title: Hyperplastic cellular remodeling of the media in ascending thoracic aortic aneurysms.
abstract: BACKGROUND
  Progressive medial degeneration and atrophy is thought to be a cause of ascending thoracic aortic aneurysms in the elderly. Extensive apoptosis of vascular smooth muscle cells (VSMCs) has been demonstrated in the media of abdominal aortic aneurysms. We investigated whether medial atrophy from loss of VSMCs occurs in primary ascending thoracic aortic aneurysms.
  
  
  RESULTS
  Morphometric analysis of 28 nonaneurysmal ascending thoracic aortas and 29 ascending thoracic aortic aneurysms was performed by directly measuring the thickness of their vascular layers and by indirectly calculating the area of their vascular compartments. The cellular and matrix composition of the media was assessed at the structural, protein, and transcript levels. Despite thinning of the media secondary to vascular dilatation, there was an overall increase in the medial area of aneurysms. VSMC density was preserved, implying cellular hyperplasia as a result of the increased medial mass. There was decreased expression of matrix proteins, despite sustained synthesis of these molecules, which was associated with evidence of increased matrix degradation. The remodeling and expansion of the media was most evident in comparisons between nonaneurysmal aortas versus smaller aneurysms and did not evolve further in larger aneurysms.
  
  
  CONCLUSIONS
  The mechanisms for luminal enlargement in thoracic and abdominal aortic aneurysms differ significantly with regard to the survival of VSMCs and atrophy of the media but share common pathophysiology involving degeneration of the matrix. Hyperplastic cellular remodeling of the media in ascending thoracic aortic aneurysms may be an initial adaptive response to minimize increased wall stress resulting from vascular dilatation.
authors.affiliation: Department of Surgery, Yale University School of Medicine, New Haven, CT, USA.
authors.forename: Paul C Y
authors.initials: PC
authors.lastname: Tang
authors.forename: Michael A
authors.initials: MA
authors.lastname: Coady
authors.forename: Constantinos
authors.initials: C
authors.lastname: Lovoulos
authors.forename: Alan
authors.initials: A
authors.lastname: Dardik
authors.forename: Mihaela
authors.initials: M
authors.lastname: Aslan
authors.forename: John A
authors.initials: JA
authors.lastname: Elefteriades
authors.forename: George
authors.initials: G
authors.lastname: Tellides
mesh_terms: D001011:Aorta / Q000201:enzymology / Q000473:pathology* / Q000503:physiopathology; D001014:Aortic Aneurysm / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D017209:Apoptosis; D001706:Biopsy; D002470:Cell Survival; D005109:Extracellular Matrix / Q000473:pathology; D006801:Humans; D006965:Hyperplasia; D020782:Matrix Metalloproteinases / Q000378:metabolism; D009131:Muscle, Smooth, Vascular / Q000201:enzymology / Q000473:pathology / Q000503:physiopathology; D017540:Tunica Media / Q000201:enzymology / Q000473:pathology* / Q000503:physiopathology; D014664:Vasodilation
chemical_list: D020782:Matrix Metalloproteinases