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Circulation. 1997;96:2115-2117

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*Substance via MeSH
Medline Plus Health Information
*Aortic Aneurysm

(Circulation. 1997;96:2115-2117.)
© 1997 American Heart Association, Inc.


Articles

Inflammation, Metalloproteinases, and Increased Proteolysis

An Emerging Pathophysiological Paradigm in Aortic Aneurysm

Prediman K. Shah, MD

From the Atherosclerosis Research Center, Division of Cardiology, and the Burns and Allen Research Institute, Cedars-Sinai Medical Center and UCLA School of Medicine, Los Angeles, Calif.

Correspondence to P.K. Shah, MD, Room 5347, Cedars-Sinai Medical Center, 8700 Beverly Blvd, Los Angeles, CA 90048. E-mail shahp@csmc.edu


Key Words: Editorials • metalloproteinases


*    Introduction
 
Abdominal aortic aneurysm is a common and potentially lethal disease with an estimated incidence of 20 to 40 cases per 100 000 persons per year.1 In the United States, nearly 45 000 operations are performed annually for AAA.2 Most aneurysms are clinically silent until the time of rupture. Elective surgical mortality for unruptured aneurysms varies from 2% to 7%, but mortality jumps to 50% to 70% when rupture occurs before surgery.2 Risk factors for the development of AAA include advancing age, male sex, chronic obstructive lung disease, cigarette smoking, hypertension, and genetic factors.2 One of the most important determinants of risk for rupture is the size of the aneurysm.2 The overall risk of rupture is 3% to 8% for aneurysms <4 cm in diameter, whereas rupture occurs in 20% to 40% of patients with an aneurysm diameter >5 cm.2 Aneurysms between 4 and 4.5 cm in diameter carry a 10% to 12% risk of rupture.2 Although there is a considerable variability in the rate of expansion, on average, expansion occurs in an exponential fashion with an {approx}10% diameter increase per year (0.3 to 0.6 cm/y for aneurysms 3 to 6 cm in size).2 Expansion rate is reduced by ß-blockers and enhanced in patients with uncontrolled diastolic hypertension, smoking, and chronic obstructive lung disease.3

Recent clinical and experimental studies have challenged the long-held notion that AAA results primarily from a complication of atherosclerosis.4 Although intimal pathological lesions characterize occlusive atherosclerotic aortic disease, one of the striking hallmarks of AAA is the . . . [Full Text of this Article]




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