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

Plos One
|February 14, 2013
PubMed

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.
Abstract

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