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Heterogeneity of Tensile Strength and Matrix Metalloproteinase Activity in the Wall of Abdominal Aortic Aneurysms
Purpose: To measure the tensile strength of the aneurysm wall and the matrix metalloproteinase (MMP) activity in similar samples of aortic tissue. Methods: Detailed mechanical testing was conducted on 124 standardized specimens of aneurysm wall harvested from 24 patients undergoing elective aneurysm...
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Published in: | Journal of endovascular therapy 2004-08, Vol.11 (4), p.494-502 |
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creator | Vallabhaneni, Srinivasa R. Gilling-Smith, Geoffrey L. How, Thien V. Carter, Stuart D. Brennan, John A. Harris, Peter L. |
description | Purpose:
To measure the tensile strength of the aneurysm wall and the matrix metalloproteinase (MMP) activity in similar samples of aortic tissue.
Methods:
Detailed mechanical testing was conducted on 124 standardized specimens of aneurysm wall harvested from 24 patients undergoing elective aneurysm repair. The intrasac pressure required to cause aneurysm rupture was calculated based upon the Law of Laplace. In addition, MMP-2 and 9 were assayed from these specimens. Sixty specimens of nonaneurysmal aorta from 6 cadaveric organ donors served as controls. Intrasubject and intersubject variations were analyzed.
Results:
In the aneurysm specimens, the Young's modulus was 1.80times106 N/m2, the load at break was 6.36 N, the strain at break was 0.30, the ultimate strength was 0.53times106 N/m2, and the MMP activity was 312 for MMP-2 and 460 for MMP-9. In the controls, the circumferential measurements were a Young's modulus of 1.82times106 N/m2, a load at break of 5.43 N, strain at break of 0.29, ultimate strength of 0.61times106 N/m2, and MMP activity of 395 for MMP-2 and 2019 for MMP-9. Longitudinal measurements in controls were a Young's modulus of 1.38times106 N/m2, a load at break of 11.39 N, a strain at break of 0.33, and ultimate strength of 1.30times106 N/m2. Intra and intersubject variation of all parameters was very high. Based upon the lowest measured tensile strength for each aneurysm, the intrasac pressure required to cause rupture varied from 142 to 982 mmHg.
Conclusions:
Localized “hot spots” of MMP hyperactivity could lead to focal weakening of the aneurysm wall and rupture at relatively low levels of intraluminal pressure. These data suggest that tensile strength of the sac is just as important as intrasac tension in determining the risk of rupture. Moreover, these observations may explain why some small aneurysms rupture and larger aneurysms do not. Assessment of rupture risk based on computation or measurement of wall stress may be subject to error and inaccuracy due to variations in wall tensile strength. |
doi_str_mv | 10.1583/04-1239.1 |
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To measure the tensile strength of the aneurysm wall and the matrix metalloproteinase (MMP) activity in similar samples of aortic tissue.
Methods:
Detailed mechanical testing was conducted on 124 standardized specimens of aneurysm wall harvested from 24 patients undergoing elective aneurysm repair. The intrasac pressure required to cause aneurysm rupture was calculated based upon the Law of Laplace. In addition, MMP-2 and 9 were assayed from these specimens. Sixty specimens of nonaneurysmal aorta from 6 cadaveric organ donors served as controls. Intrasubject and intersubject variations were analyzed.
Results:
In the aneurysm specimens, the Young's modulus was 1.80times106 N/m2, the load at break was 6.36 N, the strain at break was 0.30, the ultimate strength was 0.53times106 N/m2, and the MMP activity was 312 for MMP-2 and 460 for MMP-9. In the controls, the circumferential measurements were a Young's modulus of 1.82times106 N/m2, a load at break of 5.43 N, strain at break of 0.29, ultimate strength of 0.61times106 N/m2, and MMP activity of 395 for MMP-2 and 2019 for MMP-9. Longitudinal measurements in controls were a Young's modulus of 1.38times106 N/m2, a load at break of 11.39 N, a strain at break of 0.33, and ultimate strength of 1.30times106 N/m2. Intra and intersubject variation of all parameters was very high. Based upon the lowest measured tensile strength for each aneurysm, the intrasac pressure required to cause rupture varied from 142 to 982 mmHg.
Conclusions:
Localized “hot spots” of MMP hyperactivity could lead to focal weakening of the aneurysm wall and rupture at relatively low levels of intraluminal pressure. These data suggest that tensile strength of the sac is just as important as intrasac tension in determining the risk of rupture. Moreover, these observations may explain why some small aneurysms rupture and larger aneurysms do not. Assessment of rupture risk based on computation or measurement of wall stress may be subject to error and inaccuracy due to variations in wall tensile strength.</description><identifier>ISSN: 1526-6028</identifier><identifier>EISSN: 1545-1550</identifier><identifier>DOI: 10.1583/04-1239.1</identifier><identifier>PMID: 15298501</identifier><language>eng</language><publisher>Los Angeles, CA: SAGE Publications</publisher><subject>Aorta, Abdominal - enzymology ; Aorta, Abdominal - physiopathology ; Aortic Aneurysm, Abdominal - enzymology ; Aortic Aneurysm, Abdominal - physiopathology ; Aortic Rupture - etiology ; Case-Control Studies ; Humans ; Matrix Metalloproteinase 2 - metabolism ; Matrix Metalloproteinase 9 - metabolism ; Risk Factors ; Stress, Mechanical ; Tensile Strength</subject><ispartof>Journal of endovascular therapy, 2004-08, Vol.11 (4), p.494-502</ispartof><rights>2004 SAGE Publications</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c312t-3a0945aefc9ee4c32ed3fdc3c006f944987062174c03b12d582e6011d80f53ba3</citedby><cites>FETCH-LOGICAL-c312t-3a0945aefc9ee4c32ed3fdc3c006f944987062174c03b12d582e6011d80f53ba3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925,79364</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15298501$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Vallabhaneni, Srinivasa R.</creatorcontrib><creatorcontrib>Gilling-Smith, Geoffrey L.</creatorcontrib><creatorcontrib>How, Thien V.</creatorcontrib><creatorcontrib>Carter, Stuart D.</creatorcontrib><creatorcontrib>Brennan, John A.</creatorcontrib><creatorcontrib>Harris, Peter L.</creatorcontrib><title>Heterogeneity of Tensile Strength and Matrix Metalloproteinase Activity in the Wall of Abdominal Aortic Aneurysms</title><title>Journal of endovascular therapy</title><addtitle>J Endovasc Ther</addtitle><description>Purpose:
To measure the tensile strength of the aneurysm wall and the matrix metalloproteinase (MMP) activity in similar samples of aortic tissue.
Methods:
Detailed mechanical testing was conducted on 124 standardized specimens of aneurysm wall harvested from 24 patients undergoing elective aneurysm repair. The intrasac pressure required to cause aneurysm rupture was calculated based upon the Law of Laplace. In addition, MMP-2 and 9 were assayed from these specimens. Sixty specimens of nonaneurysmal aorta from 6 cadaveric organ donors served as controls. Intrasubject and intersubject variations were analyzed.
Results:
In the aneurysm specimens, the Young's modulus was 1.80times106 N/m2, the load at break was 6.36 N, the strain at break was 0.30, the ultimate strength was 0.53times106 N/m2, and the MMP activity was 312 for MMP-2 and 460 for MMP-9. In the controls, the circumferential measurements were a Young's modulus of 1.82times106 N/m2, a load at break of 5.43 N, strain at break of 0.29, ultimate strength of 0.61times106 N/m2, and MMP activity of 395 for MMP-2 and 2019 for MMP-9. Longitudinal measurements in controls were a Young's modulus of 1.38times106 N/m2, a load at break of 11.39 N, a strain at break of 0.33, and ultimate strength of 1.30times106 N/m2. Intra and intersubject variation of all parameters was very high. Based upon the lowest measured tensile strength for each aneurysm, the intrasac pressure required to cause rupture varied from 142 to 982 mmHg.
Conclusions:
Localized “hot spots” of MMP hyperactivity could lead to focal weakening of the aneurysm wall and rupture at relatively low levels of intraluminal pressure. These data suggest that tensile strength of the sac is just as important as intrasac tension in determining the risk of rupture. Moreover, these observations may explain why some small aneurysms rupture and larger aneurysms do not. Assessment of rupture risk based on computation or measurement of wall stress may be subject to error and inaccuracy due to variations in wall tensile strength.</description><subject>Aorta, Abdominal - enzymology</subject><subject>Aorta, Abdominal - physiopathology</subject><subject>Aortic Aneurysm, Abdominal - enzymology</subject><subject>Aortic Aneurysm, Abdominal - physiopathology</subject><subject>Aortic Rupture - etiology</subject><subject>Case-Control Studies</subject><subject>Humans</subject><subject>Matrix Metalloproteinase 2 - metabolism</subject><subject>Matrix Metalloproteinase 9 - metabolism</subject><subject>Risk Factors</subject><subject>Stress, Mechanical</subject><subject>Tensile Strength</subject><issn>1526-6028</issn><issn>1545-1550</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><recordid>eNptkE1LxDAQhoMofqwe_AOSk-ChmslHtz0WUVdQPLjiMWTT6RppG01Scf-9LS548TQD88wzw0vIKbBLUIW4YjIDLspL2CGHoKTKQCm2O_U8z3LGiwNyFOM7Yxw4wD45GAdloRgcks8FJgx-jT26tKG-oUvso2uRPqeA_Tq9UdPX9NGk4L7pIybTtv4j-ISuNxFpZZP7mjZdT9Mb0tdxPlmqVe27EWlp5UNyllY9DmETu3hM9hrTRjzZ1hl5ub1ZXi-yh6e7--vqIbMCeMqEYaVUBhtbIkorONaiqa2wjOVNKWVZzFnOYS4tEyvgtSo45gygLlijxMqIGTn_9Y7ffg4Yk-5ctNi2pkc_RJ3n87kEVY7gxS9og48xYKM_gutM2GhgespXM6mnfDWM7NlWOqw6rP_IbaB_V6NZo373QxgziP-YfgARQoHS</recordid><startdate>200408</startdate><enddate>200408</enddate><creator>Vallabhaneni, Srinivasa R.</creator><creator>Gilling-Smith, Geoffrey L.</creator><creator>How, Thien V.</creator><creator>Carter, Stuart D.</creator><creator>Brennan, John A.</creator><creator>Harris, Peter L.</creator><general>SAGE Publications</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>200408</creationdate><title>Heterogeneity of Tensile Strength and Matrix Metalloproteinase Activity in the Wall of Abdominal Aortic Aneurysms</title><author>Vallabhaneni, Srinivasa R. ; Gilling-Smith, Geoffrey L. ; How, Thien V. ; Carter, Stuart D. ; Brennan, John A. ; Harris, Peter L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c312t-3a0945aefc9ee4c32ed3fdc3c006f944987062174c03b12d582e6011d80f53ba3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Aorta, Abdominal - enzymology</topic><topic>Aorta, Abdominal - physiopathology</topic><topic>Aortic Aneurysm, Abdominal - enzymology</topic><topic>Aortic Aneurysm, Abdominal - physiopathology</topic><topic>Aortic Rupture - etiology</topic><topic>Case-Control Studies</topic><topic>Humans</topic><topic>Matrix Metalloproteinase 2 - metabolism</topic><topic>Matrix Metalloproteinase 9 - metabolism</topic><topic>Risk Factors</topic><topic>Stress, Mechanical</topic><topic>Tensile Strength</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Vallabhaneni, Srinivasa R.</creatorcontrib><creatorcontrib>Gilling-Smith, Geoffrey L.</creatorcontrib><creatorcontrib>How, Thien V.</creatorcontrib><creatorcontrib>Carter, Stuart D.</creatorcontrib><creatorcontrib>Brennan, John A.</creatorcontrib><creatorcontrib>Harris, Peter L.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of endovascular therapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Vallabhaneni, Srinivasa R.</au><au>Gilling-Smith, Geoffrey L.</au><au>How, Thien V.</au><au>Carter, Stuart D.</au><au>Brennan, John A.</au><au>Harris, Peter L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Heterogeneity of Tensile Strength and Matrix Metalloproteinase Activity in the Wall of Abdominal Aortic Aneurysms</atitle><jtitle>Journal of endovascular therapy</jtitle><addtitle>J Endovasc Ther</addtitle><date>2004-08</date><risdate>2004</risdate><volume>11</volume><issue>4</issue><spage>494</spage><epage>502</epage><pages>494-502</pages><issn>1526-6028</issn><eissn>1545-1550</eissn><abstract>Purpose:
To measure the tensile strength of the aneurysm wall and the matrix metalloproteinase (MMP) activity in similar samples of aortic tissue.
Methods:
Detailed mechanical testing was conducted on 124 standardized specimens of aneurysm wall harvested from 24 patients undergoing elective aneurysm repair. The intrasac pressure required to cause aneurysm rupture was calculated based upon the Law of Laplace. In addition, MMP-2 and 9 were assayed from these specimens. Sixty specimens of nonaneurysmal aorta from 6 cadaveric organ donors served as controls. Intrasubject and intersubject variations were analyzed.
Results:
In the aneurysm specimens, the Young's modulus was 1.80times106 N/m2, the load at break was 6.36 N, the strain at break was 0.30, the ultimate strength was 0.53times106 N/m2, and the MMP activity was 312 for MMP-2 and 460 for MMP-9. In the controls, the circumferential measurements were a Young's modulus of 1.82times106 N/m2, a load at break of 5.43 N, strain at break of 0.29, ultimate strength of 0.61times106 N/m2, and MMP activity of 395 for MMP-2 and 2019 for MMP-9. Longitudinal measurements in controls were a Young's modulus of 1.38times106 N/m2, a load at break of 11.39 N, a strain at break of 0.33, and ultimate strength of 1.30times106 N/m2. Intra and intersubject variation of all parameters was very high. Based upon the lowest measured tensile strength for each aneurysm, the intrasac pressure required to cause rupture varied from 142 to 982 mmHg.
Conclusions:
Localized “hot spots” of MMP hyperactivity could lead to focal weakening of the aneurysm wall and rupture at relatively low levels of intraluminal pressure. These data suggest that tensile strength of the sac is just as important as intrasac tension in determining the risk of rupture. Moreover, these observations may explain why some small aneurysms rupture and larger aneurysms do not. Assessment of rupture risk based on computation or measurement of wall stress may be subject to error and inaccuracy due to variations in wall tensile strength.</abstract><cop>Los Angeles, CA</cop><pub>SAGE Publications</pub><pmid>15298501</pmid><doi>10.1583/04-1239.1</doi><tpages>9</tpages></addata></record> |
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subjects | Aorta, Abdominal - enzymology Aorta, Abdominal - physiopathology Aortic Aneurysm, Abdominal - enzymology Aortic Aneurysm, Abdominal - physiopathology Aortic Rupture - etiology Case-Control Studies Humans Matrix Metalloproteinase 2 - metabolism Matrix Metalloproteinase 9 - metabolism Risk Factors Stress, Mechanical Tensile Strength |
title | Heterogeneity of Tensile Strength and Matrix Metalloproteinase Activity in the Wall of Abdominal Aortic Aneurysms |
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