Objects: To discuss the influence of PM2.5 on myocardial fibrosis and related mechanism. Methods: PM2.5 particles were prepared into different concentrations of solution to drip into the mice’s trachea twice each week. The mice were divided into five groups, Blank control group (C group), NS control group (J group), high dose group (G group, 10 mg/kg), medium dose group (Z group, 5 mg/kg), and 1ow dose group (D group, 2.5 mg/kg). After 6 weeks, the myocardial fibrosis was observed by HE and Masson staining. The expression of Ang II, ERK1/2, and TGF-β1 was examined by Western Blotting (WB) and Real time PCR (RT-PCR). Results: The higher dose PM2.5 was administrated, the worse the myocardial fibrosis was in PM2.5 groups. The expression of Ang II, ERK1/2, and TGF-β1 was increased in higher dose groups in protein and mRNA level. Conclusion: 1. PM2.5 induced the cardiac fibrosis. 2. PM2.5 dripped into trachea in mice model activated the expression of Ang II, ERK1/2, and TGF-β1. The activation of renin-angiotensin system (RAS) was suggested to participate in the cardiac fibrosis induced by PM2.5.

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Objectives To identify the predictors of long-term outcome in consecutive patients with angiographically proven stent thrombosis (ST). Methods Consecutive patients with angiographically proven ST in our centre were enrolled from January 2005 to December 2011. Demographic data, medical history, electrocardiography findings, ultrasound findings, laboratory test results and treatments administered to patients were collected. The primary endpoint of the study was cardiac death. Major adverse cardiac events (MACE) included cardiac death, recurrent definite ST, non-fatal myocardial infarction (MI) and target-vessel revascularisation (TVR). Cox regression analysis was applied to assess the association between variables and cardiac death and MACE. Results Four-nine patients with angiographically proven ST were reported in our centre from January 2005 to December 2011. Among them, 5 patients (10.2%) died from cardiac-related causes in hospital. Until September 30, 2012, 44 patients accepted follow-up. The average follow-up time was 1149.3 ± 710.1 days (274 to 2824 days). The in-hospital and one-year mortality were 10.2%, and 12.4% respectively. The cumulative incidence of in-hospital development of MACE was 12.2%. And the incidences at 2, 4 and 5 years were 18.5%, 24.8%, and 37.3%, respectively. Our study showed that family history of coronary artery disease (CAD) and two-vessel ST could be used as independent predictors of cardiac death (hazard ratio 27.70, 95% CI 2.34 to 328.81, P = 0.008 and 20.04, 95% CI 1.63 to 246.16, P = 0.019, respectively), and they could be used to predict MACE (hazard ratio 8.76, 95% CI 2.50 to 30.70, P = 0.001 and 9.21, 95% CI 1.73 to 49.19, P = 0.009, respectively) as well. Conclusions Patients who suffered from ST were considered to have a poor prognosis. In addition, family history of CAD and simultaneous two-vessel ST were associated with the cardiac death and MACE.