Document Detail


Hyperplastic cellular remodeling of the media in ascending thoracic aortic aneurysms.
MedLine Citation:
PMID:  16116068     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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. METHODS AND 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:
Paul C Y Tang; Michael A Coady; Constantinos Lovoulos; Alan Dardik; Mihaela Aslan; John A Elefteriades; George Tellides
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Circulation     Volume:  112     ISSN:  1524-4539     ISO Abbreviation:  Circulation     Publication Date:  2005 Aug 
Date Detail:
Created Date:  2005-08-23     Completed Date:  2006-02-15     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1098-105     Citation Subset:  AIM; IM    
Affiliation:
Department of Surgery, Yale University School of Medicine, New Haven, CT, USA.
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MeSH Terms
Descriptor/Qualifier:
Aorta / enzymology,  pathology*,  physiopathology
Aortic Aneurysm / metabolism,  pathology*,  physiopathology
Apoptosis
Biopsy
Cell Survival
Extracellular Matrix / pathology
Humans
Hyperplasia
Matrix Metalloproteinases / metabolism
Muscle, Smooth, Vascular / enzymology,  pathology,  physiopathology
Tunica Media / enzymology,  pathology*,  physiopathology
Vasodilation
Grant Support
ID/Acronym/Agency:
P01-HL-70295-01/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
EC 3.4.24.-/Matrix Metalloproteinases
Comments/Corrections
Comment In:
Circulation. 2005 Aug 23;112(8):1082-4   [PMID:  16116065 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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