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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.
Background:
Plaque rupture (PR) is the main cause of coronary thrombosis in non-ST segment elevation myocardial infarction (NSTEMI), but can be found in stable coronary artery disease (CAD). Our study compared the morphology and local inflammatory activity of ruptured plaques between stable CAD and NSTEMI patients using frequency-domain optical coherence tomography (FD-OCT).
Methods:
We retrospectively evaluated 70 plaques with PR at the FD-OCT (25 in stable CAD patients and 45 in NSTEMI patients). Main clinical, angiographic, and morphological features were compared.
Results:
Besides an overall equivalence in clinical and angiographic features (except for more smokers among NSTEMI patients), some important FD-OCT differences in plaque morphology emerged: PR in NSTEMI was characterized by more macrophage infiltrates (78% in NSTEMI patients vs 20% in stable CAD patients; P<.001) and intraluminal thrombosis (84% in NSTEMI patients vs 48% in stable CAD patients; P<.01). Quantitative analysis showed a higher density of macrophages in NSTEMI than in stable CAD patients: median max normalized standard deviation (NSD) was 0.0934 (IQR, 0.0796-0.1022) vs 0.0689 (IQR, 0.0598-0.0787); P<.01 and mean NSD was 0.062 (IQR, 0.060-0.065) vs 0.053 (IQR, 0.051-0.060); P<.001. Other morphological features did not differ between stable CAD and NSTEMI patients. Main FD-OCT quantitative parameters like minimal lumen area and plaque length were also equivalent between the 2 groups.
Conclusions:
Differences in morphological features of PR between stable CAD and NSTEMI patients suggest that local inflammation contributes to the unstable fate of the atherosclerotic plaque.
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