62P and FIB associated with per IQR increase (60.33 ng/m 3) in exposure to PAHs were 14.36% (95% CI:6.94%-22.28%), 9.33% (95% CI: 1.71%-17.51%) and 2.07% (95% CI:0.44%-2.07%) at prior 5 days, respectively. Blood thrombogenicity levels were significantly and positively correlated with source-specific PAHs, especially gasoline vehicle emissions, diesel vehicle emission and coal burning at prior 1 or 5 days. Stronger associations between PAHs and increased blood thrombogenicity were found in participants with high plaque vulnerability, reduced HDL function, and high levels of inflammation and oxidative stress. Conclusion:Acute exposure to ambient fine particulate matter-bound PAHs, especially PAHs from traffic sources may promote blood thrombogenicity in adults, and PAHs have stronger effects on participants with reduced vascular function and high levels of inflammation and oxidative stress.

Objective:To investigate the effects of exposure to ambient fine particulate matter-bound polycyclic aromatic hydrocarbons on blood coagulation in adults.Methods:A total of 73 adult volunteers were recruited in a cohort study and had four clinical visits from November 2014 to January 2016. Blood samples were obtained and used to measure biomarkers of blood thrombogenicity, including soluble CD40 Ligand (sCD40L), soluble P-selection (sCD62P) and Fibrinogen (FIB). White blood cell (WBC), 8-Hydroxy-2′-Deoxyguanosine (8-OHdG), matrix metalloproteinase-2 (MMP-2) and HDL cholesterol efflux capacity (HDL-CEC) were also determined. Daily concentrations of ambient fine particulate matter-bound polycyclic aromatic hydrocarbons (PAHs) were measured throughout the study period, and positive matrix factorization (PMF) approach was used to identity PAHs sources. Linear mixed-effect models including single-pollutant model, two-pollutant model and stratification analysis were constructed to estimate the effects of exposure to ambient fine particulate matter-bound PAHs on blood thrombogenicity in adults after adjusting for potential confounders.Results:The mean age of participants was (23.3±5.4) years. During the study period, the median level of PM 2.5-bound PAHs was (55.29±74.99) ng/m 3. Six sources of PM 2.5-bound PAHs were identified by PMF, with traffic sources contributing more than 50%. The linear mixed-effect model showed that PAHs exposure had a significant effect on elevated blood thrombogenicity. Significant elevations in sCD40L, sCD62P and FIB associated with per IQR increase (60.33 ng/m 3) in exposure to PAHs were 14.36% (95% CI:6.94%-22.28%), 9.33% (95% CI: 1.71%-17.51%) and 2.07% (95% CI:0.44%-2.07%) at prior 5 days, respectively. Blood thrombogenicity levels were significantly and positively correlated with source-specific PAHs, especially gasoline vehicle emissions, diesel vehicle emission and coal burning at prior 1 or 5 days. Stronger associations between PAHs and increased blood thrombogenicity were found in participants with high plaque vulnerability, reduced HDL function, and high levels of inflammation and oxidative stress. Conclusion:Acute exposure to ambient fine particulate matter-bound PAHs, especially PAHs from traffic sources may promote blood thrombogenicity in adults, and PAHs have stronger effects on participants with reduced vascular function and high levels of inflammation and oxidative stress.

Objective:The exact biological mechanism whereby exposure to ambient ozone(O3)may contribute to clinical onset of cardiovascular events remains unclear.In this study,we aim to examine the impacts of O3 exposure on cardiac arrhythmias and potential pathways involved through autonomic dysfunction and myocardial injury.Methods:Seventy-three non-smoking healthy adults were followed with 4 repeated measurements of 24-hour ambulatory arrhythmias,heart rate variability,ST-segment deviation,and blood pressure(BP)in Beijing,China,2014-2016.Generalized additive mixed models coupled with distributed lag nonlinear models were constructed to evaluate the associations and potential interlinks between O3 exposure and outcome measurements.Results:During the study period,24-hour average concentrations of ambient O3 were 47.4 μg/m3(ranging from 1.0 to 165.9 μg/m3).Increased risks of premature ventricular contraction and ventricular tachycardia were associated with interquartile range increases in O3 exposure during the last 5 days before each participant's clinic visit,with relative risks of 2.14(95％confidence interval[CI]:1.95 to 2.32)and 5.47(95％CI:3.51 to 7.43),respectively.Mediation analyses further showed that sympathetic activation,parasympathetic inhibition,and elevated BP levels,as well as heightened risks of ST-segment depression could mediate up to 47.74％of the risks of arrhythmias attributable to O3 exposure.Conclusion:Our results suggest that short-term exposure to ambient O3 could prompt the genesis of arrhythmias partially through worsening autonomic function and myocardial burden.