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Coronary Progenitor Cells and Soluble Biomarkers in Cardiovascular Prognosis after Coronary Angioplasty
Published on: January 28, 2020
Soluble TNF receptors are associated with infarct size and ventricular dysfunction in ST-elevation myocardial
Lennart Nilsson1, Aleksander Szymanowski, Eva Swahn
1Division of Cardiology, Department of Medical and Health Sciences, Linköping University, Linköping, Sweden. lennart.nilsson@liu.se
Insights
In ST-elevation myocardial infarction (STEMI) patients, elevated levels of soluble tumor necrosis factor receptors (sTNFR1 and sTNFR2) indicate larger infarct size and worse left ventricular dysfunction. These findings highlight apoptosis
Area of Science:
- Cardiovascular Medicine
- Cellular Biology
- Biomarker Research
Background:
- Primary percutaneous coronary intervention (PCI) is crucial for ST-elevation myocardial infarction (STEMI) but can cause reperfusion injury.
- Apoptosis is implicated in ischemia-reperfusion injury, leading to left ventricular (LV) dysfunction and heart failure.
Purpose of the Study:
- To investigate circulating apoptosis markers in relation to infarct size, LV dysfunction, and remodeling in STEMI patients post-primary PCI.
- To assess the association of soluble tumor necrosis factor receptors (sTNFR1, sTNFR2) and Fas pathway markers (sFas, sFasL) with clinical outcomes.
Main Methods:
- A substudy of the F.I.R.E. trial included 48 STEMI patients undergoing primary PCI.
- Blood samples were analyzed for sTNFR1, sTNFR2, sFas, and sFasL via ELISA.
- Infarct size, LV dysfunction, and remodeling were assessed using cardiac magnetic resonance imaging at 5 days and 4 months post-STEMI.
Main Results:
- Elevated sTNFR1 at 24 hours and increased sTNFR1/sTNFR2 levels correlated significantly with infarct size and LV dysfunction at 4 months.
- sTNFRs also showed strong correlations with Troponin I and matrix metalloproteinase-2.
- sFas and sFasL did not correlate with infarct size or LV dysfunction; no apoptosis markers correlated with remodeling.
Conclusions:
- Circulating sTNFR1 and sTNFR2 levels are associated with infarct size and LV dysfunction in STEMI patients.
- These findings support the role of apoptosis in ischemia-reperfusion injury following primary PCI.
Objectives:
The aim of the study was to investigate circulating markers of apoptosis in relation to infarct size, left ventricular dysfunction and remodeling in an ST-elevation myocardial infarction (STEMI) population undergoing primary percutaneous coronary intervention (PCI).
Background:
Immediate re-opening of the acutely occluded infarct-related artery via primary PCI is the treatment of choice in STEMI to limit ischemia injury. However, the sudden re-initiation of blood flow can lead to a local acute inflammatory response with further endothelial and myocardial damage, so-called reperfusion injury. Apoptosis is suggested to be a key event in ischemia-reperfusion injury, resulting in LV-dysfunction, remodeling and heart failure.
Methods:
The present study is a prespecified substudy of the F.I.R.E. trial. We included 48 patients with STEMI undergoing primary PCI. Blood samples were collected prior to PCI and after 24 hours. Plasma was separated for later analysis of soluble tumor necrosis factor receptor (sTNFR) 1, sTNFR2, sFas and sFas ligand (sFasL) by ELISA. Infarct size, left ventricular (LV) dysfunction and remodeling were assessed by cardiac magnetic resonance imaging at five days and four months after STEMI.
Results:
The levels of sTNFR1 at 24 h as well as the relative increases in sTNFR1 and sTNFR2 over 24 h showed consistent and significant correlations with infarct size and LV-dysfunction at four months. Moreover, both sTNFRs correlated strongly with Troponin I and matrix metalloproteinase (MMP)-2 measurements. Soluble Fas and sFasL did not overall correlate with measures of infarct size or LV-dysfunction. None of the apoptosis markers correlated significantly with measures of remodeling.
Conclusions:
In STEMI patients, circulating levels of sTNFR1 and sTNFR2 are associated with infarct size and LV dysfunction. This provides further evidence for the role of apoptosis in ischemia-reperfusion injury.
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