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Diffuse and Active Inflammation Occurs in Both Vulnerable and Stable Plaques of the Entire Coronary Tree

A Histopathologic Study of Patients Dying of Acute Myocardial Infarction

Alessandro Mauriello, MD^_*, Giuseppe Sangiorgi, MD, FESC, Stefano Fratoni, MD^_*, Giampiero Palmieri, MD^_*, Elena Bonanno, MD^_*, Lucia Anemona, MD^_*, Robert S. Schwartz, MD, FACC, FAHA and Luigi Giusto Spagnoli, MD^_*,_*

^_* Department of Pathology, University of Rome Tor Vergata, Rome, Italy
Department of Cardiovascular Diseases, University of Rome Tor Vergata, Rome, Italy
Minnesota Cardiovascular Research Institute, Minneapolis Heart Institute Foundation, Minneapolis, Minnesota

View larger version (108K): [in a new window]   Figure 1 Micrographs showing the coronary tree from one patient who died of acute myocardial infarction (AMI). (A1 to A4) Infarct-related coronary artery (IRA) (left circumflex coronary). (A1) Coronary section showing cap rupture near the shoulder (arrow) associated with an acute thrombus (T) (hematoxylin-eosin, x2); (A2) high-power view of the fibrous cap at the rupture site showing many macrophages cells, CD68-positive (x20); (A3) in the same plaque, numerous T-lymphocytes, CD3-positive, were present in the shoulder (alkaline phosphatase, x20); (A4) on a serial section, double immunohistochemistry showed that many T-lymphocytes were positive also for human leukocyte antigen-DR antibody, indicating an activated state (diaminobenzidine, x20). (B and C) Coronary plaques in the non-IRA segments from the same patients. (B1) A vulnerable plaque (thin fibrous cap atheromata) in the left anterior descending coronary vessel, characterized by a large lipid-necrotic core associated with a thin inflamed fibrous cap (Movat, x2); (B2) high-power view of the fibrous cap of the plaque represented in the insert of panel B1 showing many macrophages, CD68-positive (x10); (B3) immunohistochemistry stain against HLA-DR antigens showing a diffuse positive reaction in the cap of the plaque represented in the insert of panel B1 (x15). (C1) Micrograph showing another stenotic plaque present in the right coronary artery of the same patient (Movat, x2); (C2) a very large number of macrophages, CD68-positive, were present in the cap (insert of panel C1, x10), associated with numerous T-lymphocytes, CD3-positive ([C3], x10).

View larger version (30K): [in a new window]   Figure 2 Distribution of inflammatory cells in the coronary plaques (data are presented as means ± standard error of the mean). (A) Inflammatory cells in the acute myocardial infarction (AMI) group were significantly higher than those in the chronic stable angina (SA) and control (CTRL) groups, independently of the type of plaque observed (statistical analysis: A vs. B: p = 0.001; A vs. C: p = 0.001; B vs. C: p = not significant). (B) In the AMI group, no significant difference was observed between infarct-related coronary arteries (IRAs) and non-IRAs, independently of the type of plaque observed. (C) Both culprit and vulnerable plaques in the AMI group showed significantly more inflammatory infiltrates, compared with those observed in the stable plaques of the same group of patients (A vs. C: p = 0.006; B vs. C: p = 0.04). No statistically significant differences were observed between culprit and vulnerable plaques (p = 0.21). However, stable plaques in AMI patients had three-fold greater inflammation than stable and vulnerable coronary plaques of SA patients, and about four-fold of that measured in CTRL patients (C vs. D: p = 0.001; C vs. E: p = 0.001). (D) Immunohistochemical characterization of the various cytotypes in the coronary plaques. Significantly fewer CD68- and CD3-positive cells were found in stable and vulnerable plaques from SA and CTRL groups compared with those from AMI patients (AMI vs. SA and CTRL: actin p = 0.01; CD68: p = 0.01; CD3: p = 0.01).

View larger version (126K): [in a new window]   Figure 3 Micrographs showing the three major epicardial coronary arteries from a patient from the control group who died of a noncardiac cause. (A1 to A4) Left anterior descending coronary vessel. (A1) A prevalently fibrous plaque characterized by a small lipidic-necrotic core associated with a thick fibrous cap (Movat, x4). (A2) Within the plaque cap, only a small number of macrophage-type foam cells, CD68-positive, was present (x20), associated with a great number of smooth muscle cells, actin-positive ([A3], x20). In the shoulder, a small infiltrate consisting of T-lymphocytes, CD3-positive, was also observed ([A4], x20). (B and C) Left circumflex and right coronary vessels, respectively, from the same patient. Two stable plaques characterized by a concentric, predominantly fibrotic plaque with morphological features similar to those of the plaque shown in panel A are shown as an example (Movat, x2).