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Soluble suppression of tumorigenicity 2 associated with microvascular obstruction in patients with ST-segment

Xinjia Du1, Jiahua Liu1, Jingfang Zhou1

  • 1Department of Cardiology, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, China.

BMC Cardiovascular Disorders
|November 29, 2024
PubMed
Abstract

Insights

Soluble suppression of tumorigenicity 2 (sST2) is linked to microvascular obstruction (MVO) in ST-elevation myocardial infarction (STEMI) patients post-percutaneous coronary intervention. Including sST2 improves risk prediction for MVO.

Area of Science:

  • Cardiology
  • Biomarkers
  • Myocardial Infarction Research

Background:

  • Microvascular obstruction (MVO) affects 50% of ST-elevation myocardial infarction (STEMI) patients after percutaneous coronary intervention (PCI).
  • MVO correlates with inflammation, fibrosis, and poor clinical outcomes.
  • Soluble suppression of tumorigenicity 2 (sST2) indicates inflammation and fibrosis, but its role in STEMI-related MVO is unclear.

Purpose of the Study:

  • To investigate the association between sST2 levels and MVO in STEMI patients undergoing primary PCI (pPCI).
  • To determine if sST2 can enhance risk stratification for MVO.

Main Methods:

  • Retrospective analysis of 315 STEMI patients who underwent pPCI.
  • Cardiac magnetic resonance imaging (CMR) assessed MVO and myocardial infarction characteristics.
  • Serum sST2 levels were measured upon admission.

Main Results:

  • Multivariate analysis identified sST2 as an independent predictor of MVO (OR 1.01, p<0.001).
  • Other independent predictors included peak high-sensitivity troponin T, peak C-reactive protein, left ventricular ejection fraction, and age.
  • sST2 levels were significantly associated with the presence of MVO.

Conclusions:

  • sST2 is significantly associated with MVO in STEMI patients post-pPCI.
  • Integrating sST2 into risk models improves the prediction of MVO.
Keywords:
Cardiovascular magnetic resonanceMicrovascular obstructionMyocardial infarctionSoluble suppression of tumorigenicity 2

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