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OBJECTIVE: This research was designed to probe into the predictive value of glutamyltransferase (GGT) and homocysteine (Hcy) in the risk stratifications and prognoses of non-ST segment elevation acute coronary syndrome (NSTE-ACS) patients. METHODS: A total of 182 NSTE-ACS patients treated with percutaneous coronary intervention (PCI) in our hospital from February 2016 to May 2018 were recruited as a patient group (PG). They were followed up for one year, and the occurrences of any major adverse cardiovascular events (MACCE) were recorded. In addition, 90 healthy volunteers were recruited as a normal group (NG) during the same period. The GGT and Hcy expressions in the serum of both groups were tested, and the predictive values of these levels, the patient risk stratification, and the prognoses were analyzed. RESULTS: Compared with the NG, the GGT and Hcy expressions in the PG were markedly higher (P < 0.05). Compared with the patients without MACE, the GGT and Hcy expressions in the serum of those with MACE increased dramatically (P < 0.05). The serum GGT and Hcy levels were positively correlated with the NSTE-ACS patients' SYNTAX scores (P < 0.05). A Kaplan-Meier curve indicated that the MACE-free survival rate of the patients with low GGT levels was dramatically higher than the survival rate of the patients with high GGT levels, and the MACE-free survival rate of low Hcy patients was significantly higher than the MACE-free survival rate of the high Hcy patients (P < 0.05). Our COX proportional hazards regression models indicated that the serum GGT and Hcy levels are independent predictors of MACCE in NSTE-ACS patients (P < 0.05). Our ROC curve analysis indicated that the serum GGT and Hcy levels are diagnostic criteria for predicting whether MACE occurred in NSTE-ACS patients. CONCLUSION: The serum GGT and Hcy levels are positively correlated with the severity of coronary artery disease (CAD) in NSTE-ACS patients. They are independent predictors of adverse prognoses and can help refine the risk stratification management in clinical work.
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[This corrects the article DOI: 10.1371/journal.pone.0175807.].
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BACKGROUND: Skeletal myoblast transplantation seems a promising approach for the repair of myocardial infarction (MI). However, the low engraftment efficacy and impaired angiogenic ability limit the clinical efficiency of the myoblasts. Gene engineering with angiogenic growth factors promotes angiogenesis and enhances engraftment of transplanted skeletal myoblasts, leading to improved infarction recovery in myocardial ischemia. The present study evaluated the therapeutic effects of hepatocyte growth factor (HGF) gene-engineered skeletal myoblasts on tissue regeneration and restoration of heart function in a rat MI model. METHODS AND RESULTS: The skeletal myoblasts were isolated, expanded, and transduced with adenovirus carrying the HGF gene (Ad-HGF). Male SD rats underwent ligation of the left anterior descending coronary artery. After 2 weeks, the surviving rats were randomized into four groups and treated with skeletal myoblasts by direct injection into the myocardium. The survival and engraftment of skeletal myoblasts were determined by real-time PCR and in situ hybridization. The cardiac function with hemodynamic index and left ventricular architecture were monitored; The adenovirus-mediated-HGF gene transfection increases the HGF expression and promotes the proliferation of skeletal myoblasts in vitro. Transplantation of HGF-engineered skeletal myoblasts results in reduced infarct size and collagen deposition, increased vessel density, and improved cardiac function in a rat MI model. HGF gene modification also increases the myocardial levels of HGF, VEGF, and Bcl-2 and enhances the survival and engraftment of skeletal myoblasts. CONCLUSIONS: HGF engineering improves the regenerative effect of skeletal myoblasts on MI by enhancing their survival and engraftment ability.