Fig. 2

Composite of another end-stage Tg53 proximal coronary (≈320 microns) lesion phenotype: foam-cell rich, plaque rupture, erosion, hemorrhage and thrombi. (A) Masson-trichrome stained section reveals longitudinal profile of occlusive foam-cell enriched plaque with intraplaque hemorrhage and thrombosis most prominent in the proximal plaque shoulder; direction of blood flow (⇯); bar = 200 microns. (B) High magnification of lesion shoulder reveals thrombus, foam cells, globular extracellular lipid deposits (*), red blood cells, and multilobular neutrophil (➨) adhesion on the endothelium. Bar = 20 microns. (C) PTAH stained fibrin in the lesion shoulder thrombus; bar = 20 microns. (D) Few α-actin immunostained smooth muscle cells (➨) overlying thrombosed lesion shoulder; (bar = 20 microns). (E) In contrast, fibroproliferative lesion in a distal coronary artery (identical section to (D)) reveals abundant smooth muscle cells (red) in the lesion cap and media; bar = 20 microns. (F) High magnification (bar = 8 microns) shows multilobular neutrophil (➨) adhesion onto intact endothelium (▽); red blood cells (➩) in plaque; foam cells close to lesion surface. (G) High magnification (bar = 8 microns) reveals endothelial erosion () in the distal lesion shoulder with adhered neutrophils and lymphocytes (➨), and subendothelial thrombi () which stained for fibrin (PTAH data not shown). (H) ED1 immunostained macrophage-foam cells are detected close to site of rupture () and throughout lesion. Large extracellular lipid globules (delipidated during processing) are noted; bar = 20 microns. (I) Adjacent serial section reveals MMP3 immunostained smooth muscle cells, macrophage foam cells, and rupture site (); bar = 20 microns. Note: (▽), lesion surface with intact endothelium; (ad), adventitia; (fc), foam cells; (m), media; (my), myocardium, (rbcs), red blood cells; (smcs), smooth muscle cells; (thr), thrombus.