on May 28, 2009
Published online before print May 28, 2009, doi: 10.1161/STROKEAHA.108.528091
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Submitted on October 5, 2008
From the Laboratory of Hemodynamics and Cardiovascular Technology (E.F., N.S.), Swiss Federal Institute of Technology, Lausanne, Switzerland; the Institute of Anatomy (G.G.F.), Medical University of Graz, Austria; the Division of Anatomy, Department of Morphology (J.F.), CMU Geneva, Switzerland; the Biomedical Imaging Group (D.S., M.U.), Swiss Federal Institute of Technology, Lausanne, Switzerland; and the Neurointerventional Division, Clinical Neuroscience Department (D.A.R.), Geneva University Hospital, Switzerland. * To whom correspondence should be addressed. E-mail: edouard.fonck{at}a3.epfl.ch.
Background and Purpose—Aging affects elastin, a key component of the arterial wall integrity and functionality. Elastin degradation in cerebral vessels is associated with cerebrovascular disease. The goal of this study is to assess the biomechanical properties of human cerebral arteries, their composition, and their geometry, with particular focus on the functional alteration of elastin attributable to aging. Methods—Twelve posterior cranial arteries obtained from human cadavers of 2 different age groups were compared morphologically and tested biomechanically before and after enzymatic degradation of elastin. Light, confocal, and scanning electron microscopy were used to analyze and determine structural differences, potentially attributed to aging. Results—Aging affects structural morphology and the mechanical properties of intracranial arteries. In contrast to main systemic arteries, intima and media thicken while outer diameter remains relatively constant with age, leading to concentric hypertrophy. The structural morphology of elastin changed from a fiber network oriented primarily in the circumferential direction to a more heterogeneously oriented fiber mesh, especially at the intima. Biomechanically, cerebral arteries stiffen with age and lose compliance in the elastin dominated regime. Enzymatic degradation of elastin led to loss in compliance and stiffening in the young group but did not affect the structural and material properties in the older group, suggesting that elastin, though present in equal quantities in the old group, becomes dysfunctional with aging. Conclusions—Elastin loses its functionality in cerebral arteries with aging, leading to stiffer less compliant arteries. The area fraction of elastin remained, however, fairly constant. The loss of functionality may thus be attributed to fragmentation and structural reorganization of elastin occurring with age.
Accepted on February 23, 2009
Effect of Aging on Elastin Functionality in Human Cerebral Arteries
Edouard Fonck PhD*;
Key words: elastin and aging • elasticity and stiffness • structural properties • cerebral arteries