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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).