Changes in concentrations of circulating fibroblast activation protein alpha are associated with myocardial damage in

Jochen Tillmanns1, Daniela Fraccarollo1, Paolo Galuppo1

  • 1Department of Cardiology and Angiology, Hannover Medical School, 30625 Hannover, Germany.

Abstract

Insights

Fibroblast activation protein alpha (FAP) levels decrease after ST-elevation myocardial infarction (STEMI). A larger drop in FAP correlates with greater heart damage and inflammation, suggesting FAP may indicate injury severity.

Area of Science:

  • Cardiology
  • Biochemistry
  • Immunology

Background:

  • Fibroblast activation protein alpha (FAP) is a protease on activated fibroblasts post-myocardial infarction (MI).
  • Lower FAP levels are linked to higher mortality in acute coronary syndrome.
  • This study investigates FAP changes after ST-elevation MI (STEMI) and their relation to myocardial damage.

Purpose of the Study:

  • To determine if circulating FAP concentrations are altered in patients with acute STEMI.
  • To explore the relationship between FAP levels and the extent of myocardial damage and inflammation.

Main Methods:

  • Measured plasma FAP concentrations in 60 STEMI patients on days 0, 1, 3, and 5.
  • Included 25 healthy blood donors as controls.
  • Analyzed correlations between FAP levels, cardiac biomarkers (CK, hs-cTnT), and inflammatory markers (CRP).

Main Results:

  • STEMI patients had lower admission FAP levels (71ng/mL) than controls (101ng/mL).
  • FAP concentrations decreased significantly from admission to day 5 in STEMI patients.
  • Greater FAP decline (ΔFAP) correlated with worse left ventricular function, higher cardiac enzyme and CRP levels, indicating more myocardial damage and inflammation.

Conclusions:

  • Circulating FAP concentrations are significantly altered in the acute phase following STEMI.
  • A pronounced decrease in FAP levels within 5 days post-STEMI is associated with increased myocardial injury and systemic inflammation.
  • Monitoring FAP may offer insights into myocardial damage and inflammatory responses in STEMI patients.

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