doi: 10.1161/01.RES.0000261611.53084.ad
© 2007 American Heart Association, Inc.
Editorials |
Lasting Effects of Lost Vascular Elasticity
From the Department of Internal Medicine, Roy J. and Lucille Carver College of Medicine, University of Iowa, Iowa City.
Correspondence to Robert M. Weiss, MD, Department of Internal Medicine, Room E317-A GH, University of Iowa College of Medicine, 200 Hawkins Drive, Iowa City, IA 52242 E-mail robert-weiss@uiowa.edu
See related article, pages 738–746
Key Words: aneurysm • aortic valve • mouse model
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
The term elasticity, in materials science terms, indicates the degree to which energy is conserved during a deformation-recoil reaction. When a steel ball is dropped onto a rigid surface, it rebounds closer to its initial height than, say, a rubber ball. In that configuration, steel is said to be more elastic than rubber, because more of its potential energy is recovered during the reaction. In cardiovascular science, the term elasticity is sometimes appropriated to indicate compliance or deformability, but such license can sometimes lead to erroneous mechanistic constructs. A spoiled plum is deformable but, when dropped, interacts with the floor in a highly inelastic manner.
Aortic aneurysm is primarily responsible for more than 13 000 deaths and is a contributing factor in 61 000 hospital discharges annually in the United States,1 statistics that tend to underestimate comorbid contributions to processes such as systolic heart failure, atheroembolic stroke, and kidney disease. Traditional cardiovascular risk factors such as hypertension, hyperlipidemia, diabetes, and tobacco abuse are associated with aortic aneuryms when incurred during old age, when aneurysm prevalence reaches 12.5% in men.1 But a significant minority of catastrophic aortic disease events occurs in younger patients, often enough during childhood, arising as a result of deficiencies in the inherent material properties of the aorta itself, along with putatively maladaptive tissue responses to subsequent vascular injury.
The diverse processes leading to catastrophic events share a common end result: loss of elasticity in the aortic wall (Figure). Hypertension and hyperlipidemia, especially when combined, evoke
Related Article:
Circ. Res. 2007 100: 738-746.