Pancoronary Plaque Characteristics in STEMI Caused by Culprit Plaque Erosion Versus Rupture: 3-Vessel OCT Study

Muhua Cao1, Linlin Zhao1, Xuefeng Ren1

  • 1Department of Cardiology, Second Affiliated Hospital of Harbin Medical University, Harbin, China; Key Laboratory of Myocardial Ischemia, Chinese Ministry of Education, Harbin, China.

Insights

Patients with ST-segment elevation myocardial infarction (STEMI) experiencing plaque erosion (PE) show less widespread plaque vulnerability compared to those with plaque rupture (PR), potentially explaining better outcomes.

Area of Science:

  • Cardiovascular Medicine
  • Interventional Cardiology
  • Optical Coherence Tomography (OCT)

Background:

  • Plaque erosion (PE) and plaque rupture (PR) are distinct mechanisms of ST-segment elevation myocardial infarction (STEMI).
  • PE is generally associated with better clinical outcomes than PR.
  • Limited data exists on pancoronary plaque characteristics differentiating culprit PE from culprit PR.

Purpose of the Study:

  • To investigate and compare nonculprit plaque characteristics in STEMI patients with culprit PE versus culprit PR.
  • To assess pancoronary vulnerability at nonculprit sites using Optical Coherence Tomography (OCT) criteria.
  • To determine if culprit PE is associated with reduced overall plaque burden and vulnerability.

Main Methods:

  • A prospective study included 523 STEMI patients undergoing 3-vessel OCT during primary percutaneous intervention (October 2016 - September 2018).
  • Nonculprit plaques were analyzed for high-risk features defined by the CLIMA study criteria (e.g., small lumen area, thin fibrous cap, large lipid arc, macrophage accumulation).
  • Plaques were also assessed for presence of rupture or thin-cap fibroatheromas (TCFA).

Main Results:

  • STEMI patients with culprit PR (n=321) had significantly more nonculprit high-risk plaques (25.2%) compared to those with culprit PE (n=202) (11.4%).
  • A gradient of increasing nonculprit plaque vulnerability (thin fibrous cap, macrophages, TCFA) was observed from PE (fibrous) to PE (lipid-rich plaque) to PR.
  • Culprit PE was an independent predictor of decreased pancoronary vulnerability.

Conclusions:

  • STEMI patients with culprit PE exhibit less pancoronary plaque vulnerability compared to those with culprit PR.
  • This reduced vulnerability in PE patients may contribute to their generally better clinical outcomes.
  • OCT imaging provides valuable insights into the diffuse coronary disease burden associated with different STEMI etiologies.
Abstract

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