Circ_0004104 participates in the regulation of ox-LDL-induced endothelial cells injury via miR-942-5p/ROCK2 axis.

BACKGROUND: Cardiovascular disease was the most common disease among the elderly with high morbidity and mortality. Circ_0004104 was demonstrated to be involved in the regulation of atherosclerosis. METHODS: Quantitative real-time polymerase chain reaction was employed to measure the expression of circ_0004104, miR-942-5p and Rho associated coiled-coil containing protein kinase 2 (ROCK2). Cell proliferation was tested by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Cell apoptosis was measured by flow cytometry, and tube formation assay was used to detect the angiogenesis ability of cells. Western blot assay was performed to assess protein levels. Enzyme­linked immunosorbent assay was used to detect the release of IL-1ß and TNF-α. The relationship between miR-942-5p and circ_0004104 or ROCK2 was identified by dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay, and RNA pull-down assay. RESULTS: Oxidized low-density lipoprotein (ox-LDL) inhibited the proliferation of human umbilical vein endothelial cells (HUVECs) and promoted apoptosis in a dose-dependent manner. Circ_0004104 was increased in serum of atherosclerosis patients and ox-LDL-treated HUVECs, and silence of circ_0004104 promoted the proliferation of ox-LDL-exposed HUVECs and inhibited cell apoptosis. MiR-942-5p downregulation reversed si-circ_0004104-mediated influences in HUVECs upon ox-LDL exposure. ROCK2 was the target of miR-942-5p and circ_0004104 regulated the expression of ROCK2 through sponging miR-942-5p. ROCK2 abated the influences of miR-942-5p in ox-LDL-stimulated HUVECs. Circ_0004104 was increased in the exosomes derived from ox-LDL-exposed HUVECs, and the expression of circ_0004104 was promoted in HUVECs after stimulation with ox-LDL-treated HUVECs cells-derived exosomes. CONCLUSION: Circ_0004104 downregulation receded ox-LDL-induced injury in HUVECs through miR-942-5p and ROCK2.

Transcatheter closure of ventricular septal rupture with prolonged support of intra-aortic balloon pump after primary PCI: a case report.

BACKGROUND: Ventricular septal rupture (VSR) is a rare but severe complication of acute myocardial infarction (AMI). For such cases, surgical repair is recommended by major guidelines, but not always possible for such cases. CASE PRESENTATION: A 72-year-old man presented to the emergency room. ECG showed the ST-segment was elevated by 2-3 mm in lead II, III, and aVF, with Q-waves. Coronary angiography (CAG) showed multi-vessel disease with a total occlusion of the right coronary artery (RCA) and severe stenosis of the left anterior descending artery (LAD). A diagnosis of acute inferior myocardial infarction was made. VSR occurred immediately after percutaneous coronary intervention (a 2.5 × 20 mm drug-eluting stent implanted in RCA), and the patient developed cardiogenic shock. An intra-aortic balloon pump (IABP) was used to stabilize the hemodynamics. Transthoracic echocardiography (TTE) revealed an 11.4-mm left-to-right shunt in the interventricular septum. An attempt was made to reduce the IABP augmentation ratio for weaning on day 12 but failed. Transcatheter closure was conducted using a 24-mm double-umbrella occluder on day 28. The patient was weaned from IABP on day 31 and underwent secondary PCI for LAD lesions on day 35. The patient was discharged on day 41. Upon the last follow-up 6 years later, CAG and TTE revealed no in-stent restenosis, no left-to-right shunt, and 51% left ventricular ejection fraction. CONCLUSIONS: Prolonged implementation of IABP can be a viable option to allow deferred closure of VSR in AMI patients, and transcatheter closure may be considered as a second choice for the selected senior and vulnerable patients, but the risk is still high.

High red blood cell distribution width is closely associated with in-stent restenosis in patients with unstable angina pectoris.

BACKGROUND: In-stent restenosis remains an unresolved issue. Inflammation plays a pivotal role in the process of in-stent restenosis. Significant and positive associations were found between red blood cell distribution width (RDW) and inflammation. But whether there is a close relationship between higher RDW and in-stent restenosis is still not clarified. METHODS: This retrospective observational study investigated 214 consecutive patients with unstable angina pectoris who underwent successful percutaneous coronary interventions with drug-eluting stents. Patients were divided into three groups according to baseline RDW before percutaneous coronary interventions (low RDW group:≤12.5%; intermediate RDW group:> 12.5% and ≤ 13.5%; high RDW group:> 13.5%). The follow-up angiographies were routinely performed 9-12 months after the initial percutaneous coronary interventions. The multivariate logistic regression analysis was employed to determine the independent predictors of in-stent restenosis. RESULTS: The in-stent restenosis rate was significantly higher in group with higher baseline RDW value (12.3, 19.7, 47.7% in low, intermediate, and high RDW groups respectively, P < 0.001). The baseline RDWs were significantly higher in patients with in-stent restenosis compared with those in patients without in-stent restenosis (13.7 ± 0.8% vs. 13.0 ± 0.8%, P < 0.001). For prediction of in-stent restenosis, the ROC (receiver operating characteristic) curve analysis demonstrated the optimal RDW cutoff value was 13.37 (sensitivity: 65.5%, specificity: 73.6%); the diagnosis cutoff value was 13.89 (sensitivity: 40.0%, specificity: 91.8%); the screening cutoff value was 12.99 (sensitivity: 83.6%, specificity: 49.1%). By multivariate logistic analysis, higher baseline RDW (odds ratio [OR], 5.179; 95% confidence interval [CI], 2.568 to 10.446; P<0.001) together with lower baseline indirect bilirubin (OR, 0.413; 95% CI, 0.305 to 0.559; P<0.001) and diabetes (OR, 4.077; 95% CI, 1.654 to 10.054; P = 0.002) were closely associated with in-stent restenosis at followup (11.1 ± 5.8 months). CONCLUSIONS: The baseline RDW was closely associated with in-stent restenosis at follow-up. The patients with higher baseline RDW might have more chances to develop in-stent restenosis at followup.