Circulating microparticles are associated with clinical severity of persistent ST-segment elevation myocardial

A Sionis1, R Suades2, J Sans-Roselló3

  • 1Acute and Intensive Cardiac Care Unit, Cardiology Department, Hospital Santa Creu i Sant Pau, Biomedical Research Institute Sant Pau (IIB Sant Pau), Barcelona, Spain; CiberCV, Institute of Health Carlos III, Hospital Santa Creu i Sant Pau, Biomedical Research Institute Sant Pau (IIB Sant Pau), Barcelona, Spain.

Insights

Cardiogenic shock (CS) patients exhibit elevated levels of circulating microparticles (cMPs) from activated leukocytes and platelets. This cMP signature can identify CS patients and predict mortality, aiding in risk stratification and improved patient outcomes.

Area of Science:

  • Cardiovascular Medicine
  • Biomarkers
  • Cellular Biology

Background:

  • Cardiogenic shock (CS) is a severe complication of acute myocardial infarction (MI), associated with high mortality despite advancements in treatment.
  • The role of circulating microparticles (cMPs) as potential biomarkers in CS remains largely unexplored.
  • Investigating cMP subtypes may offer insights into cellular activation and damage in CS patients.

Purpose of the Study:

  • To investigate circulating microparticle (cMP) subtypes and their parental activated cells in ST-elevation myocardial infarction (STEMI) patients with and without cardiogenic shock (CS).
  • To identify a cMP signature that can aid in the risk stratification of CS patients.
  • To explore the association of specific cMPs with clinical outcomes and myocardial reperfusion in CS.

Main Methods:

  • Triple-labeling flow cytometry was used to characterize cMPs in STEMI patients with and without CS (36 patients per group).
  • Patients received guideline-directed medical therapy, including primary percutaneous coronary intervention.
  • cMPs were analyzed for their origin from platelets, leukocytes (neutrophils, granulocytes, monocytes), and endothelium.

Main Results:

  • CS patients showed significantly increased levels of leukocyte-derived (neutrophil, granulocyte) and platelet-derived cMPs compared to non-CS patients.
  • A distinct cMP signature comprising platelet, leukocyte, and endothelial microparticles effectively discriminated CS patients (AUC 0.743) and predicted mortality (AUC 0.869).
  • In CS patients, elevated platelet-, monocyte-, and tissue factor-rich cMPs correlated with poorer myocardial reperfusion (blush grade, TIMI flow).

Conclusions:

  • Elevated levels of prothrombotic and proinflammatory cMPs are characteristic of CS patients.
  • Activated granulocytes and neutrophils continuously release cMPs in CS patients, even with guideline-directed treatment.
  • These cMPs serve as valuable biomarkers for adverse prognosis in cardiogenic shock, potentially guiding clinical management.
Abstract

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