Inflammatory aortic aneurysms - A clinical review with new perspectives in pathogenesis

Objective The authors present a review of abdominal aortic aneurysms (AAAs) and to examine the literature on the diagnosis, operative management, and long-term survival of patients with inflammatory AAAs. Furthermore, to review current theories on the cause of inflammatory AAAs and present recent studies that provoke new thought on the cause of these aneurysms. Background Data inflammatory AAAs represent 3% to 10% of all AAAs and present the surgical team with a unique challenge. Progress has occurred in the technical approach to these aneurysms, and operative morbidity and mortality have been reduced. However, the pathogenesis remains an enigma. Recent studies raise questions regarding the influence of tobacco and genetic factors that accentuate an antigen-driven inflammatory response. Methods The authors conduct a review of the literature on both noninflammatory and inflammatory AAAs. Results Review of the literature of inflammatory AAAs reveals advancement in the definition, diagnosis, management, and long-term survival of patients with inflammatory AAAs. This review found an evolution in thought regarding the cause of inflammatory AAAs. In contrast to initial reports describing a distinct clinical entity, recent evidence suggests that inflammatory AAAs arise from the same causal stimulus responsible for noninflammatory AAAs. Finally, recent studies show an influence of tobacco and genetic factors on the pathogenesis. Conclusions The literature supports the theory that inflammatory AAAs arise from the same or similar antigenic stimulus which is responsible for the noninflammatory AAA. Genetic and chemical factors such as tobacco use predispose certain persons to the development of noninflammatory AAAs and others to develop the extreme end of an inflammatory spectrum, the inflammatory AAA. Furthermore, inflammatory AAAs can be managed with the same operative morbidity, mortality, and long-term survival as noninflammatory AAAs.