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Atrial endocardial changes in mitral valve disease: A scanning electron microscopy study

Background The precise contribution of left atrial appendage (LAA) endocardial damage and dysfunction to the process of thrombus formation in patients with mitral valve (MV) disease, especially in the presence of atrial fibrillation (AF), has not as yet been clearly described. This may be important...

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Published in:The American heart journal 2000-11, Vol.140 (5), p.777-784
Main Authors: Goldsmith, Ira, Kumar, Patricia, Carter, Peter, Blann, Andrew D., Patel, Ramesh L., Lip, Gregory Y.H.
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description Background The precise contribution of left atrial appendage (LAA) endocardial damage and dysfunction to the process of thrombus formation in patients with mitral valve (MV) disease, especially in the presence of atrial fibrillation (AF), has not as yet been clearly described. This may be important because the LAA is the usual site for thrombus formation. Methods The purpose of this study was to describe endocardial surface changes, through the use of scanning electron microscopy, in the left and right atrial appendages of patients with MV disease and the differences, if any, between patients with mitral stenosis and mitral regurgitation as well as between those with AF and sinus rhythm. Our second objective was to relate endocardial changes to plasma levels of von Willebrand factor (vWf), an established marker for endothelial damage. LAA specimens were obtained immediately after commencement of cardiopulmonary bypass from 35 patients (18 men; mean age 65 years, range 20 to 85) during surgery for MV repair or replacement. Right atrial appendage (RAA) specimens were similarly obtained as controls for individual patients. The specimens were fixed in 2.5% glutaraldehyde solution overnight, stored in Sorensen’s phosphate buffer, and examined by means of scanning electron microscopy. Two independent observers documented the most advanced lesion in each specimen as follows: (1) “minimal” changes, with minimal disruption of the endocardium; (2) “intermediate” changes or prethrombotic lesions; and (3) “advanced” changes, with endocardial disruption and thrombotic lesions. Plasma levels of vWf were also measured (enzyme-linked immunosorbent assay) in all patients, and results were compared with those of age- and sex-matched healthy control patients. Results Advanced changes were more frequently seen in the endocardium of the LAA when compared with the RAA (31% vs 6%), whereas minimal changes were more frequently seen in the RAA compared with the LAA (23% vs 6%) (P =.00167). Similarly, the LAA from patients with mitral stenosis had a higher proportion of “advanced” endocardial changes when compared with patients with mitral regurgitation (67% vs 24%; P =.0066). The LAA in patients with AF had more “advanced” changes (39% vs 27%), but this was not statistically significant. Plasma vWf levels were significantly higher in patients with MV disease compared with healthy control patients (132 ± 33 IU/dL vs 99 ± 37 IU/dL; P =.0004) and in patients with advanced LAA changes
doi_str_mv 10.1067/mhj.2000.110284
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This may be important because the LAA is the usual site for thrombus formation. Methods The purpose of this study was to describe endocardial surface changes, through the use of scanning electron microscopy, in the left and right atrial appendages of patients with MV disease and the differences, if any, between patients with mitral stenosis and mitral regurgitation as well as between those with AF and sinus rhythm. Our second objective was to relate endocardial changes to plasma levels of von Willebrand factor (vWf), an established marker for endothelial damage. LAA specimens were obtained immediately after commencement of cardiopulmonary bypass from 35 patients (18 men; mean age 65 years, range 20 to 85) during surgery for MV repair or replacement. Right atrial appendage (RAA) specimens were similarly obtained as controls for individual patients. The specimens were fixed in 2.5% glutaraldehyde solution overnight, stored in Sorensen’s phosphate buffer, and examined by means of scanning electron microscopy. Two independent observers documented the most advanced lesion in each specimen as follows: (1) “minimal” changes, with minimal disruption of the endocardium; (2) “intermediate” changes or prethrombotic lesions; and (3) “advanced” changes, with endocardial disruption and thrombotic lesions. Plasma levels of vWf were also measured (enzyme-linked immunosorbent assay) in all patients, and results were compared with those of age- and sex-matched healthy control patients. Results Advanced changes were more frequently seen in the endocardium of the LAA when compared with the RAA (31% vs 6%), whereas minimal changes were more frequently seen in the RAA compared with the LAA (23% vs 6%) (P =.00167). Similarly, the LAA from patients with mitral stenosis had a higher proportion of “advanced” endocardial changes when compared with patients with mitral regurgitation (67% vs 24%; P =.0066). The LAA in patients with AF had more “advanced” changes (39% vs 27%), but this was not statistically significant. Plasma vWf levels were significantly higher in patients with MV disease compared with healthy control patients (132 ± 33 IU/dL vs 99 ± 37 IU/dL; P =.0004) and in patients with advanced LAA changes compared with earlier changes (149 ± 34 IU/dL vs 121 ± 31 IU/dL; P =.042). Conclusions Endocardial damage occurs in the atrial appendages of patients with MV disease. Potentially thrombogenic changes are more commonly seen in the LAA compared with the RAA and in patients with mitral stenosis compared with mitral regurgitation. These anatomic appearances may contribute to the risk of intra-atrial thrombus formation in patients with mitral valve disease, especially if AF is present. (Am Heart J 2000;140:777-84.)</description><identifier>ISSN: 0002-8703</identifier><identifier>EISSN: 1097-6744</identifier><identifier>DOI: 10.1067/mhj.2000.110284</identifier><identifier>PMID: 11054625</identifier><identifier>CODEN: AHJOA2</identifier><language>eng</language><publisher>New York, NY: Mosby, Inc</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Atrial Fibrillation - pathology ; Biological and medical sciences ; Cardiology. Vascular system ; Case-Control Studies ; Disease Progression ; Endocardial and cardiac valvular diseases ; Endocardium - pathology ; Enzyme-Linked Immunosorbent Assay ; Female ; Heart ; Heart Atria - pathology ; Heart Diseases - pathology ; Humans ; Male ; Medical sciences ; Microscopy, Electron, Scanning ; Middle Aged ; Mitral Valve Insufficiency - pathology ; Mitral Valve Stenosis - blood ; Mitral Valve Stenosis - classification ; Mitral Valve Stenosis - complications ; Mitral Valve Stenosis - pathology ; Thrombosis - pathology ; von Willebrand Factor - metabolism</subject><ispartof>The American heart journal, 2000-11, Vol.140 (5), p.777-784</ispartof><rights>2000 Mosby, Inc.</rights><rights>2001 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c371t-1979551538f90f93ac3c38039f6fa8d5fd86ff48eef4f73bf28556a32c0e0daa3</citedby><cites>FETCH-LOGICAL-c371t-1979551538f90f93ac3c38039f6fa8d5fd86ff48eef4f73bf28556a32c0e0daa3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=794700$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11054625$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Goldsmith, Ira</creatorcontrib><creatorcontrib>Kumar, Patricia</creatorcontrib><creatorcontrib>Carter, Peter</creatorcontrib><creatorcontrib>Blann, Andrew D.</creatorcontrib><creatorcontrib>Patel, Ramesh L.</creatorcontrib><creatorcontrib>Lip, Gregory Y.H.</creatorcontrib><title>Atrial endocardial changes in mitral valve disease: A scanning electron microscopy study</title><title>The American heart journal</title><addtitle>Am Heart J</addtitle><description>Background The precise contribution of left atrial appendage (LAA) endocardial damage and dysfunction to the process of thrombus formation in patients with mitral valve (MV) disease, especially in the presence of atrial fibrillation (AF), has not as yet been clearly described. This may be important because the LAA is the usual site for thrombus formation. Methods The purpose of this study was to describe endocardial surface changes, through the use of scanning electron microscopy, in the left and right atrial appendages of patients with MV disease and the differences, if any, between patients with mitral stenosis and mitral regurgitation as well as between those with AF and sinus rhythm. Our second objective was to relate endocardial changes to plasma levels of von Willebrand factor (vWf), an established marker for endothelial damage. LAA specimens were obtained immediately after commencement of cardiopulmonary bypass from 35 patients (18 men; mean age 65 years, range 20 to 85) during surgery for MV repair or replacement. Right atrial appendage (RAA) specimens were similarly obtained as controls for individual patients. The specimens were fixed in 2.5% glutaraldehyde solution overnight, stored in Sorensen’s phosphate buffer, and examined by means of scanning electron microscopy. Two independent observers documented the most advanced lesion in each specimen as follows: (1) “minimal” changes, with minimal disruption of the endocardium; (2) “intermediate” changes or prethrombotic lesions; and (3) “advanced” changes, with endocardial disruption and thrombotic lesions. Plasma levels of vWf were also measured (enzyme-linked immunosorbent assay) in all patients, and results were compared with those of age- and sex-matched healthy control patients. Results Advanced changes were more frequently seen in the endocardium of the LAA when compared with the RAA (31% vs 6%), whereas minimal changes were more frequently seen in the RAA compared with the LAA (23% vs 6%) (P =.00167). Similarly, the LAA from patients with mitral stenosis had a higher proportion of “advanced” endocardial changes when compared with patients with mitral regurgitation (67% vs 24%; P =.0066). The LAA in patients with AF had more “advanced” changes (39% vs 27%), but this was not statistically significant. Plasma vWf levels were significantly higher in patients with MV disease compared with healthy control patients (132 ± 33 IU/dL vs 99 ± 37 IU/dL; P =.0004) and in patients with advanced LAA changes compared with earlier changes (149 ± 34 IU/dL vs 121 ± 31 IU/dL; P =.042). Conclusions Endocardial damage occurs in the atrial appendages of patients with MV disease. Potentially thrombogenic changes are more commonly seen in the LAA compared with the RAA and in patients with mitral stenosis compared with mitral regurgitation. These anatomic appearances may contribute to the risk of intra-atrial thrombus formation in patients with mitral valve disease, especially if AF is present. (Am Heart J 2000;140:777-84.)</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Atrial Fibrillation - pathology</subject><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Case-Control Studies</subject><subject>Disease Progression</subject><subject>Endocardial and cardiac valvular diseases</subject><subject>Endocardium - pathology</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Female</subject><subject>Heart</subject><subject>Heart Atria - pathology</subject><subject>Heart Diseases - pathology</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Microscopy, Electron, Scanning</subject><subject>Middle Aged</subject><subject>Mitral Valve Insufficiency - pathology</subject><subject>Mitral Valve Stenosis - blood</subject><subject>Mitral Valve Stenosis - classification</subject><subject>Mitral Valve Stenosis - complications</subject><subject>Mitral Valve Stenosis - pathology</subject><subject>Thrombosis - pathology</subject><subject>von Willebrand Factor - metabolism</subject><issn>0002-8703</issn><issn>1097-6744</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><recordid>eNp1kM1LwzAUwIMobk7P3qQgeOuWNm2SehvDLxh4UfAWsuRly2jTmXSD_femdOjJ0_v6vcfjh9BthqcZpmzWbLbTHONYZTjnxRkaZ7hiKWVFcY7GcZCnnGEyQlchbGNJc04v0SjSZUHzcoy-5p23sk7A6VZJr_tcbaRbQ0isSxrb-dg5yPoAibYBZIDHZJ4EJZ2zbp1ADarzbU8q3wbV7o5J6Pb6eI0ujKwD3JziBH0-P30sXtPl-8vbYr5MFWFZl2YVq8oyKwk3FTYVkYoowjGpDDWS69JoTo0pOIApDCMrk_OypJLkCgPWUpIJehju7nz7vYfQicYGBXUtHbT7IFhOKCWMRXA2gP2fwYMRO28b6Y8iw6KXKaJM0csUg8y4cXc6vV81oP_4k70I3J8AGYXUxkunbPjlWFUwjCNVDRREDQcLXgRlwSnQ1kd5Qrf23xd-ACJJkC8</recordid><startdate>20001101</startdate><enddate>20001101</enddate><creator>Goldsmith, Ira</creator><creator>Kumar, Patricia</creator><creator>Carter, Peter</creator><creator>Blann, Andrew D.</creator><creator>Patel, Ramesh L.</creator><creator>Lip, Gregory Y.H.</creator><general>Mosby, Inc</general><general>Elsevier</general><scope>IQODW</scope><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>20001101</creationdate><title>Atrial endocardial changes in mitral valve disease: A scanning electron microscopy study</title><author>Goldsmith, Ira ; Kumar, Patricia ; Carter, Peter ; Blann, Andrew D. ; Patel, Ramesh L. ; Lip, Gregory Y.H.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c371t-1979551538f90f93ac3c38039f6fa8d5fd86ff48eef4f73bf28556a32c0e0daa3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Atrial Fibrillation - pathology</topic><topic>Biological and medical sciences</topic><topic>Cardiology. Vascular system</topic><topic>Case-Control Studies</topic><topic>Disease Progression</topic><topic>Endocardial and cardiac valvular diseases</topic><topic>Endocardium - pathology</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Female</topic><topic>Heart</topic><topic>Heart Atria - pathology</topic><topic>Heart Diseases - pathology</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Microscopy, Electron, Scanning</topic><topic>Middle Aged</topic><topic>Mitral Valve Insufficiency - pathology</topic><topic>Mitral Valve Stenosis - blood</topic><topic>Mitral Valve Stenosis - classification</topic><topic>Mitral Valve Stenosis - complications</topic><topic>Mitral Valve Stenosis - pathology</topic><topic>Thrombosis - pathology</topic><topic>von Willebrand Factor - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Goldsmith, Ira</creatorcontrib><creatorcontrib>Kumar, Patricia</creatorcontrib><creatorcontrib>Carter, Peter</creatorcontrib><creatorcontrib>Blann, Andrew D.</creatorcontrib><creatorcontrib>Patel, Ramesh L.</creatorcontrib><creatorcontrib>Lip, Gregory Y.H.</creatorcontrib><collection>Pascal-Francis</collection><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>The American heart journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Goldsmith, Ira</au><au>Kumar, Patricia</au><au>Carter, Peter</au><au>Blann, Andrew D.</au><au>Patel, Ramesh L.</au><au>Lip, Gregory Y.H.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Atrial endocardial changes in mitral valve disease: A scanning electron microscopy study</atitle><jtitle>The American heart journal</jtitle><addtitle>Am Heart J</addtitle><date>2000-11-01</date><risdate>2000</risdate><volume>140</volume><issue>5</issue><spage>777</spage><epage>784</epage><pages>777-784</pages><issn>0002-8703</issn><eissn>1097-6744</eissn><coden>AHJOA2</coden><abstract>Background The precise contribution of left atrial appendage (LAA) endocardial damage and dysfunction to the process of thrombus formation in patients with mitral valve (MV) disease, especially in the presence of atrial fibrillation (AF), has not as yet been clearly described. This may be important because the LAA is the usual site for thrombus formation. Methods The purpose of this study was to describe endocardial surface changes, through the use of scanning electron microscopy, in the left and right atrial appendages of patients with MV disease and the differences, if any, between patients with mitral stenosis and mitral regurgitation as well as between those with AF and sinus rhythm. Our second objective was to relate endocardial changes to plasma levels of von Willebrand factor (vWf), an established marker for endothelial damage. LAA specimens were obtained immediately after commencement of cardiopulmonary bypass from 35 patients (18 men; mean age 65 years, range 20 to 85) during surgery for MV repair or replacement. Right atrial appendage (RAA) specimens were similarly obtained as controls for individual patients. The specimens were fixed in 2.5% glutaraldehyde solution overnight, stored in Sorensen’s phosphate buffer, and examined by means of scanning electron microscopy. Two independent observers documented the most advanced lesion in each specimen as follows: (1) “minimal” changes, with minimal disruption of the endocardium; (2) “intermediate” changes or prethrombotic lesions; and (3) “advanced” changes, with endocardial disruption and thrombotic lesions. Plasma levels of vWf were also measured (enzyme-linked immunosorbent assay) in all patients, and results were compared with those of age- and sex-matched healthy control patients. Results Advanced changes were more frequently seen in the endocardium of the LAA when compared with the RAA (31% vs 6%), whereas minimal changes were more frequently seen in the RAA compared with the LAA (23% vs 6%) (P =.00167). Similarly, the LAA from patients with mitral stenosis had a higher proportion of “advanced” endocardial changes when compared with patients with mitral regurgitation (67% vs 24%; P =.0066). The LAA in patients with AF had more “advanced” changes (39% vs 27%), but this was not statistically significant. Plasma vWf levels were significantly higher in patients with MV disease compared with healthy control patients (132 ± 33 IU/dL vs 99 ± 37 IU/dL; P =.0004) and in patients with advanced LAA changes compared with earlier changes (149 ± 34 IU/dL vs 121 ± 31 IU/dL; P =.042). Conclusions Endocardial damage occurs in the atrial appendages of patients with MV disease. Potentially thrombogenic changes are more commonly seen in the LAA compared with the RAA and in patients with mitral stenosis compared with mitral regurgitation. These anatomic appearances may contribute to the risk of intra-atrial thrombus formation in patients with mitral valve disease, especially if AF is present. (Am Heart J 2000;140:777-84.)</abstract><cop>New York, NY</cop><pub>Mosby, Inc</pub><pmid>11054625</pmid><doi>10.1067/mhj.2000.110284</doi><tpages>8</tpages></addata></record>
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source ScienceDirect Freedom Collection 2022-2024
subjects Adult
Aged
Aged, 80 and over
Atrial Fibrillation - pathology
Biological and medical sciences
Cardiology. Vascular system
Case-Control Studies
Disease Progression
Endocardial and cardiac valvular diseases
Endocardium - pathology
Enzyme-Linked Immunosorbent Assay
Female
Heart
Heart Atria - pathology
Heart Diseases - pathology
Humans
Male
Medical sciences
Microscopy, Electron, Scanning
Middle Aged
Mitral Valve Insufficiency - pathology
Mitral Valve Stenosis - blood
Mitral Valve Stenosis - classification
Mitral Valve Stenosis - complications
Mitral Valve Stenosis - pathology
Thrombosis - pathology
von Willebrand Factor - metabolism
title Atrial endocardial changes in mitral valve disease: A scanning electron microscopy study
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