plaining of persistent chest pain for 4 h after dinner, accompanied by profuse sweating. The electrocardiogram (ECG) immediately revealed sinus tachycardia with no obvious abnormality of the ST-T segment in each lead (Figure 1a). After a while, the patient suddenly lost consciousness because of ventricular fibrillation, and he regained consciousness after extra-cardiac compression and electrical cardioversion. The ECG was rechecked and found to be normal with no significant changes (Figure 1b). The patient continued to complain of excruciating chest pain. Meanwhile, the laboratory tests revealed:Myo 124 ng/ml (0-107 ng/ml); cTnI 0.05 ng/mL (0-0.05 ng/ml); D-Dimer 0.4 ng/ml (<0.5 ng/ml). An urgent contrast-enhanced CT of the chest ruled out the diagnoses of "acute aortic dissection" and "acute pulmonary embolism." The third ECG revealed sinus tachycardia, 0.1 mV ST-segment elevation in leads II, III, and aVF compared to the first and second ECGs, without mirror changes in other leads (Figure 1c). The patient was highly suspected of having "acute inferior myocardial infarction" and was prepared for emergency PCI after receiving loading doses of aspirin and ticagrelor. The fourth ECG showed no obvious abnormality within 2 hours after admission before the operation (Figure 1d). Emergency transthoracic echocardiography showed normal sizes of cardiac chambers decreased anterior wall motion of the left ventricle, with LVEF of 55%. After adequate heparin anticoagulation, the emergency CAG showed total

Background：Endothelial cell apoptosis plays an important role in the progression of atherosclerosis. Oxidized low density lipoprotein (Ox-LDL) induces endothelial cell apoptosis through multiple signaling pathways. We investigated the role of FOXO3 activation in the development of atherosclerosis and ox-LDL induced mouse aortic endothelial cell (MAEC) apoptosis. Methods: In vivo, ApoE-/- mice atherosclerosis model was induced by high fat feeding and the FOXO3 expression in aorta endothelium were measured by IHC. In vitro，MAECs were induced with ox-LDL to establish an atherosclerosis model. The cell viability and apoptosis were measured by MTT and Hoechst 33342 staining. The FOXO3 expression was measured by Q-PCR. Then we constructed two plasmids: the interference vector for FOXO3 and the expression vector for FOXO3. The effects of the two plasmids on MAECs were evaluated. Results: The results of in vivo experiments showed that FOXO3 activation in mouse aortic endothelium was associated with atherosclerosis (ApoE mice model of atherosclerosis). Furthermore, ox-LDL triggers MAEC apoptosis. FOXO3 activation was associated with Ox-LDL-induced MAEC apoptosis. RNA interference-mediated reduction of FOXO3 expression blunted Ox-LDL-induced MAEC apoptosis. In contrast, overexpression of FOXO3 promoted Ox-LDL-induced MAEC apoptosis. Conclusions: FOXO3 activation is therefore involved in the development of atherosclerosis and MAEC apoptosis.

Background The triglyceride (TG)to high-density lipoprotein cholesterol (HDL-C) ratio has been regarded as an independent predictor of cardiovascular events. However, the association of TG/HDL-C ratio with survival in patients with diabetes and coronary artery disease (CAD) on statin therapy remains uncertain. The aim of the present study was to explore whether TG/HDL-C ratio predicts mortality in diabetic patients with CAD on statin treatment. Methods A total of 2080 consecutive patients with type 2 diabetes and angiographic-proven CAD who were treated with statin were enrolled in the presents study. Patients were divided into tertiles according to baseline TG/HDL-C ratio. The primary endpoints were all-cause and cardiovascular mortality. Results During 4-year follow-up, 209(10.0%) patients died, 136(65.1%) caused by cardiovascular disease (CVD). The Kaplan-Meier analyses showed that all-cause and cardiovascular mortality increased gradually with rising TG/HDL-C ratio tertiles (log-rank test, P < 0.001, respectively). Multivariate cox hazard regression analysis revealed that patients in tertile 3 but not teretile 2 had significantly higher rate of all-cause and cardiovascular mortality (P < 0.001, P < 0.05, respectively). Moreover, TG/HDL-C ratio was independently associated with all-cause mortality (HR: 1.21, 95% CI:1.11–1.31; P < 0.001) and cardiovascular mortality (HR:1.28, 95% CI: 1.19–1.37; P < 0.001). For all-cause mortality, TG/HDL-C ratio significantly improved the C-statistic (0.799[0.766–0.833] to 0.813[0.780–0.845]; P = 0.018), net reclassification index (NRI) (0.315; P < 0.001), and integrated discrimination index (IDI) (0.012; P = 0.003). For cardiovascular mortality, TG/HDL-C ratio significantly improved the C-statistic (0.769[0.727–0.812] to 0.810[0.771–0.849]; P = 0.001), NRI (0.442; P < 0.001), and IDI (0.039; P < 0.001). Conclusions TG/HDL-C ratio may predict mortality risk among diabetic CAD patients receiving statin treatment. These findings suggest that assessing TG/HDL-C ratio may be useful for risk stratification for mortality risk in patients with diabetes and CAD.