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Few prospective studies have assessed the blood pressure effect of extremely high air pollution encountered in Asia's megacities. The objective of this study was to evaluate the association between combustion-related air pollution with ambulatory blood pressure and autonomic function. During February to July 2012, personal black carbon was determined for 5 consecutive days using microaethalometers in patients with metabolic syndrome in Beijing, China. Simultaneous ambient fine particulate matter concentration was obtained from the Beijing Municipal Environmental Monitoring Center and the US Embassy. Twenty-four-hour ambulatory blood pressure and heart rate variability were measured from day 4. Arterial stiffness and endothelial function were obtained at the end of day 5. For statistical analysis, we used generalized additive mixed models for repeated outcomes and generalized linear models for single/summary outcomes. Mean (SD) of personal black carbon and fine particulate matter during 24 hours was 4.66 (2.89) and 64.2 (36.9) μg/m(3). Exposure to high levels of black carbon in the preceding hours was associated significantly with adverse cardiovascular responses. A unit increase in personal black carbon during the previous 10 hours was associated with an increase in systolic blood pressure of 0.53 mm Hg and diastolic blood pressure of 0.37 mm Hg (95% confidence interval, 0.17-0.89 and 0.10-0.65 mm Hg, respectively), a percentage change in low frequency to high frequency ratio of 5.11 and mean interbeat interval of -0.06 (95% confidence interval, 0.62-9.60 and -0.11 to -0.01, respectively). These findings highlight the public health effect of air pollution and the importance of reducing air pollution. [ABSTRACT FROM AUTHOR]

Lipid abnormalities are an important cause of premature atherosclerosis in patients with systemic lupus erythematosus (SLE). This longitudinal study investigates the changes in lipid profile and arterial stiffness with SLE disease activity index (SLEDAI) reduction.Fifty one female SLE patients with baseline SLEDAI ≥ 6 and SLEDAI reduction >3 at 1-year follow-up were included. Neutrophil-to-lymphocyte ratio (NLR), erythrocyte sedimentation rate (ESR), high-sensitivity C-reactive protein (hsCRP), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), triglyceride (TG), and mean brachial-ankle pulse wave velocity (baPWV) were measured and compared between baseline and 1-year follow-up. Correlations between inflammation biomarkers, SLEDAI, mean baPWV and lipid profile were assessed.We observed significant decreases in ESR, mean baPWV, TG and TC to HDL-C ratio compared with baseline at 1-year follow up, while HDL-C, hsCRP, and NLR were not significantly changed. Significant correlations were found between the reductions in ESR and TG, and SLEDAI and mean baPWV, with adjustment to age, disease duration, blood pressure, and medications (prednisone, immunosuppressants and ARB/ACEI).SLE patients experiencing SLEDAI reductions showed improvements in arterial stiffness. This finding may provide insight into the beneficial effects of reducing SLEDAI on atherosclerosis risk in SLE.

Background: Several updated meta-analyses comparing percutaneous coronary intervention (PCI) with coronary artery bypass grafting (CABG) for left main coronary artery disease (LM CAD) have been published recently. However, the risk of false-positive results could be high in conventional updated meta-analyses due to repetitive testing of accumulating data. Therefore, we compared these treatment approaches via trial sequential analysis (TSA)., Methods: The MEDLINE, Embase, and Cochrane Central Register of Controlled Trials databases were searched for published randomized controlled trials (RCTs) or subgroups of RCTs comparing PCI and CABG in patients with LM CAD. The primary outcome was major cardiac and cerebrovascular adverse events (MACCE). TSA was used to confirm the conclusions derived from conventional meta-analysis., Results: Six RCTs with 4700 patients were included. PCI was associated with a greater risk of MACCE compared with CABG (pooled relative risk [RR] 1.21, 95% confidence interval [CI]: 1.05-1.40, P = .008). In addition, PCI resulted in a significantly higher risk of revascularization than CABG (pooled RR 1.61, 95% CI: 1.33-1.95, P < .0001). TSA provided firm evidence for the reduction of MACCE and revascularization with CABG compared with PCI (cumulative z-curve crossed the monitoring boundary). In the subgroup analysis, CABG was better than PCI in patients with SYNTAX score >32 (pooled RR 1.41, 95% CI: 1.12-1.76, P = .003), which was confirmed by the TSA. There was no difference in patients with a SYNTAX score from 0 to 32., Conclusions: In patients with LM CAD, CABG may be better than PCI for reducing MACCE due to a reduced risk of revascularization. CABG remains the first choice for LM CAD patients with high anatomic complexity, while PCI could be an alternative for those with low-to-moderate anatomic complexity.

The plasma levels of asymmetric dimethylarginine (ADMA) had been proved to be an independent cardiovascular risk factor. Few studies involved the entire arginine methylation dysfunction. This study was designed to investigate whether arginine methylation dysfunction is associated with acute coronary syndrome risk in coronary artery disease population.In total 298 patients undergoing coronary angiography because of chest pain with the diagnosis of stable angina pectoris or acute coronary syndrome from February 2013 to June 2014 were included. Plasma levels of free arginine, citrulline, ornithine, and the methylated form of arginine, ADMA, and symmetric dimethylarginine (SDMA) were measured with high-performance liquid chromatography coupled with tandem mass spectrometry. We examined the relationship between arginine metabolism-related amino acids or arginine methylation index (AMI, defined as ratio of [arginine + citrulline + ornithine]/[ADMA + SDMA]) and acute coronary events.We found that plasma ADMA levels were similar in the stable angina pectoris group and the acute coronary syndrome group (P = 0.88); the AMI differed significantly between 2 groups (P < 0.001). Multivariate logistic regression demonstrated that AMI was an independent risk factor of acute coronary events in patients with coronary artery disease (OR = 0.975, 95% confidence interval 0.956-0.993; P = 0.008).Our study suggested that ADMA levels were very similar in the stable angina and acute coronary syndrome patients; AMI might be an independent risk factor of acute coronary events in coronary artery disease population.

Introduction: We herein describe a patient with chronic disseminated intravascular coagulation (DIC) induced by a giant thrombus in the left atrium.A 63-year-old woman was admitted to our hospital for evaluation of extensive mucocutaneous hemorrhage, especially at the sites of venipuncture, on May 21, 2015. Considering her long history of rheumatic heart disease and atrial fibrillation and her mitral valve replacement performed several years previously, we strongly suspected that the bleeding was closely related to postoperative over-anticoagulation of warfarin. After careful investigation, we found that her coagulopathy was induced by the chronic DIC, which was in turn secondary to a left atrial giant thrombus. This is a rarely reported cause of chronic DIC. Cardiac computed tomography and echocardiography showed apparent biatrial enlargement; the morphology and function of the ventricles were unaffected. After anticoagulant therapy, the bleeding tendency and coagulation index were significantly improved., Conclusion: A left atrial thrombus should be considered as a differential diagnosis of chronic DIC, especially in patients with predisposing heart conditions. Because treatment of the underlying cause is paramount in the management of chronic DIC, this case is of great clinical value., Competing Interests: The authors have no conflicts of interest to disclose.

Background: An increased prevalence of arterial stiffness in systemic lupus erythematosus (SLE) patients has been established, but the mechanisms of progression of arterial stiffness with increasing age have not been fully explored., Objectives: To investigate age-related progression of arterial stiffness among SLE patients relative to healthy controls., Methods: A total of 161 female SLE patients who were enrolled in the Chinese SLE Treatment and Research group (CSTAR) registry and 135 age-matched healthy control subjects participated in this cross-sectional investigation. Traditional cardiovascular risk factors and SLE-related parameters were assessed on the day that brachial-ankle pulse wave velocity (baPWV) was examined. SAS 9.3 was used to perform all statistical analyses in this study. Linear regression and curvilinear regression models were utilized to analyze the association between age and arterial stiffness., Results: Arterial stiffness based on baPWV significantly differed between the SLE patients and controls in the different age groups, and within the SLE group. The baPWV increments for each age group (<25, 25-34, 35-45, and >45) were 30 cm/s, 52 cm/s, and 121 cm/s for the controls and 61 cm/s, 132 cm/s, and 155 cm/s for the SLE patients, respectively. Curvilinear regression and linear regression revealed various trends of increased arterial stiffness among the SLE patients compared with the healthy controls. The correlation coefficients between age and arterial stiffness significantly differed among the SLE patients relative to the healthy controls (correlation coefficients of 0.46478 and 0.52612, respectively; t = 2.05; P = 0.0409). Multivariate analysis revealed that age, mean blood pressure (BP) (P < 0.0001), erythrocyte sedimentation rate (ESR) (P = 0.0073), prednisone course (P = 0.0144), and SLE disease activity (P = 0.0405) were associated with arterial stiffness among the SLE patients. Further, these patients exhibited earlier exposure to and higher frequencies of several risk factors compared with the controls in each age group (<25 years: OR = 6.3253; 25-34 years: OR = 3.1043; 35-45 years: OR = 3.1316; >45 years: OR = 3.6020)., Conclusions: The mechanisms of the age-related progression of arterial stiffness differed among the SLE patients relative to the healthy controls. Furthermore, accelerated arterial stiffness was observed among the SLE patients relative to the healthy controls with advancing age.

Objectives: This study was performed to determine the relationship between systemic lupus erythematosus (SLE) and the interarm blood pressure difference (IAD) and to elucidate the role of the IAD as a surrogate marker for early detection of peripheral artery disease (PAD) in patients with SLE., Methods: In total, 135 patients with SLE and 135 age- and gender-matched subjects were enrolled. The IAD and risk of an abnormal IAD were compared between the SLE and control groups, and logistic regression analysis was performed to determine the relationship between SLE and an abnormal IAD. The specificity and sensitivity of an IAD of 10 mm Hg or greater for diagnosis of PAD (ankle brachial index of <0.90) were calculated., Results: Both the systolic and diastolic IADs were significantly higher in the SLE group than in the control group (P < 0.001). After adjustment for confounding factors, SLE remained significantly associated with an abnormal IAD (P = 0.039). Both the systolic and diastolic IADs were negatively associated with the ankle brachial index. Using a systolic IAD of 10 mm Hg or greater as the cutoff point, the specificity and sensitivity for PAD were 90% and 41%, respectively. A diastolic IAD of 10 mm Hg or greater exhibited higher specificity (92%), but lower sensitivity (30%)., Conclusions: Systemic lupus erythematosus is independently associated with an abnormal IAD, and an IAD of 10 mm Hg or greater predicts PAD with high specificity but low sensitivity. Blood pressure should be measured at least once in both arms in patients with SLE for early detection of asymptomatic PAD.

We compared the efficacy of cilostazol for the prevention of late restenosis and acute or subacute stent thrombosis with that of ticlopidine. Cilostazol has been used for antiplatelet therapy after coronary stent implantation, but the results are controversial. Patients scheduled for stent implantation were randomly assigned to receive either cilostazol (100 mg twice daily for 6 months, n=201) or ticlopidine (250 mg twice daily for 1 month, n=196). All patients also received oral aspirin (100 mg once daily for 6 months). Coronary angiography was performed at baseline and immediately and 6 months after coronary stenting. Clinical follow-up was continued up to 9 months postprocedure. There was no significant difference in the composite incidence of death, myocardial infarction, stroke, and stent thrombosis between the 2 groups [cilostazol (1.5%) versus ticlopidine (3.6%), P=0.216], but the target lesion revascularization rate per patient was significantly lower in the cilostazol group than in the ticlopidine group (22.9% vs 32.7%, P=0.030) 9 months post-coronary stenting. Medication withdrawn because of drug-related side effects tended to be higher in the ticlopidine group than that in the cilostazol group (3.5% vs 8.2%, P=0.054). At follow-up angiography, the minimal luminal diameters (2.31+/-1.06 vs 2.10+/-1.16, P=0.057) tended to be larger and the restenosis rates lower (23.3% vs 30.9%, P=0.086) in the cilostazol group than in the ticlopidine group. Aspirin plus cilostazol is a comparable antithrombotic regimen to aspirin plus ticlopidine after elective coronary stenting, but the rate of target lesion revascularization was significantly lower in the cilostazol group than in the ticlopidine group.