Invited commentary
Article Outline
The clinical predictors of abdominal aortic aneurysm (AAA) expansion and rupture have recently been better delineated in randomized trials, but the dominant factor for rupture risk remains aortic diameter. Indeed, an aortic diameter of >5.5 cm is the cutoff for risk benefit-ratio for operative repair.1 Many large AAAs do not rupture, and it would be ideal to have additional patient-level information that might better predict the risk of an AAA rupture. It is now clear from recent sophisticated computed tomography imaging studies that geometry and wall stress play a significant role in local aortic wall stress. For example, significant aortic tortuosity and asymmetric geometry confer a greater AAA rupture risk.2
The study by Martino et al highlights a correlative measure of aortic wall strength and thickness in humans. Specifically, comparison was made of wall thickness and tensile strength between ruptured AAA and elective AAA tissue. The authors show that mean aortic wall thickness was greater in ruptured compared with nonruptured tissue. Further, tensile strength of the ex vivo specimen was lower in ruptured aortic tissue than nonruptures (P = .04, noncorrected). Although this study is limited by its small patient number, lack of a normal aorta control group for biomechanical parameters and imaging, and heterogeneity of specimens, this study is intriguing and hypothesis generating.
While it is not counterintuitive that ruptured AAA tissue specimens may have weaker tissue than intact AAAs, it is important to note that the tissue analyzed was not from the site of rupture but the anterior wall. Thus, patients with any given size AAA may have intrinsically weaker walls throughout the aorta. Supportive of this, but not necessarily intuitive, is the finding that ruptured AAAs have thicker walls. This is consistent with greater inflammatory processes in these aortas. The molecular pathologic remodeling process was not evaluated in this study, but likely involves leukocyte-driven matrix breakdown via matrix metalloproteinase activity. Complementary studies with gene array and single nucleotide polymorphism analysis hold further promise to elucidate these mechanisms.
The current paper adds to our understanding of end-stage AAA pathophysiology in humans. These data require further validation in larger patient imaging studies, particularly to determine a threshold thickness of aortic wall as a prognostic variable. In addition to the well known risk factors of AAA growth including size, smoking, diastolic, hypertension, and emphysema, we should now also consider the finer points of imaging analysis.
References
- . Guidelines for the treatment of abdominal aortic aneurysms (report of a subcommittee of the joint council of the American Association for Vascular Surgery and Society for Vascular Surgery) . J Vasc Surg . 2003;37:1106–1117
- Anatomic characteristics of ruptured abdominal aortic aneurysm on conventional CT scans (implications for rupture risk) . J Vasc Surg . 2004;39:1243–1252
PII: S0741-5214(05)01923-3
doi:10.1016/j.jvs.2005.11.011
© 2006 The Society for Vascular Surgery. Published by Elsevier Inc. All rights reserved.
