Objective: To analyze the trends on constituent ratio of non-ST-segment-elevation (NSTEMI) and ST-segment-elevation myocardial infarction (STEMI) and related in-hospital mortality in acute myocardial infarction (AMI) patients hospitalized in Beijing Anzhen Hospital from 2004 to 2014. Methods: This is a single-center, retrospective study. We reviewed all patients hospitalized for AMI in Beijing Anzhen Hospital from January 1 2004 to December 31 2014, and collected all related information including hospitalization stay, the type of AMI, revascularization and in-hospital mortality. We analyzed the trends of constituent ratio of NSTEMI and STEMI, and their in-hospital mortalities during the 11 years. Results: Data from a total of 23 864 patients with AMI, including 5 539 STEMI and 18 325 NSTEMI, were analyzed. Compared with STEMI patients, NSTEMI patients were older, less likely to be male (P<0.001), had higher prevalence of hypertension, hyperlipidemia, diabetes (P<0.001), and lower prevalence of smoking (P<0.001). Additionally, patients with NSTEMI were more likely to have prior history of MI (12.6% (695/5 539) vs. 7.4% (1 354/18 325), P<0.001) and coronary artery bypass graft surgery (2.7% (152/5 539) vs. 0.7% (124/18 325), P<0.001). The constituent ratio of NSTEMI was significantly increased during the observation period, rising from 15.8% (107/802) in 2004 to 35.7% (1 273/3 583) in 2014 (P value for trend <0.001). The in-hospital mortality of NSTEMI patients was significantly lower compared with those with STEMI (1.84% (102 cases) vs. 2.74% (502 cases), P<0.001). The mortality of both STEMI and NSTEMI were significantly decreased during the 11 years (both P value for χ² trend test <0.001). After adjusting for other risk factors, NSTEMI was independently associated with lower in-hospital mortality (OR=0.50, 95%CI 0.40-0.63, P<0.001). Conclusions In patients with AMI, the constituent ratio of NSTEMI versus STEMI is increased during the 11 years. The in-hospital mortality is decreased for both STEMI and NSTEMI patients in the past 11 years, and the in-hospital mortality rate of NSTEMI patients is lower than STEMI patients in this patient cohort during the observation period.

Background::Hyperglycemia frequently induces apoptosis in endothelial cells and ultimately contributes to microvascular dysfunction in patients with diabetes mellitus (DM). Previous research reported that the expression of integrins as well as their ligands was elevated in the diseased vessels of DM patients. However, the association between integrins and hyperglycemia-induced cell death is still unclear. This research was designed to investigate the role played by integrin subunit β5 (ITGB5) in hyperglycemia-induced endothelial cell apoptosis.Methods::We used leptin receptor knockout (Lepr-KO) ( db/ db) mice as spontaneous diabetes animal model. Selective deletion of ITGB5 in endothelial cell was achieved by injecting vascular targeted adeno-associated virus via tail vein. Besides, we also applied small interfering RNA in vitro to study the mechanism of ITGB5 in regulating high glucose-induced cell apoptosis. Results::ITGB5 and its ligand, fibronectin, were both upregulated after exposure to high glucose in vivo and in vitro. ITGB5 knockdown alleviated hyperglycemia-induced vascular endothelial cell apoptosis and microvascular rarefaction in vivo. In vitro analysis revealed that knockdown of either ITGB5 or fibronectin ameliorated high glucose-induced apoptosis in human umbilical vascular endothelial cells (HUVECs). In addition, knockdown of ITGB5 inhibited fibronectin-induced HUVEC apoptosis, which indicated that the fibronectin-ITGB5 interaction participated in high glucose-induced endothelial cell apoptosis. By using RNA-sequencing technology and bioinformatic analysis, we identified Forkhead Box Protein O1 (FoxO1) as an important downstream target regulated by ITGB5. Moreover, we demonstrated that the excessive macroautophagy induced by high glucose can contribute to HUVEC apoptosis, which was regulated by the ITGB5-FoxO1 axis. Conclusion::The study revealed that high glucose-induced endothelial cell apoptosis was positively regulated by ITGB5, which suggested that ITGB5 could potentially be used to predict and treat DM-related vascular complications.