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      Age-Related Changes in the Elastic Tissue of the Human Aorta

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          Abstract

          Background: Age-related arterial alterations affecting cells, matrix and biomolecules are the main culprit for initiation and progression of cardiovascular disease. The objective of this study is to gain further insights into the complex mechanism of elastic tissue ageing in human aortic blood vessels. Methods: One hundred and nineteen human aortic tissue samples were collected from adult patients (101 males, 18 females; age 40–86 years) undergoing coronary artery bypass grafting. Overall extracellular matrix architecture was examined by multiphoton laser scanning microscopy and histology. Matrix metalloproteinases 2 and 9, corresponding tissue inhibitors 1 and 2 as well as desmosine were determined. mRNA levels of tropoelastin were assessed by quantitative RT-PCR. Results: Age-related destruction of the vascular elastic laminas as well as a loss of interlamina cross-links were observed by laser scanning microscopy. These results were confirmed by histology indicating increasing interlamina gaps. There were no significant differences in matrix turnover or desmosine content. A steady decrease in tropoelastin mRNA by about 50% per 10 years of age increase was observed. Conclusions: Our findings indicate that ageing is accompanied by a destruction of the elastic vascular structure. However, tropoelastin expression analysis suggests that elastogenesis occurs throughout life with constantly decreasing levels.

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          Mechanical factors in arterial aging: a clinical perspective.

          Michael F O'Rourke, Junichiro Hashimoto (2007)
          The human arterial system in youth is beautifully designed for its role of receiving spurts of blood from the left ventricle and distributing this as steady flow through peripheral capillaries. Central to such design is "tuning" of the heart to arterial tree; this minimizes aortic pressure fluctuations and confines flow pulsations to the larger arteries. With aging, repetitive pulsations (some 30 million/year) cause fatigue and fracture of elastin lamellae of central arteries, causing them to stiffen (and dilate), so that reflections return earlier to the heart; in consequence, aortic systolic pressure rises, diastolic pressure falls, and pulsations of flow extend further into smaller vessels of vasodilated organs (notably the brain and kidney). Stiffening leads to increased left ventricular (LV) load with hypertrophy, decreased capacity for myocardial perfusion, and increased stresses on small arterial vessels, particularly of brain and kidney. Clinical manifestations are a result of diastolic LV dysfunction with dyspnea, predisposition to angina, and heart failure, and small vessel degeneration in brain and kidney with intellectual deterioration and renal failure. While aortic stiffening is the principal cause of cardiovascular disease with age in persons who escape atherosclerotic complications, it is not a specific target for therapy. The principal target is the smooth muscle in distributing arteries, whose relaxation has little effect on peripheral resistance but causes substantial reduction in the magnitude of wave reflection. Such relaxation is achieved through regular exercise and with the vasodilating drugs that are used in modern treatment of hypertension and cardiac failure.
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            Arterial and Cardiac Aging: Major Shareholders in Cardiovascular Disease Enterprises: Part I: Aging Arteries: A “Set Up” for Vascular Disease

            Edward G. Lakatta, Daniel Levy (2003)
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              Ageing of the conduit arteries.

              S E Greenwald (2007)
              Conduit arteries become stiffer with age due to alterations in their morphology and the composition of the their major structural proteins, elastin and collagen. The elastic lamellae undergo fragmentation and thinning, leading to ectasia and a gradual transfer of mechanical load to collagen, which is 100-1000 times stiffer than elastin. Possible causes of this fragmentation are mechanical (fatigue failure) or enzymatic (driven by matrix metallo proteinases (MMP) activity), both of which may have genetic or environmental origins (fetal programming). Furthermore, the remaining elastin itself becomes stiffer, owing to calcification and the formation of cross-links due to advanced glycation end-products (AGEs), a process that affects collagen even more strongly. These changes are accelerated in the presence of disease such as hypertension, diabetes and uraemia and may be exacerbated locally by atherosclerosis. Raised MMP activity, calcification and impaired endothelial function are also associated with a high level of plasma homocysteine, which itself increases with age. Impaired endothelial function leads to increased resting vascular smooth muscle tone and further increases in vascular stiffness and mean and/or pulse pressure. The effect of increased stiffness, whatever its underlying causes, is to reduce the reservoir/buffering function of the conduit arteries near the heart and to increase pulse wave velocity, both of which increase systolic and pulse pressure. These determine the peak load on the heart and the vascular system as a whole, the breakdown of which, like that of any machine, depends more on the maximum loads they must bear than on their average. Reversing or stabilising the increased arterial stiffness associated with age and disease by targeting any or all of its causes provides a number of promising new approaches to the treatment of systolic hypertension and its sequelae, the main causes of mortality and morbidity in the developed world. Copyright (c) 2007 Pathological Society of Great Britain and Ireland.
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                Author and article information

                Journal
                Journal ID (publisher-id): JVR
                Journal ID (nlm-ta): J Vasc Res
                Journal ID (doi): 10.1159/issn.1018-1172
                Title: Journal of Vascular Research
                Publisher: S. Karger AG
                ISSN (Print): 1018-1172
                ISSN (Electronic): 1423-0135
                Publication date Subscription-year: 2012
                Publication date (Print): December 2011
                Publication date (Electronic): 18 November 2011
                Volume: 49
                Issue: 1
                Pages: 77-86
                Affiliations
                aDepartment of Thoracic and Cardiovascular Surgery, University Hospital Tübingen, and bInter-University Centre for Medical Technology, Eberhard Karls University, Tübingen, cInstitute for Microbiology and Hygiene, Charité – Universitätsmedizin Berlin, Berlin, dDepartment of Cell and Tissue Engineering, Fraunhofer Institute for Interfacial Engineering and Biotechnology , Stuttgart, Germany; eFaculty of Medicine, University of Alcalá de Henares, Madrid, Spain; fINSERM, Hôpital Bichat, Université Paris 7, Paris, France; gUniversity of Texas Health Center at Tyler, Tyler, Tex., USA
                Author notes
                *Dr. Ulrich Stock, Department of Thoracic and Cardiovascular Surgery, University Hospital Tübingen, Silcher Strasse 7/1, DE–72076 Tübingen (Germany), Tel. +49 707 1298 6638, E-Mail Ulrich.Stock@med.uni-tuebingen.de
                Article
                Publisher ID: 331278 Other ID: J Vasc Res 2012;49:77–86
                DOI: 10.1159/000331278
                PubMed ID: 22105095
                SO-VID: be3de975-82a5-4d38-ac5c-00d1a7669094
                Copyright © © 2011 S. Karger AG, Basel
                License:

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                Date received : 23 December 2010
                Date accepted : 27 July 2011
                Page count
                Figures: 6, Tables: 1, Pages: 10
                Categories
                Subject: Research Paper

                ScienceOpen disciplines: General medicine,Neurology,Cardiovascular Medicine,Internal medicine,Nephrology
                Keywords: Vascular ageing,Ageing,Elastin,Vascular imaging,Aorta
                Data availability:
                ScienceOpen disciplines: General medicine, Neurology, Cardiovascular Medicine, Internal medicine, Nephrology
                Keywords: Vascular ageing, Ageing, Elastin, Vascular imaging, Aorta

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