OBJECTIVE: To investigate the role of SIRT1 in ventricular remodeling after myocardial infarction using ultrasound three-dimensional speckle tracking (3D-STI). PATIENTS AND METHODS: Fifty-eight patients with acute myocardial infarction diagnosed in the Second Affiliated Hospital of Qiqihar Medical College from June 2015 to July 2017 were enrolled in the study. They were divided into ventricular remodeling group and ventricular non-remodeling group. Fifty-eight healthy people underwent physical examination were controls. 3D-STI was used to detect end-diastolic ventricular septal thickness (LVST), end-diastolic left ventricular posterior wall thickness (LVPWT), left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV), left ventricular ejection fraction (LVEF), systolic peak radial strain (PRS). SIRT1 expression levels in peripheral blood samples of the 3 groups were measured. Rats with acute myocardial infarction were treated with SIRT1 agonist. After 4 weeks, LVEDV, LVESV, LVEF, stroke volume (SV) were recorded by three-dimensional ultrasound; rat myocardial tissue protein was extracted, and SIRT1 and TGF-β, α-SMA, Vimentin and other fibrosis indicators were detected to explore the effects of SIRT1 on ventricular remodeling and myocardial fibrosis. RESULTS: At the time of initial diagnosis, SIRT1 level in healthy group > non-ventricular remodeling group > remodeling group (p<0.05); at the return visit, SIRT1 levels in the remodeling group and non-ventricular remodeling group were significantly elevated (p<0.05), but that in the remodeling group was significantly lower than that in the non-ventricular group (p<0.05). The expression level of SIRT1 in H9c2 hypoxia-reperfusion cell model control group > SIRT agonist treatment model group > model group. CONCLUSIONS: In summary, SIRT1 in the peripheral blood is negatively correlated with the degree of ventricular remodeling. The expression of SIRT1 in myocardial tissue is related to the cardiac morphology expansion and relief of reduced function in vivo after acute myocardial infarction. Up-regulation of SIRT1 expression in cell models can reduce cardiomyocyte apoptosis and inhibit cardiomyocyte fibrosis. SIRT1 has a good application prospect in predicting and treating myocardial infarction and delaying ventricular remodeling.
OBJECTIVE: To investigate the role of SIRT1 in ventricular remodeling after myocardial infarction using ultrasound three-dimensional speckle tracking (3D-STI). PATIENTS AND METHODS: Fifty-eight patients with acute myocardial infarction diagnosed in the Second Affiliated Hospital of Qiqihar Medical College from June 2015 to July 2017 were enrolled in the study. They were divided into ventricular remodeling group and ventricular non-remodeling group. Fifty-eight healthy people underwent physical examination were controls. 3D-STI was used to detect end-diastolic ventricular septal thickness (LVST), end-diastolic left ventricular posterior wall thickness (LVPWT), left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV), left ventricular ejection fraction (LVEF), systolic peak radial strain (PRS). SIRT1 expression levels in peripheral blood samples of the 3 groups were measured. Rats with acute myocardial infarction were treated with SIRT1 agonist. After 4 weeks, LVEDV, LVESV, LVEF, stroke volume (SV) were recorded by three-dimensional ultrasound; rat myocardial tissue protein was extracted, and SIRT1 and TGF-β, α-SMA, Vimentin and other fibrosis indicators were detected to explore the effects of SIRT1 on ventricular remodeling and myocardial fibrosis. RESULTS: At the time of initial diagnosis, SIRT1 level in healthy group > non-ventricular remodeling group > remodeling group (p<0.05); at the return visit, SIRT1 levels in the remodeling group and non-ventricular remodeling group were significantly elevated (p<0.05), but that in the remodeling group was significantly lower than that in the non-ventricular group (p<0.05). The expression level of SIRT1 in H9c2 hypoxia-reperfusion cell model control group > SIRT agonist treatment model group > model group. CONCLUSIONS: In summary, SIRT1 in the peripheral blood is negatively correlated with the degree of ventricular remodeling. The expression of SIRT1 in myocardial tissue is related to the cardiac morphology expansion and relief of reduced function in vivo after acute myocardial infarction. Up-regulation of SIRT1 expression in cell models can reduce cardiomyocyte apoptosis and inhibit cardiomyocyte fibrosis. SIRT1 has a good application prospect in predicting and treating myocardial infarction and delaying ventricular remodeling.