Analysis of the relationship between central adiposity and biomechanical, histological, and immunohistochemical properties of the anterior wall of abdominal aortic aneurysms
Adipose tissue plays a role in atherogenesis and degeneration of the vascular wall. However, the relationship between aortic abdominal aneurysm (AAA) and adipose tissue is controversial. This study aimed to correlate the biomechanical properties (elasticity and resistance), histology and immunohisto...
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Published in | JVS-vascular science Vol. 6; p. 100283 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
01.01.2025
Elsevier |
Subjects | |
Online Access | Get full text |
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Summary: | Adipose tissue plays a role in atherogenesis and degeneration of the vascular wall. However, the relationship between aortic abdominal aneurysm (AAA) and adipose tissue is controversial. This study aimed to correlate the biomechanical properties (elasticity and resistance), histology and immunohistochemistry findings of aortic tissue fragments from abdominal aortic aneurysms (AAAs) with the abdominal fat distribution determined by computed tomography scans.
This retrospective study analyzed data from biomechanical tests performed on fragments of the anterior wall of AAA obtained during open surgical repair. A uniaxial test was used to determine the tissue's failure tensile strength, tension, stress, and elasticity (strain). Preoperative computed tomography scans were used to quantify abdominal circumference at the L3-L4 and umbilical levels. Visceral and subcutaneous fat areas were quantified at these levels using tissue radiodensity. Univariate analysis and multiple regression models were used to correlate adiposity measures with biomechanical variables, considering factors such as hypertension, diabetes, and smoking status. Histological analysis (hematoxylin and eosin staining) was performed on twenty-five specimens, and immunohistochemical analysis (CD20, CD68, CD45, peroxisome proliferator activated receptor-γ [PPAR-γ], KLF5, and tumor necrosis factor-α) was performed on 13 specimens.
The most common risk factors were hypertension (82%) and smoking (85%). Diabetes mellitus was present in 21.8%. No correlation was found between visceral fat area and biomechanical parameters or maximum AAA diameter. Predominance of visceral adipose tissue at L3-L4 and the umbilical level was associated with lower fibrosis in all layers of the abdominal wall (subcutaneous, 61% vs visceral, 41%), higher PPAR-γ expression in the tunica media (subcutaneous, 170.5-199.0 positive cells/mm2 vs visceral, 957.88-1038.50 positive cells/mm2; P = .033), and lower elastic fiber concentration in the tunica media. (subcutaneous, 40.5% vs visceral, 31.5%).
No relationship was found between the biomechanical parameters of the AAA wall and visceral or subcutaneous fat areas. The predominance of visceral fat was associated with increased adipocyte cellularity and decreased elastic fiber concentration in the tunica media of the anterior AAA wall.
This study provides valuable insights into the complex relationship between adiposity and abdominal aortic aneurysms (AAAs). Although epidemiological studies have linked obesity to AAA, this research uniquely examines the microstructural effects of visceral fat on the AAA wall. Our findings suggest that visceral fat may influence the histological composition of the AAA wall, specifically by increasing peroxisome proliferator activated receptor-γ expression, decreasing fibrosis, and reducing elastic fibers in the medial layer. However, visceral and subcutaneous fat do not seem to affect the overall biomechanical properties of established AAA significantly. This finding may indicate that the metabolic and inflammatory effects of visceral fat are not the primary drivers of AAA expansion or rupture risk, potentially guiding future research and clinical management strategies. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 2666-3503 2666-3503 |
DOI: | 10.1016/j.jvssci.2025.100283 |