Department of Ultrasound, The Second Affiliated Hospital of Qiqihar Medical College, Qiqihar, P.R. China.
Eur Rev Med Pharmacol Sci. 2020 Oct;24(20):10632-10645. doi: 10.26355/eurrev_202010_23421.
To investigate the role of SIRT1 in ventricular remodeling after myocardial infarction using ultrasound three-dimensional speckle tracking (3D-STI).
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.
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.
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.
利用超声三维斑点追踪（3D-STI）技术探讨 SIRT1 在心肌梗死后心室重构中的作用。
选取 2015 年 6 月至 2017 年 7 月在齐齐哈尔医学院第二附属医院就诊的急性心肌梗死患者 58 例，根据是否发生心室重构分为重构组和非重构组。选择同期健康体检者 58 例作为对照组。应用 3D-STI 检测舒张末期室间隔厚度（LVST）、舒张末期左心室后壁厚度（LVPWT）、左心室舒张末期容积（LVEDV）、左心室收缩末期容积（LVESV）、左心室射血分数（LVEF）、收缩期径向应变峰值（PRS）。检测三组外周血样本中 SIRT1 表达水平。采用 SIRT1 激动剂处理急性心肌梗死大鼠，4 周后通过三维超声记录 LVEDV、LVESV、LVEF、每搏量（SV）；提取大鼠心肌组织蛋白，检测 SIRT1 及 TGF-β、α-SMA、Vimentin 等纤维化指标，探讨 SIRT1 对心室重构及心肌纤维化的影响。
初诊时健康组>SIRT1 水平非重构组>重构组（p<0.05）；随访时，重构组和非重构组 SIRT1 水平均显著升高（p<0.05），但重构组显著低于非重构组（p<0.05）。H9c2 缺氧复氧细胞模型对照组>SIRT 激动剂处理模型组>SIRT1 模型组。
综上所述，外周血中 SIRT1 与心室重构程度呈负相关。心肌组织中 SIRT1 的表达与急性心肌梗死后体内心脏形态扩张和心功能降低的缓解有关。细胞模型中 SIRT1 表达上调可减少心肌细胞凋亡，抑制心肌细胞纤维化。SIRT1 在预测和治疗心肌梗死、延缓心室重构方面具有良好的应用前景。
