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ObjectiveTo assess both short-term and long-term prognosis in consecutive patients with coronary heart disease treated with drug-eluting stents in a high-volume percutaneous coronary intervention (PCI) centre.DesignObservational cohort study.SettingA hospital in the Henan province, China, between 2009 and 2011.ParticipantsA total of 2533 patients were enrolled. Patients with ST-elevation myocardial infarction (STEMI) treated with urgent PCI accounted for 3.9% of cases; patients with STEMI treated with delayed PCI accounted for 20.5% of cases; patients with stable angina accounted for 16.5% of cases; and patients with non-ST elevation acute coronary syndrome (NSTE-ACS) accounted for 58.6% of cases.Primary outcomesDeath, major adverse cardiac and cerebrovascular events (MACCE: death/myocardial infarction/stroke), and target vessel revascularisation.ResultsFollow-up after a median of 29.8 months was obtained for 2533 patients (92.6%). The mortality rate during hospitalisation was highest in the urgent PCI group (p<0.001). During follow-up, although the incidences of death and MACCE were highest in the urgent PCI group, no significant differences were observed among the different groups. The incidences of cardiac death and myocardial infarction were significantly higher in the paclitaxel-eluting stent (PES) group than in the sirolimus-eluting stent (SES) group. Independent predictors of death during follow-up were age, left ventricular ejection function <40%, diabetes mellitus, prior coronary artery bypass graft and chronic total occlusion.ConclusionsPCI patients with STEMI had the worst hospital and long-term prognosis. The mortality rate after hospital increased markedly in patients with NSTE-ACS. SESs seem to be more effective than PESs.

Maslinic acid (MA) is a natural triterpenoid widely distributed in edible and medicinal plants and has been demonstrated to possess bioactivity. However, its effect on vascular smooth muscle cells (VSMC) has not been explored yet. In this study, we found that heme oxygenase-1 (HO-1) expression was increased in VSMCs treated with MA. Furthermore, MA was found to induce Akt activation in a dose- and time-dependent manner. Wortmannin suppression of Akt was able to abolish HO-1 upregulation in VSMCs, suggesting the requirement of Akt activation for MA effect on HO-1. Further investigation indicated that Akt activation resulted in the elevated expression of Nrf2, a HO-1 promoter, in MA-treated VMSCs. Finally, we found that MA was able to protect VSMCs from oxidative stress induced by H2O2. Blocking the activation of Akt/Nrf2/HO-1 was able to compromise the protective effect of MA on VSMCs. Collectively, we provided evidence that MA protected VMSCs from oxidative stress through Akt/Nrf2/HO-1 pathway.

TSN exerts antifibrotic effects in postinfarct cardiac fibrosis by upregulating the expression of miR-29b, which is mediated by the TGF-β-Smad3 signaling pathway.