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Updated: Dec 1, 2025
Ultrasonic Assessment of Myocardial Microstructure
Published on: January 14, 2014
Using ultrasound three-dimensional speckle tracking technology to explore the role of SIRT1 in ventricular remodeling
1Department of Ultrasound, The Second Affiliated Hospital of Qiqihar Medical College, Qiqihar, P.R. China. FSEY-CSK@qmu.edu.cn.
Insights
Sirtuin 1 (SIRT1) levels in peripheral blood are negatively correlated with ventricular remodeling after myocardial infarction. Upregulating SIRT1 may reduce cardiomyocyte apoptosis and fibrosis, offering potential for treating heart attacks and delaying remodeling.
Area of Science:
- Cardiology
- Molecular Biology
- Biochemistry
Background:
- Ventricular remodeling is a significant complication following myocardial infarction, leading to heart failure.
- Sirtuin 1 (SIRT1) is a protein deacetylase implicated in various cellular processes, including stress response and aging.
- Understanding the role of SIRT1 in post-myocardial infarction ventricular remodeling is crucial for developing therapeutic strategies.
Purpose of the Study:
- To investigate the role of SIRT1 in ventricular remodeling after myocardial infarction.
- To assess the correlation between SIRT1 expression levels and the degree of ventricular remodeling.
- To explore the therapeutic potential of SIRT1 modulation in mitigating myocardial fibrosis and cardiomyocyte apoptosis.
Main Methods:
- Utilized three-dimensional speckle tracking (3D-STI) to evaluate cardiac structure and function in patients with myocardial infarction.
- Measured SIRT1 expression levels in peripheral blood of patients and healthy controls.
- Induced myocardial infarction in rats and treated them with a SIRT1 agonist, assessing cardiac remodeling and fibrosis markers.
- Established a H9c2 hypoxia-reperfusion cell model to investigate the effects of SIRT1 on cardiomyocyte apoptosis and fibrosis.
Main Results:
- SIRT1 levels were significantly lower in patients with ventricular remodeling compared to those without and healthy controls at initial diagnosis.
- SIRT1 levels increased in both remodeling and non-remodeling groups at follow-up, but remained lower in the remodeling group.
- SIRT1 agonist treatment in a rat model of myocardial infarction reduced ventricular volumes and improved ejection fraction.
- In vitro, SIRT1 upregulation in a hypoxia-reperfusion cell model decreased cardiomyocyte apoptosis and inhibited fibrosis.
Conclusions:
- Peripheral blood SIRT1 levels are negatively correlated with the severity of ventricular remodeling post-myocardial infarction.
- SIRT1 expression in myocardial tissue is associated with cardiac morphology and function after infarction.
- Upregulating SIRT1 shows promise in reducing cardiomyocyte apoptosis and fibrosis, suggesting therapeutic potential for myocardial infarction treatment 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.
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