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Diffuse and Active Inflammation Occurs in Both Vulnerable and Stable Plaques of the Entire Coronary Tree
Open accessAbstract
Objectives This study was undertaken to define and compare geographic coronary artery inflammation in patients who were dying of acute myocardial infarction (AMI), chronic stable angina (SA), and noncardiac causes (CTRL).Background Biochemical markers and flow cytometry provide indirect evidence of diffuse coronary inflammation in patients dying of acute coronary syndromes. Yet no histopathologic studies have corroborated these findings. A key unanswered question is whether the inflammatory burden involves the entire coronary tree or is limited to a few plaques.Methods We examined 544 coronary artery segments from 16 patients with AMI, 109 segments from 5 patients with SA, and 304 coronary segments from 9 patients with CTRL.Results An average of 6.8 +/- 0.5 vulnerable segments per patient were found in the AMI group (in addition to culprit lesions) compared with an average of 0.8 +/- 0.3 and 1.4 +/- 0.3 vulnerable lesions/patient in the SA and CTRL groups, respectively. The AMI group, independent of the type of plaque observed, showed significantly more inflammatory infiltrates compared with the SA and CTRL groups (121.6 +/- 12.4 cell x mm2 vs. 37.3 +/- 11.9 cell x mm2 vs. 26.6 +/- 6.8 cell x mm2, p = 0.0001). In AMI patients, active inflammation was not only evident within the culprit lesion and vulnerable plaques but also involved stable plaques. These showed a three- to four-fold higher inflammation than vulnerable and stable plaques from the SA and CTRL groups, respectively.Conclusions This histopathologic study found that both vulnerable and stable coronary plaques of patients dying of AMI are diffusely infiltrated by inflammatory cells.
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“Histopathological studies have shown that patients dying from acute myocardial infarction have widespread inflammation not only in culprit plaques but also in plaques within other major coronary arteries83.”
From Perspectives and opportunities for nanomedicine in the management of atherosclerosis (2011) · cites this paper as [83]
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Metadata
- Authors
- Mauriello, A., Sangiorgi, G., Fratoni, S., Palmieri, G., Bonanno, E., Anemona, L., Schwartz, R. S., & Spagnoli, L. G.
- Affiliations
- University of Rome Tor Vergata (IT)
- Minneapolis Heart Institute Foundation (US)
- Corresponding author
- Spagnoli, Luigi Giusto
- ORCID
- Venue
- Journal of the American College of Cardiology
- Publisher
- Elsevier BV
- Published
- 2005-05
- Volume
- 45
- Issue
- 10
- Pages
- 1585-1593
- ISSN
- 0735-1097 (ISSN-L)
- OpenAlex
- W201422399
- Cited by
- 238
- References
- 33
- Citations by year
- 2026: 3 · 2025: 9 · 2024: 7 · 2023: 4 · 2022: 12 · 2021: 11 · 2020: 18 · 2019: 7 · 2018: 8 · 2017: 6 · 2016: 9 · 2015: 4 · 2014: 11 · 2013: 11 · 2012: 12
- FWCI
- 7.33
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Journal of the American College of Cardiology (publishedVersion)
- PubMed (publishedVersion)
- Cineca Institutional Research Information System (Tor Vergata University) (submittedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Coronary Interventions and Diagnostics
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Cardiac Imaging and Diagnostics
- Keywords
- active inflammation, vulnerable plaque, stable plaque, acute myocardial infarction, stable angina, coronary artery disease, inflammatory cell infiltration, acute coronary syndrome
- MeSH terms
- CD68 Molecule, Aged, Aged, 80 and over, Angina Pectoris, Arteritis, Cause of Death, Chronic Disease, Coronary Artery Disease, Coronary Disease, Coronary Thrombosis, Coronary Vessels, Female, Flow Cytometry, HLA-DR Antigens, Humans, Immunoenzyme Techniques, Leukocytes, Macrophages, Male, Middle Aged, Myocardial Infarction, T-Lymphocytes, Antigens, Differentiation, Myelomonocytic, Antigens, CD, CD3 Complex, Inflammation Mediators, Coronary Stenosis
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