Long-term endothelin receptor antagonism attenuates coronary plaque progression in patients with early

Myeong Ho Yoon1, Martin Reriani, Gössl Mario

  • 1Division of Cardiovascular Diseases, Mayo Clinic Rochester, 200 First Street, SW, Rochester, MN 55905, United States.

Insights

The endothelin-A (ETA) receptor antagonist Atrasentan significantly reduced coronary plaque progression in patients with endothelial dysfunction over six months. This suggests ETA receptor blockade may be a therapeutic strategy for managing coronary artery disease.

Area of Science:

  • Cardiology
  • Pharmacology

Background:

  • Coronary endothelial dysfunction is a key factor in the progression of coronary artery disease.
  • Endothelin-A (ETA) receptor antagonists have shown potential in preclinical models for cardiovascular protection.

Purpose of the Study:

  • To evaluate the efficacy of the ETA receptor antagonist Atrasentan in attenuating coronary plaque progression in patients with endothelial dysfunction.

Main Methods:

  • A double-blind, randomized study involving 35 patients with coronary endothelial dysfunction treated with Atrasentan or placebo for six months.
  • Coronary endothelial function assessed via intracoronary acetylcholine.
  • Coronary plaque volume evaluated using intravascular ultrasound (IVUS) at baseline and follow-up.

Main Results:

  • Atrasentan treatment led to a significant decrease in total atheroma volume (TAVMEAN) and percent atheroma volume (PAV) in segments with endothelial dysfunction compared to placebo.
  • No significant changes in TAV or PAV were observed in segments with normal endothelial function.
  • The observed changes in TAVMEAN and PAV were statistically significant (p=0.0024 and p=0.010, respectively).

Conclusions:

  • Six-month treatment with Atrasentan effectively attenuates the progression of coronary plaque in patients with endothelial dysfunction.
  • These findings support the potential role of ETA receptor antagonism in managing coronary atherosclerosis in this patient population.
Abstract

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