Abstract
The pathogenesis of the abdominal aortic aneurysm (AAA) shows several hallmarks of atherosclerotic and atherothrombotic disease, but comprises an additional, predominant feature of proteolysis resulting in the degradation and destabilization of the aortic wall. This review aims to summarize the current knowledge on AAA development, involving the accumulation of neutrophils in the intraluminal thrombus and their central role in creating an oxidative and proteolytic environment. Particular focus is placed on the controversial role of heme oxygenase 1/carbon monoxide and nitric oxide synthase/peroxynitrite, which may exert both protective and damaging effects in the development of the aneurysm. Treatment indications as well as surgical and pharmacological options for AAA therapy are discussed in light of recent reports.
Highlights
The Intraluminal ThrombusIn 70–80% of abdominal aortic aneurysm (AAA) patients, the vessel wall is covered by an intraluminal thrombus (ILT, Figure 2), which generally does not preclude blood flow and shows little compression throughout the cardiac cycle [13, 14]
Specialty section: This article was submitted to Thrombosis, a section of the journal Frontiers in Cardiovascular Medicine
This review aims to summarize the current knowledge on abdominal aortic aneurysm (AAA) development, involving the accumulation of neutrophils in the intraluminal thrombus and their central role in creating an oxidative and proteolytic environment
Summary
In 70–80% of AAA patients, the vessel wall is covered by an intraluminal thrombus (ILT, Figure 2), which generally does not preclude blood flow and shows little compression throughout the cardiac cycle [13, 14]. The effect is accompanied by a reduction in leukocyte infiltration and lower release of proteases within the mural thrombus, which results in decreased degradation of elastic fibers, and promotes thrombus colonization by SMCs. by sequestering and activating platelets, erythrocytes, neutrophils, and macrophages, the ILT exposes the vessel wall to a local milieu of highly concentrated cytokines, proteases, and reactive oxygen species (ROS) that promotes aneurysm development. The presence of a large thrombus leads to localized hypoxia at the underlying aortic wall, which triggers adventitial angiogenesis and aggravates inflammatory infiltration from the outer vessel layers [21] Despite this role in supporting the inflammatory and proteolytic mechanisms of AAA pathogenesis, the mural thrombus has repeatedly been suggested to protect the aneurysm from rupture by reducing the peak wall stress and altering wall stress distribution [22]. The relation between AAA development and Hmox promoter polymorphism requires further analysis
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