AHA 2019 — Icosapent ethyl slowed coronary plaque progression but missed primary endpoint


  • Daniel M. Keller, Ph.D
  • Conference Reports
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Takeaway

  • Icosapent ethyl (ethyl eicosapentaenoic acid, IPE) slowed progression of several forms of coronary artery plaque in an interim analysis of the EVAPORATE trial but missed the primary endpoint.

Why this matters

  • Further protection from plaque progression needed beyond the protective effects of statins to lessen risk of cardiovascular events.
  • Although IPE slowed progression, progression occurred.

Study design

  • Patients ≥45 years with elevated fasting triglycerides (TG; 135-499 mg/dL) on stable statin therapy, low-density-lipoprotein cholesterol >40 and ≤115 mg/dL, ≥1 coronary stenosis ≥20% on CT, normal kidney function.
  • EVAPORATE double-blind study: patients randomly assigned to IPE (n=40) 4 g/day or placebo (n=40) for 18 months.
  • Primary endpoint: progression of low-attenuation plaque.
  • Amarin Pharma funded the study and provided drug.

Key results

  • Plaque change from baseline, IPE (n=30) vs placebo (n=37), adjusted P-value (9-month interim data):
    • Calcification: −1% vs 9%; P=.001. IPE slowed progression 89%.
    • Fibrous: 17% vs 40%; P=.0109. IPE slowed progression 57%
    • Total noncalcified: 35% vs 43%; P=.0103. IPE slowed progression 19%.
    • Total plaque: 15% vs 26%; P=.0004. IPE slowed progression 42%.
    • No significant differences between IPE and placebo in fibro-fatty or low-attenuation plaques.
  • Consistent efficacy of IPE across multiple subgroups and full range of baseline TG’s.

Limitations

  • Short time frame.
  • Small cohort with some dropouts.
  • Unknown effect of IPE on other lipid parameters.
  • Effect on future cardiovascular outcomes unknown.