Editorials |
From the Department of Internal Medicine, University of Iowa, Iowa City.
Correspondence to Francis J. Miller, Jr., MD, Department of Internal Medicine, E314-4 GH, University of Iowa Hospitals, Iowa City, IA 52242. E-mail francis-miller@uiowa.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Abdominal aortic aneurysms (AAAs) are present in 8% of men >60 years of age.1 The diagnosis of AAA in many patients is made only after aneurysm rupture, after which mortality is high. Depending on the size of the AAA, often times the only treatment available after its discovery is "watchful waiting." Although aneurysm diameter is generally used to assess timing of surgical repair, rupture also occurs in AAAs less than 5 cm in diameter.2 The absence of effective medical therapy for AAA is explained in part by a poor understanding of the processes involved in the development of aneurysms. Treatment that could slow AAA growth would have important therapeutic value.
See page 2017
An emerging concept is that AAAs develop in the setting of oxidative stress, whereby reactive oxygen species (ROS) mediate activation of matrix degrading proteins and smooth muscle cell apoptosis, resulting in loss of medial elastic lamellae and thinning of the tunica media. This concept is supported by the observations that infiltration of inflammatory cells into the vessel wall and subsequent elaboration of matrix metalloproteinases (MMPs) are associated with formation of AAAs. ROS are abundantly produced by inflammatory cells and activate MMPs.3 And, in humans, ROS levels and oxidative injury are greater in AAAs compared with adjacent nonaneurysmal aortic segments.4
Mechanical forces also contribute to aortic remodeling. The artery wall is subject to three distinct fluid-induced forces: (1) pressure created by hydrostatic forces, (2) circumferential stretch exerting longitudinal forces, and (3) shear stress created by the movement of
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