Heterogeneity in the remodeling of aneurysms of the ascending aorta with tricuspid aortic valves.
OBJECTIVE
The study addresses mechanisms driving the formation of ascending aortic aneurysms by comparing the maximal dilatation area with the transition area immediately adjacent to the normal aortic tissue left in place during surgical repair.


METHODS
Aortic wall specimens were taken from the maximal dilatation area and transition area in 10 patients undergoing surgery for ascending aortic aneurysms and fixed for histology and immunohistochemistry for vascular smooth muscle cells (alpha-actin), endothelial cells (CD31), and macrophages (CD68). Tissue concentrations of vascular endothelial growth factor, matrix metalloproteinase-2, and matrix metalloproteinase-9 were determined by enzyme-linked immunosorbent assay. The results are expressed as medians with their 25th and 75th centiles.


RESULTS
Vascular smooth muscle cells were significantly more abundant in the maximal dilatation area than in the transition area (20.3 [14.8-24.4]/10(-2) mm2 vs 8.0 [6.4-9.3]/10(-2) mm2, respectively, P = .002). In the maximal dilatation area, vascular smooth muscle cells had lost their typical lamellar organization, whereas it was preserved in the transition area. Microvessels were significantly more abundant in the media of transition area than in the maximal dilatation area (7.5 [2.9-10.1]/mm2 vs 1.75 [1.5-2.0]/mm2, respectively, P = .008) and were associated with an inflammatory cell infiltration that predominated in their immediate vicinity. There were no significant differences in vascular endothelial growth factor, matrix metalloproteinase-2, and matrix metalloproteinase-9 between both areas.


CONCLUSIONS
The transition area appears as a disease progression front characterized by microvessel formation and inflammatory cell infiltration. In contrast, increased vascular smooth muscle cell density in the maximal dilatation area suggests a healing process, although inefficient to prevent aortic dilatation.
Kirsch
E W Matthias
EW
Surgical Research Center, Paris XII University, IFR de Médecine, Hôpital Henri Mondor, Créteil, France. matthias.kirsch@hmn.aphp.fr
Radu
N Costin
NC
Gervais
Marianne
M
Allaire
Eric
E
Loisance
Daniel Y
DY
D000199:Actins / Q000032:analysis; D000368:Aged; D015703:Antigens, CD / Q000032:analysis; D015214:Antigens, Differentiation, Myelomonocytic / Q000032:analysis; D001011:Aorta / Q000473:pathology*; D001014:Aortic Aneurysm / Q000473:pathology*; D001021:Aortic Valve; D004108:Dilatation, Pathologic; D018450:Disease Progression; D042783:Endothelial Cells / Q000473:pathology; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006349:Heart Valve Diseases / Q000150:complications / Q000473:pathology*; D006801:Humans; D008264:Macrophages / Q000473:pathology; D008297:Male; D020778:Matrix Metalloproteinase 2 / Q000032:analysis; D020780:Matrix Metalloproteinase 9 / Q000032:analysis; D008875:Middle Aged; D032389:Myocytes, Smooth Muscle / Q000473:pathology; D009389:Neovascularization, Pathologic; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000032:analysis; D042461:Vascular Endothelial Growth Factor A / Q000032:analysis; D000097382:CD68 Molecule
D000199:Actins; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D020778:Matrix Metalloproteinase 2; D020780:Matrix Metalloproteinase 9; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D042461:Vascular Endothelial Growth Factor A; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C467484:VEGFA protein, human