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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.
Objectives:
This study sought to investigate nonculprit plaque characteristics in patients with ST-segment elevation myocardial infarction (STEMI) presenting with plaque erosion (PE) and plaque rupture (PR). Pancoronary vulnerability was considered at nonculprit sites: 1) the CLIMA (Relationship Between OCT Coronary Plaque Morphology and Clinical Outcome) study (NCT02883088) defined high-risk plaques with simultaneous presence of 4 optical coherence tomography (OCT) features (minimum lumen area <3.5 mm2; fibrous cap thickness [FCT] <75 μm; maximum lipid arc >180º; and macrophage accumulation); and 2) the presence of plaque ruptures or thin-cap fibroatheromas (TCFA).
Background:
PE is a unique clinical entity associated with better outcomes than PR. There is limited evidence regarding pancoronary plaque characteristics of patients with culprit PE versus culprit PR.
Methods:
Between October 2016 and September 2018, 523 patients treated by 3-vessel OCT at the time of primary percutaneous intervention were included with 152 patients excluded from final analysis.
Results:
Overall, 458 nonculprit plaques were identified in 202 STEMI patients with culprit PE; and 1,027 nonculprit plaques were identified in 321 STEMI patients with culprit PR. At least 1 CLIMA-defined OCT nonculprit high-risk plaque was seen in 11.4% of patients with culprit PE, but twice as many patients were seen with culprit PR (25.2%; p < 0.001). This proportion was also seen when individual high-risk features were analyzed separately. When patients with PE were divided by a heterogeneous substrate (fibrous or lipid-rich plaque) underlying the culprit site, the prevalence of nonculprits with FCT <75 μm, macrophages, and TCFA showed a significant gradient from PE(Fibrous) to PElipid-rich plaque (LRP) to PR. Interestingly, nonculprit rupture was rarely found in patients with culprit PE(Fibrous) (1.9%), although it was exhibited with comparable prevalence in patients with culprit PE(LRP) (16.3%) versus PR (17.8%). Culprit PE predicted decreased pancoronary vulnerability independent of conventional risk factors.
Conclusions:
STEMI patients with culprit PE have a limited pancoronary vulnerability that may explain better outcomes in these patients than in STEMI patients with culprit PR.
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