A coronary artery fistula between a coronary artery and a cardiac chamber is a rare condition. We reported a case of right coronary artery fistula to the left ventricle in a 57-year-old man who had 2-year history of chest pain and exercise dyspnea without significant coronary atherosclerosis with abnormal left ventricular size and function. It was important to recognize this anomaly and our experience showed that transcatheter occlusion of coronary artery fistula was a safe and effective procedure in the presence of symptoms of congestive heart failure, significant left-to-right shunt or refractory to medical treatment.

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The human Hole gene (hHole) encodes a six-transmembrane protein with 319- amino acids. Our previous study showed that hHole was strongly expressed in adult heart and may act as a suppressor of extracellular signal-regulated kinases (ERKs), overactivation of which contributed to pathological cardiac hypertrophy. In this study, it was observed that Hole expression was up-regulated in murine hypertrophic hearts. In a cardiac specific transgenic mouse model, it was observed that overexpression of hHole specifically in heart attenuated cardiac hypertrophy and fibrosis induced by isoproterenol (ISO), with blunted transcriptions of ERK1/2, total ERK1/2 proteins and phosphorylated ERK1/2 (p-ERK1/2) levels. Furthermore, overexpression of hHole in mice by hydrodynamic tail-vein injection with hHole plamids also inhibited cardiac hypertrophy induced by ISO. Our work identified hHole as a novel repressor of cardiac hypertrophy, and provided new insights into the possible target for the prevention or treatment of cardiac diseases.

Myocardial ischemia-reperfusion injury (IRI) is a severe trauma which is characterized by inflammatory reaction, oxidative stress and cardiomyocyte apoptosis. Anesthetics such as sevoflurane have been proved to exhibit cardioprotective effect on IRI and the present study aimed to explore the underlying mechanism. In this study, H9C2 cells were randomly divided into the following groups: Control group; hypoxia/reoxygenation (H/R) group; 2.5% sevoflurane (Sev) 1 h group (H9C2 cells were exposed to 1 h of 2.5% sevoflurane 24 h before H/R); 2.5% Sev 2 h group (H9C2 cells were exposed to 2 h of 2.5% sevoflurane 24 h before H/R); 2.5% sevoflurane (Sev) 2 h þ LY294002 group (H9C2 cells were pretreated with 10 lL LY294002 for 24 h before sevoflurane treatment). Cell proliferation and apoptosis were examined by CCK8 assay and Flow cytometry. Then, the expression levels of key proteins, including Bcl-2, Mcl-1, iNOS, p-AKT, t-AKT, PIM1, P-Bad, p-GSK3b, t-GSK3b and cyclinD1, were examined by western blot. Furthermore, nitric oxide (NO) concentration was detected with an ELISA kit, and TNF-a, IL-1b, IL-6 and IL-10 levels were examined by western blot. The CCK8 assay and flow cytometry results indicated that sevoflurane pretreatment reduced the apoptosis of H9C2 cells with H/R injury. In addition, sevoflurane pretreatment significantly inhibited the inflammatory injury induced by H/R. Furthermore, sevoflurane activated AKT/Pim-1 and AKT/GSK3b signaling pathway. These beneficial effects of sevoflurane were canceled by phosphoinositide-3-kinase inhibitor LY294002. In conclusion, these results verified that sevoflurane attenuates H/R-induced cardiomyocyte injury via AKT/Pim-1 and AKT/GSK3b signaling pathways.