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Isolated ascending aorta dilatation is associated with increased risk of abdominal aortic aneurysm.

ABSTRACT:

Background

Abdominal aortic aneurysm (AAA) is an asymptomatic condition characterized by progressive dilatation of the aorta. The purpose of this study is to identify important 2D-TTE aortic indices associated with AAA as predictive tools for undiagnosed AAA.

Methods

In this retrospective study, we evaluated the size of the ascending aorta in patients without known valvular diseases or hemodynamic compromise as predictive tool for undiagnosed AAA. We studied the tubular ascending aorta of 170 patients by 2-dimensional transthoracic echocardiography (2D-TTE). Patients were further divided into two groups, 70 patients with AAA and 100 patients without AAA with normal imaging results.

Results

Dilatation of tubular ascending aorta was measured in patients with AAA compared to the group with absent AAA (37.5 ± 4.8 mm vs. 31.2 ± 3.6 mm, p < 0.001, respectively) and confirmed by computed tomographic (CT) (35.6 ± 5.1 mm vs. 30.8 ± 3.7 mm, p < 0.001, respectively). An increase in tubular ascending aorta size was associated with the presence of AAA by both 2D-TTE and CT (r = 0.40, p < 0.001 and r = 0.37, p < 0.001, respectively). The tubular ascending aorta (D diameter) size of ≥33 mm or ≥ 19 mm/m² presented with 2-4 times more risk of AAA presence (OR 4.68, CI 2.18-10.25, p = 0.001 or OR 2.63, CI 1.21-5.62, p = 0.02, respectively). In addition, multiple logistic regression analysis identified tubular ascending aorta (OR 1.46, p < 0.001), age (OR 1.09, p = 0.013), gender (OR 0.12, p = 0.002), and LVESD (OR 1.24, p = 0.009) as independent risk factors of AAA presence.

Conclusions

An increased tubular ascending aortic diameter, measured by 2D-TTE, is associated with the presence of AAA. Routine 2D-TTE screening for silent AAA by means of ascending aorta analysis, may appear useful especially in older patients with a dilated tubular ascending aorta (≥33 mm).

SUBMITTER: Gallego-Colon E

PROVIDER: S-EPMC8063334 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:ObjectiveMurine models have proved instrumental in studying various aspects of abdominal aortic aneurysm (AAA), from identification of underlying pathophysiologic changes to the development of novel therapeutic strategies. In the current study, we describe a new model in which an elastase-treated donor aorta is transplanted to a recipient mouse and allowed to progress to aneurysm. We hypothesized that by transplanting an elastase-treated abdominal aorta of one genotype to a recipient mouse of a different genotype, one can differentiate pathophysiologic factors that are intrinsic to the aortic wall from those stemming from circulation and other organs.MethodsElastase-treated aorta was transplanted to the infrarenal abdominal aorta of recipient mice by end-to-side microsurgical anastomosis. Heat-inactivated elastase-treated aorta was used as a control. Syngeneic transplants were performed with use of 12-week-old C57BL/6 littermates. Transplant grafts were harvested from recipient mice on day 7 or day 14 after surgery. The aneurysm outcome was measured by aortic expansion, elastin degradation, proinflammatory cytokine expression, and inflammatory cell infiltration and compared with that produced with the established, conventional elastase infusion model.ResultsThe surgical technique success rate was 75.6%, and the 14-day survival rate was 51.1%. By day 14 after surgery, all of the elastase-treated transplanted abdominal aortas had dilated and progressed to AAAs, defined as 100% or more increase in the maximal external diameter compared with that measured before elastase perfusion, whereas none of the transplanted aortas pretreated with inactive elastase became aneurysmal (percentage increase in maximum aortic diameter: 159.36% ± 23.27%, transplanted elastase, vs 41.46% ± 9.34%, transplanted inactive elastase). Aneurysm parameters, including elastin degradation and infiltration of macrophages and T lymphocytes, were found to be identical to those observed in the conventional elastase model. Quantitative polymerase chain reaction analysis revealed similarly increased levels of proinflammatory cytokines (relative changes of mRNA in the conventional elastase model vs transplant model: tumor necrosis factor α, 1.71 ± 0.27 vs 2.93 ± 0.86; monocyte chemoattractant protein 1, 2.36 ± 0.58 vs 2.87 ± 0.51; chemokine (C-C motif) ligand 5, 3.37 ± 0.92 vs 3.46 ± 0.83; and interferon γ, 3.09 ± 0.83 vs 5.30 ± 1.69). Using green fluorescent protein transgenic mice as donors or recipients, we demonstrated that a small quantity of mononuclear leukocytes in the transplant grafts bared the genotype of the donors.ConclusionsTransplanted elastase-treated abdominal aorta could develop to aneurysm in recipient mice. This AAA transplant model can be used to examine how the microenvironment of a transplanted aneurysmal aorta may be altered by the contributions of the "global" environment of the recipient.