Factors associated with microvascular occlusion in patients with ST elevation myocardial infarction after primary percutaneous coronary intervention.

OBJECTIVE: This study aimed to determine predictors of microvascular occlusion (MVO) in patients with ST elevation myocardial infarction (STEMI) after primary percutaneous coronary intervention (pPCI). METHODS: This retrospective, observational study consecutively included 113 patients with STEMI undergoing pPCI. Cardiac magnetic resonance imaging was used to determine the presence of MVO in these patients. Biomarkers in serum were routinely tested 1 day after pPCI. Multivariable logistic regression analysis was used to evaluate significant predictors of occurrence of MVO. RESULTS: There were 62 patients in the MVO group and 51 patients in the non-MVO group. C-reactive protein (CRP), thrombomodulin, lymphatic vessel endothelial hyaluronan receptor-1, syndecan-1, and troponin T (TnT) levels after the procedure were significantly higher in the MVO group than in the non-MVO group. CRP (hazard ratio [HR]=1.036), TnT (HR=1.316), and syndecan-1 (HR=1.986) levels were independently associated with MVO in patients with acute myocardial infarction after pPCI. CONCLUSIONS: Levels of CRP, TnT, and syndecan-1 can be used as serum biomarkers for MVO in patients with STEMI receiving pPCI.

Prognostic relevance and clinical features of papillary muscle infarction with mitral regurgitation in patients with ST segment elevation myocardial infarction.

BACKGROUND: Papillary muscle infarction (PapMI) combined with mitral regurgitation (MR) is a severe complication of ST-segment elevation myocardial infarction (STEMI). The features detected by cardiac magnetic resonance (CMR) imaging in PapMI have not been characterized. The aim of the present study was to assess the incidence, determinants, and the prognostic significance of PapMI with MR at 1-year follow-up in a study of patients with STEMI after primary percutaneous coronary intervention (pPCI). METHODS: We enrolled 209 patients with STEMI reperfused by pPCI (<12 hours after symptom onset) at 2 centers. CMR and echocardiography were performed within 1 week after infarction using a standardized protocol. According to the results of CMR and echocardiography, patients were divided into PapMI with MR, PapMI (PapMI without MR), and non-PapMI groups. The primary clinical endpoint of the study was the occurrence of major adverse cardiovascular events (MACE). RESULTS: PapMI with MR was found in 27 patients (13%). The existence of PapMI with MR was associated with age (P<0.001), impaired left ventricular ejection fraction (LVEF) (P=0.005), higher SYNTAX score (P=0.002), concentration of troponin I (P<0.001), longer time to reperfusion (P<0.001), more diabetics (P<0.001), and microvascular occlusion (MVO) (P<0.001). Binary logistic regression with stepwise backward selection analysis showed that advanced age, MVO, and impaired LVEF were independent risk factors for PapMI with MR. Patients in the PapMI with MR group had significantly more MACE compared with the PapMI and non-PapMI groups [PapMI with MR, 23 (85.2%) vs. PapMI, 21 (55.3%) vs. non-PapMI, 29 (20.1%)] at 1-year follow-up (P<0.001). However, there were no pronounced differences in mortality rates among the 3 groups (P=0.071). CONCLUSIONS: The presence of PapMI with MR in patients with STEMI is associated with advanced age, MVO, and impaired LVEF, which can increase the rates of MACE.

Circ_0010729 regulates hypoxia-induced cardiomyocyte injuries by activating TRAF5 via sponging miR-27a-3p.

Ischemic cardiomyopathy is a severe cardiovascular disease with high mortality. Circular RNAs (circRNAs) are widely regulated in diverse human diseases, including Ischemic cardiomyopathy. This study aimed to investigate a novel functional mechanism of circRNA circ_0010729 in hypoxia-induced cardiomyocyte injuries. Human cardiomyocytes (AC16) were exposed to hypoxia to mimic ischemic cardiomyopathy in vitro. Cell viability, apoptosis/necrosis and glycolysis progress, were determined using 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay, flow cytometry assay and glycolysis stress test, respectively. Cell apoptosis was also assessed by the activity of cleaved caspase-3/7. The levels of glycolysis-related proteins and tumor necrosis factor receptor-associated factor 5 (TRAF5) were examined by western blot. The expression of circ_0010729 and miR-27a-3p was measured by real-time quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The prediction about the targeted relationship was verified by dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay and RNA pull-down assay. As a result, hypoxia treatment inhibited cell viability, induced cell apoptosis and blocked glycolysis, however, these injuries were alleviated by circ_0010729 knockdown. MiR-27a-3p was targeted by circ_0010729, and miR-27a-3p inhibition reversed the role of circ_0010729 knockdown, leading to the deterioration of cell injuries. Further, TRAF5 was a target of miR-27a-3p, and circ_0010729 upregulated the expression of TRAF5 by sponging miR-27a-3p. MiR-27a-3p restoration enhanced cell viability, depleted cell apoptosis and promoted glycolysis of hypoxia-induced AC16 cells, while these effects were abolished by TRAF5 overexpression. In conclusion, circ_0010729 knockdown alleviated hypoxia-induced AC16 cell injuries by mediating the miR-27a-3p/TRAF5 axis.

MicroRNA-29b-3p Targets SPARC Gene to Protect Cardiocytes against Autophagy and Apoptosis in Hypoxic-Induced H9c2 Cells.

MicroRNAs participate in the regulation of abnormal cardiomyocyte apoptosis and autophagy, which leads to heart failure (HF). Lower miR-29b-3p levels were found in HF patients in this study. However, the role of miR-29b-3p in the molecular pathogenesis of HF remains unclear. Hypoxia-stimulated H9c2 cells were used an in vitro model of HF. It was found that hypoxia stimulation decreased the miR-29b-3p expression and enhanced cell apoptosis and autophagy response in H9c2 cells. While the effects of hypoxia on cell apoptosis and autophagy were reversed by miR-29b-3p transfection, especially 100 nM. The secreted protein acidic and rich in cysteine (SPARC), predicted as a direct target of miR-29b-3p, aggravated the hypoxia-induced cells apoptosis, autophagy, and TGFß1/Smad3 activation. While the changes were dramatically reversed by miR-29b-3p. Taken together, our data suggest that miR-29b-3p plays an important role in the progression of HF through targeting SPARC and regulating TGFß1/Smad3 pathway.