Focus on the unique mechanisms involved in thoracic aortic aneurysm formation in bicuspid aortic valve versus tricuspid aortic valve patients: clinical implications of a pilot study
OBJECTIVES The involvement of different factors in the onset of thoracic aortic aneurysm (TAA) in patients with a bicuspid aortic valve (BAV) vs those with a tricuspid aortic valve (TAV) is well recognized. However, the molecular, genetic and cellular mechanisms driving TAA remain unclear. The aim o...
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| Veröffentlicht in: | European journal of cardio-thoracic surgery 2013-06, Vol.43 (6), p.e180-e186 |
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| container_title | European journal of cardio-thoracic surgery |
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| creator | Balistreri, Carmela Rita Pisano, Calogera Candore, Giuseppina Maresi, Emiliano Codispoti, Massimiliano Ruvolo, Giovanni |
| description | OBJECTIVES
The involvement of different factors in the onset of thoracic aortic aneurysm (TAA) in patients with a bicuspid aortic valve (BAV) vs those with a tricuspid aortic valve (TAV) is well recognized. However, the molecular, genetic and cellular mechanisms driving TAA remain unclear. The aim of this study was to identify the different mechanisms involved in TAA development in patients with BAV vs TAV.
METHODS
Aorta specimens and DNA samples were collected from 24 BAV (18 men and 6 women; mean age: 54.2 ± 14.39 years) and 110 TAV (79 men and 31 women, mean age: 66 ± 9.8 years) patients. A control group of 128 subjects (61 men and 67 woman, mean age: 61.1 ± 5.8 years) was also enrolled. Histopathological and immunoistochemical analyses were performed, as well as genotyping of 10 polymorphisms.
RESULTS
In BAV-associated ascending aortas, significant severe plurifocal apoptosis of smooth muscle cells and matrix metalloproteinase-9 (MMP-9) amounts were detected. In contrast, TAV-associated ascending aortas were characterized by a significant severity of elastic fragmentation, cystic medial necrosis, medial fibrosis and inflammation. In addition, in BAV cases, the −1562TMMP-9 and −735TMMP-2 alleles represent independent risk factors for TAA. The effects of these genotypes combined with hypertension and smoking in BAV cases result in an increase in both the apoptosis (P = 0.0001) and levels of MMP-9 (P = 0.001). In TAV cases, the D angiotensin-converting enzyme and +896A Toll-like receptor-4 alleles seem to be the predictive factors for TAA risk. They, combined with hypertension and age, significantly increase both the microscopic lesions and inflammation.
CONCLUSIONS
Our data seem to suggest that TAA in BAV and TAV patients arises from different molecular, cellular and genetic mechanisms. They might help to identify the potential molecular and genetic biomarkers that are useful to detect BAV subjects at high TAA risk, to monitor and treat them differently from those with TAV, with approaches such as the complete removal of the ascending aorta, including the aortic root with or without dilatation. |
| doi_str_mv | 10.1093/ejcts/ezs630 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1353042947</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><oup_id>10.1093/ejcts/ezs630</oup_id><sourcerecordid>1353042947</sourcerecordid><originalsourceid>FETCH-LOGICAL-c427t-cfec197b4f9a27c1de254e702e7298439f2b6caa48b824f87691a651cad87fb13</originalsourceid><addsrcrecordid>eNp9kU1P3DAQhq2qqAvb3nqufGsPBPy1cdIbQiwgIXEBqbfIccbCKIlTj7PS8r_6_-plWU5VTzOSn3k89kvIV87OOKvlOTzbhOfwgqVkH8gxr7QstFS_PuaecVboWrEFOUF8ZoyVUuhPZCGkUJVg5TH5sw52RhpGmp6AzqP_PQMdwD6Z0eOA1I-b0G-gy00mQjTWW2pCTLsywhy3OFAX4mCSz5JMtT4LJ98dqI3J83QDEfM9Kf7zdMrTMCb8SW3vR29NT_0w9bnZWfN6jho6-T4kimnutp_JkTM9wpe3uiSP66uHy5vi7v769vLirrBK6FRYB5bXulWuNkJb3oFYKdBMgBZ1pWTtRFtaY1TVVkK5Spc1N-WKW9NV2rVcLsmPvXeKIX8MpmbwaKHv89PDjA2XK8mUqJXO6OketTEgRnDNFP1g4rbhrNkF1bwG1eyDyvi3N_PcDtC9w4dkMvB9D4R5-r_qL5DVo94</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1353042947</pqid></control><display><type>article</type><title>Focus on the unique mechanisms involved in thoracic aortic aneurysm formation in bicuspid aortic valve versus tricuspid aortic valve patients: clinical implications of a pilot study</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Oxford University Press Journals All Titles (1996-Current)</source><source>Alma/SFX Local Collection</source><creator>Balistreri, Carmela Rita ; Pisano, Calogera ; Candore, Giuseppina ; Maresi, Emiliano ; Codispoti, Massimiliano ; Ruvolo, Giovanni</creator><creatorcontrib>Balistreri, Carmela Rita ; Pisano, Calogera ; Candore, Giuseppina ; Maresi, Emiliano ; Codispoti, Massimiliano ; Ruvolo, Giovanni</creatorcontrib><description>OBJECTIVES
The involvement of different factors in the onset of thoracic aortic aneurysm (TAA) in patients with a bicuspid aortic valve (BAV) vs those with a tricuspid aortic valve (TAV) is well recognized. However, the molecular, genetic and cellular mechanisms driving TAA remain unclear. The aim of this study was to identify the different mechanisms involved in TAA development in patients with BAV vs TAV.
METHODS
Aorta specimens and DNA samples were collected from 24 BAV (18 men and 6 women; mean age: 54.2 ± 14.39 years) and 110 TAV (79 men and 31 women, mean age: 66 ± 9.8 years) patients. A control group of 128 subjects (61 men and 67 woman, mean age: 61.1 ± 5.8 years) was also enrolled. Histopathological and immunoistochemical analyses were performed, as well as genotyping of 10 polymorphisms.
RESULTS
In BAV-associated ascending aortas, significant severe plurifocal apoptosis of smooth muscle cells and matrix metalloproteinase-9 (MMP-9) amounts were detected. In contrast, TAV-associated ascending aortas were characterized by a significant severity of elastic fragmentation, cystic medial necrosis, medial fibrosis and inflammation. In addition, in BAV cases, the −1562TMMP-9 and −735TMMP-2 alleles represent independent risk factors for TAA. The effects of these genotypes combined with hypertension and smoking in BAV cases result in an increase in both the apoptosis (P = 0.0001) and levels of MMP-9 (P = 0.001). In TAV cases, the D angiotensin-converting enzyme and +896A Toll-like receptor-4 alleles seem to be the predictive factors for TAA risk. They, combined with hypertension and age, significantly increase both the microscopic lesions and inflammation.
CONCLUSIONS
Our data seem to suggest that TAA in BAV and TAV patients arises from different molecular, cellular and genetic mechanisms. They might help to identify the potential molecular and genetic biomarkers that are useful to detect BAV subjects at high TAA risk, to monitor and treat them differently from those with TAV, with approaches such as the complete removal of the ascending aorta, including the aortic root with or without dilatation.</description><identifier>ISSN: 1010-7940</identifier><identifier>EISSN: 1873-734X</identifier><identifier>DOI: 10.1093/ejcts/ezs630</identifier><identifier>PMID: 23248206</identifier><language>eng</language><publisher>Germany: Oxford University Press</publisher><subject>Adult ; Aged ; Aortic Aneurysm, Thoracic - genetics ; Aortic Aneurysm, Thoracic - pathology ; Aortic Valve - abnormalities ; Aortic Valve - pathology ; Apoptosis - physiology ; Bicuspid Aortic Valve Disease ; Comorbidity ; Female ; Gene Frequency ; Genetic Predisposition to Disease ; Genotype ; Heart Valve Diseases - epidemiology ; Heart Valve Diseases - genetics ; Heart Valve Diseases - pathology ; Histocytochemistry ; Humans ; Male ; Matrix Metalloproteinase 9 - genetics ; Middle Aged ; Pilot Projects ; Polymorphism, Single Nucleotide ; Risk Factors ; Tricuspid Valve - abnormalities</subject><ispartof>European journal of cardio-thoracic surgery, 2013-06, Vol.43 (6), p.e180-e186</ispartof><rights>The Author 2012. Published by Oxford University Press on behalf of the European Journal of Cardio-Thoracic Surgery. All rights reserved. 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c427t-cfec197b4f9a27c1de254e702e7298439f2b6caa48b824f87691a651cad87fb13</citedby><cites>FETCH-LOGICAL-c427t-cfec197b4f9a27c1de254e702e7298439f2b6caa48b824f87691a651cad87fb13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,1579,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23248206$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Balistreri, Carmela Rita</creatorcontrib><creatorcontrib>Pisano, Calogera</creatorcontrib><creatorcontrib>Candore, Giuseppina</creatorcontrib><creatorcontrib>Maresi, Emiliano</creatorcontrib><creatorcontrib>Codispoti, Massimiliano</creatorcontrib><creatorcontrib>Ruvolo, Giovanni</creatorcontrib><title>Focus on the unique mechanisms involved in thoracic aortic aneurysm formation in bicuspid aortic valve versus tricuspid aortic valve patients: clinical implications of a pilot study</title><title>European journal of cardio-thoracic surgery</title><addtitle>Eur J Cardiothorac Surg</addtitle><description>OBJECTIVES
The involvement of different factors in the onset of thoracic aortic aneurysm (TAA) in patients with a bicuspid aortic valve (BAV) vs those with a tricuspid aortic valve (TAV) is well recognized. However, the molecular, genetic and cellular mechanisms driving TAA remain unclear. The aim of this study was to identify the different mechanisms involved in TAA development in patients with BAV vs TAV.
METHODS
Aorta specimens and DNA samples were collected from 24 BAV (18 men and 6 women; mean age: 54.2 ± 14.39 years) and 110 TAV (79 men and 31 women, mean age: 66 ± 9.8 years) patients. A control group of 128 subjects (61 men and 67 woman, mean age: 61.1 ± 5.8 years) was also enrolled. Histopathological and immunoistochemical analyses were performed, as well as genotyping of 10 polymorphisms.
RESULTS
In BAV-associated ascending aortas, significant severe plurifocal apoptosis of smooth muscle cells and matrix metalloproteinase-9 (MMP-9) amounts were detected. In contrast, TAV-associated ascending aortas were characterized by a significant severity of elastic fragmentation, cystic medial necrosis, medial fibrosis and inflammation. In addition, in BAV cases, the −1562TMMP-9 and −735TMMP-2 alleles represent independent risk factors for TAA. The effects of these genotypes combined with hypertension and smoking in BAV cases result in an increase in both the apoptosis (P = 0.0001) and levels of MMP-9 (P = 0.001). In TAV cases, the D angiotensin-converting enzyme and +896A Toll-like receptor-4 alleles seem to be the predictive factors for TAA risk. They, combined with hypertension and age, significantly increase both the microscopic lesions and inflammation.
CONCLUSIONS
Our data seem to suggest that TAA in BAV and TAV patients arises from different molecular, cellular and genetic mechanisms. They might help to identify the potential molecular and genetic biomarkers that are useful to detect BAV subjects at high TAA risk, to monitor and treat them differently from those with TAV, with approaches such as the complete removal of the ascending aorta, including the aortic root with or without dilatation.</description><subject>Adult</subject><subject>Aged</subject><subject>Aortic Aneurysm, Thoracic - genetics</subject><subject>Aortic Aneurysm, Thoracic - pathology</subject><subject>Aortic Valve - abnormalities</subject><subject>Aortic Valve - pathology</subject><subject>Apoptosis - physiology</subject><subject>Bicuspid Aortic Valve Disease</subject><subject>Comorbidity</subject><subject>Female</subject><subject>Gene Frequency</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotype</subject><subject>Heart Valve Diseases - epidemiology</subject><subject>Heart Valve Diseases - genetics</subject><subject>Heart Valve Diseases - pathology</subject><subject>Histocytochemistry</subject><subject>Humans</subject><subject>Male</subject><subject>Matrix Metalloproteinase 9 - genetics</subject><subject>Middle Aged</subject><subject>Pilot Projects</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Risk Factors</subject><subject>Tricuspid Valve - abnormalities</subject><issn>1010-7940</issn><issn>1873-734X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU1P3DAQhq2qqAvb3nqufGsPBPy1cdIbQiwgIXEBqbfIccbCKIlTj7PS8r_6_-plWU5VTzOSn3k89kvIV87OOKvlOTzbhOfwgqVkH8gxr7QstFS_PuaecVboWrEFOUF8ZoyVUuhPZCGkUJVg5TH5sw52RhpGmp6AzqP_PQMdwD6Z0eOA1I-b0G-gy00mQjTWW2pCTLsywhy3OFAX4mCSz5JMtT4LJ98dqI3J83QDEfM9Kf7zdMrTMCb8SW3vR29NT_0w9bnZWfN6jho6-T4kimnutp_JkTM9wpe3uiSP66uHy5vi7v769vLirrBK6FRYB5bXulWuNkJb3oFYKdBMgBZ1pWTtRFtaY1TVVkK5Spc1N-WKW9NV2rVcLsmPvXeKIX8MpmbwaKHv89PDjA2XK8mUqJXO6OketTEgRnDNFP1g4rbhrNkF1bwG1eyDyvi3N_PcDtC9w4dkMvB9D4R5-r_qL5DVo94</recordid><startdate>20130601</startdate><enddate>20130601</enddate><creator>Balistreri, Carmela Rita</creator><creator>Pisano, Calogera</creator><creator>Candore, Giuseppina</creator><creator>Maresi, Emiliano</creator><creator>Codispoti, Massimiliano</creator><creator>Ruvolo, Giovanni</creator><general>Oxford University Press</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>20130601</creationdate><title>Focus on the unique mechanisms involved in thoracic aortic aneurysm formation in bicuspid aortic valve versus tricuspid aortic valve patients: clinical implications of a pilot study</title><author>Balistreri, Carmela Rita ; Pisano, Calogera ; Candore, Giuseppina ; Maresi, Emiliano ; Codispoti, Massimiliano ; Ruvolo, Giovanni</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c427t-cfec197b4f9a27c1de254e702e7298439f2b6caa48b824f87691a651cad87fb13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aortic Aneurysm, Thoracic - genetics</topic><topic>Aortic Aneurysm, Thoracic - pathology</topic><topic>Aortic Valve - abnormalities</topic><topic>Aortic Valve - pathology</topic><topic>Apoptosis - physiology</topic><topic>Bicuspid Aortic Valve Disease</topic><topic>Comorbidity</topic><topic>Female</topic><topic>Gene Frequency</topic><topic>Genetic Predisposition to Disease</topic><topic>Genotype</topic><topic>Heart Valve Diseases - epidemiology</topic><topic>Heart Valve Diseases - genetics</topic><topic>Heart Valve Diseases - pathology</topic><topic>Histocytochemistry</topic><topic>Humans</topic><topic>Male</topic><topic>Matrix Metalloproteinase 9 - genetics</topic><topic>Middle Aged</topic><topic>Pilot Projects</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Risk Factors</topic><topic>Tricuspid Valve - abnormalities</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Balistreri, Carmela Rita</creatorcontrib><creatorcontrib>Pisano, Calogera</creatorcontrib><creatorcontrib>Candore, Giuseppina</creatorcontrib><creatorcontrib>Maresi, Emiliano</creatorcontrib><creatorcontrib>Codispoti, Massimiliano</creatorcontrib><creatorcontrib>Ruvolo, Giovanni</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>European journal of cardio-thoracic surgery</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Balistreri, Carmela Rita</au><au>Pisano, Calogera</au><au>Candore, Giuseppina</au><au>Maresi, Emiliano</au><au>Codispoti, Massimiliano</au><au>Ruvolo, Giovanni</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Focus on the unique mechanisms involved in thoracic aortic aneurysm formation in bicuspid aortic valve versus tricuspid aortic valve patients: clinical implications of a pilot study</atitle><jtitle>European journal of cardio-thoracic surgery</jtitle><addtitle>Eur J Cardiothorac Surg</addtitle><date>2013-06-01</date><risdate>2013</risdate><volume>43</volume><issue>6</issue><spage>e180</spage><epage>e186</epage><pages>e180-e186</pages><issn>1010-7940</issn><eissn>1873-734X</eissn><abstract>OBJECTIVES
The involvement of different factors in the onset of thoracic aortic aneurysm (TAA) in patients with a bicuspid aortic valve (BAV) vs those with a tricuspid aortic valve (TAV) is well recognized. However, the molecular, genetic and cellular mechanisms driving TAA remain unclear. The aim of this study was to identify the different mechanisms involved in TAA development in patients with BAV vs TAV.
METHODS
Aorta specimens and DNA samples were collected from 24 BAV (18 men and 6 women; mean age: 54.2 ± 14.39 years) and 110 TAV (79 men and 31 women, mean age: 66 ± 9.8 years) patients. A control group of 128 subjects (61 men and 67 woman, mean age: 61.1 ± 5.8 years) was also enrolled. Histopathological and immunoistochemical analyses were performed, as well as genotyping of 10 polymorphisms.
RESULTS
In BAV-associated ascending aortas, significant severe plurifocal apoptosis of smooth muscle cells and matrix metalloproteinase-9 (MMP-9) amounts were detected. In contrast, TAV-associated ascending aortas were characterized by a significant severity of elastic fragmentation, cystic medial necrosis, medial fibrosis and inflammation. In addition, in BAV cases, the −1562TMMP-9 and −735TMMP-2 alleles represent independent risk factors for TAA. The effects of these genotypes combined with hypertension and smoking in BAV cases result in an increase in both the apoptosis (P = 0.0001) and levels of MMP-9 (P = 0.001). In TAV cases, the D angiotensin-converting enzyme and +896A Toll-like receptor-4 alleles seem to be the predictive factors for TAA risk. They, combined with hypertension and age, significantly increase both the microscopic lesions and inflammation.
CONCLUSIONS
Our data seem to suggest that TAA in BAV and TAV patients arises from different molecular, cellular and genetic mechanisms. They might help to identify the potential molecular and genetic biomarkers that are useful to detect BAV subjects at high TAA risk, to monitor and treat them differently from those with TAV, with approaches such as the complete removal of the ascending aorta, including the aortic root with or without dilatation.</abstract><cop>Germany</cop><pub>Oxford University Press</pub><pmid>23248206</pmid><doi>10.1093/ejcts/ezs630</doi><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Oxford University Press Journals All Titles (1996-Current); Alma/SFX Local Collection |
| subjects | Adult Aged Aortic Aneurysm, Thoracic - genetics Aortic Aneurysm, Thoracic - pathology Aortic Valve - abnormalities Aortic Valve - pathology Apoptosis - physiology Bicuspid Aortic Valve Disease Comorbidity Female Gene Frequency Genetic Predisposition to Disease Genotype Heart Valve Diseases - epidemiology Heart Valve Diseases - genetics Heart Valve Diseases - pathology Histocytochemistry Humans Male Matrix Metalloproteinase 9 - genetics Middle Aged Pilot Projects Polymorphism, Single Nucleotide Risk Factors Tricuspid Valve - abnormalities |
| title | Focus on the unique mechanisms involved in thoracic aortic aneurysm formation in bicuspid aortic valve versus tricuspid aortic valve patients: clinical implications of a pilot study |
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