Coronary Plaque Rupture in Stable Coronary Artery Disease and Non-ST Segment Elevation Myocardial Infarction: An

Luca Mariani1, Francesco Burzotta, Cristina Aurigemma

  • 1Institute of Cardiology, Mazzoni Hospital, Ascoli Piceno, Italy, Via degli Iris 1, 63100 Ascoli Piceno, Italy. lm0281@gmail.com.

Insights

Plaque rupture in non-ST segment elevation myocardial infarction (NSTEMI) shows significantly more macrophage infiltrates and thrombosis compared to stable coronary artery disease (CAD). This suggests inflammation drives plaque instability.

Area of Science:

  • Cardiology
  • Biomedical Imaging
  • Pathology

Background:

  • Plaque rupture (PR) is a primary cause of coronary thrombosis in non-ST segment elevation myocardial infarction (NSTEMI).
  • Ruptured plaques can also occur in stable coronary artery disease (CAD).
  • Understanding morphological and inflammatory differences in PR is crucial for differentiating disease states.

Purpose of the Study:

  • To compare the morphology and local inflammatory activity of ruptured plaques between stable CAD and NSTEMI patients.
  • To utilize frequency-domain optical coherence tomography (FD-OCT) for detailed plaque analysis.
  • To identify key differences that may explain plaque instability in NSTEMI.

Main Methods:

  • Retrospective evaluation of 70 ruptured plaques using FD-OCT (25 in stable CAD, 45 in NSTEMI).
  • Comparison of clinical, angiographic, and morphological features.
  • Quantitative analysis of macrophage density using normalized standard deviation (NSD).

Main Results:

  • NSTEMI patients had significantly more macrophage infiltrates (78% vs. 20%) and intraluminal thrombosis (84% vs. 48%) in ruptured plaques compared to stable CAD patients.
  • Higher macrophage density was observed in NSTEMI patients (mean NSD 0.062 vs. 0.053).
  • Clinical and angiographic features were largely similar, except for a higher prevalence of smokers in the NSTEMI group.

Conclusions:

  • Morphological differences in ruptured plaques, particularly increased macrophage infiltration and thrombosis, distinguish NSTEMI from stable CAD.
  • These findings highlight the role of local inflammation in the progression of atherosclerotic plaque instability.
  • FD-OCT is effective in characterizing plaque features related to acute coronary events.
Abstract

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