To systematically review early surgery and the optimal timing of surgery in patients with infective endocarditis (IE), a search for foreign and domestic articles on cohort studies about the association between early surgery and infective endocarditis published from inception to January 2015 was conducted in the PubMed, EMBASE, Chinese Biomedical Literature (CBM), Wanfang and Chinese National Knowledge Infrastructure (CNKI) databases. The studies were screened according to the inclusion and exclusion criteria, the data were extracted and the quality of the method of the included studies was assessed. Then, the meta-analysis was performed using the Stata 12.0 software. Sixteen cohort studies, including 8141 participants were finally included. The results of the meta-analysis revealed that, compared with non-early surgery, early surgery in IE lowers the incidence of in-hospital mortality [odds ratio (OR) = 0.57, 95% confidence interval (CI) (0.42, 0.77); P = 0.000, I(2) = 73.1%] and long-term mortality [OR = 0.57, 95% CI (0.43, 0.77); P = 0.001, I(2) = 67.4%]. Further, performing operation within 2 weeks had a more favourable effect on long-term mortality [OR = 0.63, 95% CI (0.41, 0.97); P = 0.192, I(2) = 39.4%] than non-early surgery. In different kinds of IE, we found that early surgery for native valve endocarditis (NVE) had a lower in-hospital [OR = 0.46, 95% CI (0.31, 0.69); P = 0.001, I(2) = 73.0%] and long-term [OR = 0.57, 95% CI (0.40, 0.81); P = 0.001, I(2) = 68.9%] mortality than the non-early surgery group. However, for prosthetic valve endocarditis (PVE), in-hospital mortality did not differ significantly [OR = 0.83, 95% CI (0.65, 1.06); P = 0.413, I(2) = 0.0%] between early and non-early surgery. We concluded that early surgery was associated with lower in-hospital and long-term mortality compared with non-early surgical treatment for IE, especially in NVE. However, the optimal timing of surgery remains unclear. Additional larger prospective clinical trials will be required to clarify the optimal timing for surgical intervention and determine its efficacy in PVE.

A coronary heart disease leads to increase in obesity and metabolic dysfunction. Protocatechuic acid (PCA), due to its antioxidant, anti-inflammatory, neuro protective activities was found efficient as cardio-protective in coronary heart disease. Our study investigated hypolipidemic and cardioprotective effects of protocatechuic acid in the coronary artery disease induced by high fat and fructose diet (HFD) rat models. A diet rich in fat and fructose was fed to male wistar rats prior to the start of experimental procedures. Serum lipid levels and hepatic triglycerides (TG) and total cholesterol (TC) levels were examined and analyzed. Both in-vitro an in-vivo pancreatic lipase activity was determined as well. Histopathological examination was performed and their results were noted. Noteworthy reduction of serum lipid levels and hepatic TG and TC levels was seen in groups treated with simvastatin (SIM; 20 mg/kg) and PCA (50 & 100 mg/kg) in comparison to HFD groups. Pancreatic lipase activity was reduced in the SIM group and the group treated with doses of PCA (50 and 100 mg/kg). A marked increase in gain in body weight per week (p < 0.05) was achieved in HFD group. Coronary risk index (CRI) and Atherogenic index of plasma (AIP) showed decreased index values after treatments with SIM and PCA (50 and 100 mg/kg) respectively. Our findings confirmed the efficacious cardio-protective and hypolipidaemic activities of protocatechuic acid in coronary artery disease induced in rats with fat and fructose rich diet.

Aims Myocardial infarction (MI) is a type of cardiovascular disease caused by myocardial necrosis. Growing evidences have suggested that circular RNAs (circRNAs) play crucial roles in cardiac hypoxia/reoxygenation (H/R)-induced injury of MI. Methods and resultsHypoxia/reoxygenation model of H9C2 cells was established and circ_0001206 expression was detected via quantitative real-time polymerase chain reaction. Ribonuclease R (RNase R) and Actinomycin D (Act D) assays verified the stability. Cell counting kit-8 (CCK-8), western blot, TUNEL, and flow cytometry assays evaluated cell viability and cell apoptosis. RNA pull-down, RNA binding protein immunoprecipitation (RIP), and luciferase reporter assays explored the mechanisms underlying MI. All experimental data were presented with mean ± standard deviation (SD) and P < 0.05 indicated statistical significance. Circ_0001206 was low-expressed in H9C2 cells under H/R treatment. Circ_0001206 was formed by cyclization of CRK like proto-oncogene, adaptor protein (CRKL). Circ_0001206 overexpression promoted cell viability and inhibited cardiomyocyte apoptosis. It was confirmed that circ_0001206 regulated CRKL expression via acting as a competing endogenous RNA (ceRNA) of microRNA-665 (miR-665). CRKL played a protective role in MI. Conclusions Circ_0001206 regulates miR-665/CRKL axis to alleviate H/R-induced cardiomyocyte injury in MI. Our findings suggest that circ_0001206 might be a potential target for MI treatment.

Purpose: MicroRNA (miRNA) is known to be involved in the pathological process of congenital heart disease (CHD), and nodal modulator1 (NOMO1) is a critical determinant of heart formation. The present study aims to discover the effect of miR-33a-5p and NOMO1 on CHD. Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect expressions of miR-33a-5p mimic or inhibitor and overexpressed NOMO1 plasmid orNOMO1 knockdown. Human cardiomyocyte progenitor cells (hCMPCs) proliferation was measured by cell counting kit-8 (CCK-8) at 24, 48 and 72 h. Flow cytometry was applied to investigate hCMPCs cell cycle progression and apoptosis. Expressions of cell apoptotic proteins Bax, Cleaved(C) caspase-3 and Bcl-2, and expressions of cardiomyocyte differentiation markers GATA4, troponin T (cTnT) and myocyte enhancer factor2C (MEF2C) in hCMPCs were identified by qRT-PCR and western blot. Target genes and potential binding sites of NOMO1 and miR-33a-5p were predicted with Targetscan 7.2, and was confirmed through dualluciferase reporter assay. Results: Up-regulation of miR-33a-5p inhibited hCMPCs proliferation, cell cycle G0/S transition but promoted hCMPCs apoptosis, which was partially mitigated by overexpressed NOMO1. NOMO1 was the target gene of miR-33a-5p. Expressions of Bax and C caspase-3 were enhanced but expressions of Bcl-2, GATA4, cTnT and MEF2C were reduced by up-regulation of miR-33a-5p, which was partially mitigated by overexpressed NOMO1. Conclusion: Up-regulation of miR-33a-5p inhibited hCMPCs proliferation, cell cycle G0/S transition and differentiation into cardiomyocytes but promoted apoptosis via targeting NOMO1.