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Endothelin in coronary artery disease and myocardial infarction

Theofilos M Kolettis1, Matthias Barton, David Langleben

  • 1Department of Cardiology, University of Ioannina, Ioannina, Greece. thkolet@cc.uoi.gr

Cardiology in Review
|February 21, 2013
PubMed

Insights

Endothelin-1 plays a complex role in coronary artery disease, influencing inflammation and plaque formation. Its blockade shows mixed results, prompting ongoing research into its clinical impact.

Area of Science:

  • Cardiovascular Medicine
  • Endocrinology
  • Pharmacology

Background:

  • Coronary artery disease (CAD) is a leading cause of death.
  • Endothelin-1 (ET-1) is implicated in various stages of CAD, from endothelial dysfunction to atherosclerotic plaque development.
  • ET-1's role shifts from detrimental during acute myocardial infarction (MI) to potentially favorable for healing, then detrimental again in chronic post-MI remodeling.

Purpose of the Study:

  • To review the multifaceted roles of endothelin-1 in coronary artery disease.
  • To summarize the experimental and clinical evidence regarding endothelin receptor blockade in CAD and heart failure.
  • To discuss the controversies and potential clinical implications of targeting the endothelin system.

Main Methods:

  • Literature review of experimental and clinical studies.
  • Analysis of data on endothelin-1's effects at different stages of coronary artery disease.
  • Examination of outcomes from endothelin receptor blockade trials.

Main Results:

  • Endothelin-1 contributes to endothelial dysfunction, inflammation, and atherogenesis.
  • During acute MI, ET-1 increases necrosis but aids infarct healing and remodeling.
  • In chronic phases, ET-1 elevates afterload and promotes fibrosis, while receptor blockade yields conflicting results.

Conclusions:

  • Endothelin-1 has complex, stage-dependent effects in coronary artery disease.
  • Endothelin receptor blockade in CAD and heart failure has produced contradictory outcomes.
  • Further research is needed to clarify the clinical utility of targeting the endothelin system.

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