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Association of autoantibodies targeting endothelin type-A receptors with no-reflow in ST-elevation myocardial

Francesco Tona1, Marta Vadori1, Giovanni Civieri1

  • 1Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padua, Italy.

Atherosclerosis
|July 8, 2023
PubMed

Insights

Autoantibodies activating endothelin-1 receptor type A (ETAR-AAs) are linked to no-reflow (NR) in ST-elevation myocardial infarction (STEMI) patients. This suggests ETAR-AAs may be a target for improving perfusion after heart attack treatment.

Area of Science:

  • Cardiology
  • Immunology
  • Vascular Biology

Background:

  • No-reflow (NR) phenomenon after ST-elevation myocardial infarction (STEMI) treatment is linked to adverse patient outcomes.
  • Understanding the mechanisms behind NR is crucial for improving treatment efficacy.

Purpose of the Study:

  • To investigate the association between autoantibodies activating endothelin-1 receptor type A (ETAR-AAs) and NR in STEMI patients undergoing primary percutaneous coronary intervention (PPCI).

Main Methods:

  • A cohort of 50 STEMI patients treated with PPCI within 6 hours of symptom onset was studied.
  • ETAR-AA levels were measured within 12 hours post-PPCI, and NR was assessed using cardiac magnetic resonance imaging (microvascular obstruction - MVO).
  • A control group of 40 healthy individuals was included for comparison.

Main Results:

  • Microvascular obstruction (MVO) was observed in 48% of STEMI patients.
  • ETAR-AA seropositivity was significantly higher in patients with MVO (72% vs. 38%, p=0.03).
  • ETAR-AA levels were elevated in patients with MVO, and seropositivity was independently associated with MVO (OR 3.2, p=0.03). A cut-off of ≥6.74 U/mL predicted MVO with 72% accuracy.

Conclusions:

  • ETAR-AA seropositivity is associated with no-reflow (microvascular obstruction) in STEMI patients.
  • These findings highlight a potential role for ETAR-AAs in the pathophysiology of NR after myocardial infarction.
  • Targeting ETAR-AAs could represent a novel therapeutic strategy for managing myocardial infarction, pending further validation in larger studies.
Abstract

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