Overcontraction and excess actin filaments. Basic elements of hypertrophic cardiomyopathy
Endomyocardial biopsies were taken from the right ventricular aspect of the interventricular septum in three patients with hypertrophic cardiomyopathy and were subjected to electronmicroscopical examination. Longitudinal sections confirmed already well-established findings. In the transverse section...
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Veröffentlicht in: | British Heart Journal 1981-05, Vol.45 (5), p.494-499 |
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description | Endomyocardial biopsies were taken from the right ventricular aspect of the interventricular septum in three patients with hypertrophic cardiomyopathy and were subjected to electronmicroscopical examination. Longitudinal sections confirmed already well-established findings. In the transverse sections disarray in the arrangement of the actin filaments and expansion of the myosin lattice, indicating clear overcontraction, were observed. The number of actin filaments varied from seven to 14 per hexagon; a number exceeding 12, however, was found in only one case. From our findings we conclude that overcontraction leads to a progressive deviation of the action filaments during systole caused by double overlap. The majority of these mechanisms results in a "self-impeding contraction" of the fibres. Functionally the excess of actin filaments may provide a balance between the unequal forces of contraction. |
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The majority of these mechanisms results in a "self-impeding contraction" of the fibres. Functionally the excess of actin filaments may provide a balance between the unequal forces of contraction.</description><identifier>ISSN: 0007-0769</identifier><identifier>ISSN: 1355-6037</identifier><identifier>EISSN: 1468-201X</identifier><identifier>EISSN: 2053-5864</identifier><identifier>DOI: 10.1136/hrt.45.5.494</identifier><identifier>PMID: 6894542</identifier><language>eng</language><publisher>England: BMJ Publishing Group Ltd and British Cardiovascular Society</publisher><subject>Actins - analysis ; Adult ; Cardiomyopathy, Hypertrophic - metabolism ; Cardiomyopathy, Hypertrophic - pathology ; Cardiomyopathy, Hypertrophic - physiopathology ; Endocardium - ultrastructure ; Heart Septum - ultrastructure ; Humans ; Male ; Microscopy, Electron ; Middle Aged ; Myocardial Contraction ; Myocardium - ultrastructure</subject><ispartof>British Heart Journal, 1981-05, Vol.45 (5), p.494-499</ispartof><rights>Copyright BMJ Publishing Group LTD May 1981</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-b3484-b068ea18be867dd0a00cb8fd06223ae50d58334660e5ecb3753ac4c477f611ed3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC482555/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC482555/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27922,27923,53789,53791</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/6894542$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Harmjanz, D</creatorcontrib><creatorcontrib>Reale, E</creatorcontrib><title>Overcontraction and excess actin filaments. Basic elements of hypertrophic cardiomyopathy</title><title>British Heart Journal</title><addtitle>Br Heart J</addtitle><description>Endomyocardial biopsies were taken from the right ventricular aspect of the interventricular septum in three patients with hypertrophic cardiomyopathy and were subjected to electronmicroscopical examination. Longitudinal sections confirmed already well-established findings. In the transverse sections disarray in the arrangement of the actin filaments and expansion of the myosin lattice, indicating clear overcontraction, were observed. The number of actin filaments varied from seven to 14 per hexagon; a number exceeding 12, however, was found in only one case. From our findings we conclude that overcontraction leads to a progressive deviation of the action filaments during systole caused by double overlap. The majority of these mechanisms results in a "self-impeding contraction" of the fibres. Functionally the excess of actin filaments may provide a balance between the unequal forces of contraction.</description><subject>Actins - analysis</subject><subject>Adult</subject><subject>Cardiomyopathy, Hypertrophic - metabolism</subject><subject>Cardiomyopathy, Hypertrophic - pathology</subject><subject>Cardiomyopathy, Hypertrophic - physiopathology</subject><subject>Endocardium - ultrastructure</subject><subject>Heart Septum - ultrastructure</subject><subject>Humans</subject><subject>Male</subject><subject>Microscopy, Electron</subject><subject>Middle Aged</subject><subject>Myocardial Contraction</subject><subject>Myocardium - ultrastructure</subject><issn>0007-0769</issn><issn>1355-6037</issn><issn>1468-201X</issn><issn>2053-5864</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1981</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kU1v1DAQhi1EVZbCjStSJCS4kGDHnzlwoCuglQpFfAm4WI4zId4mcbCzVfff18uuVsCB02jmfcYz4xehRwQXhFDxogtzwXjBC1axO2hBmFB5icm3u2iBMZY5lqK6h-7HuEopq5Q4RsdCVYyzcoG-X15DsH6cg7Gz82NmxiaDGwsxZtvKmLWuNwOMcyyyUxOdzaCH33nm26zbTBDm4KcuCdaExvlh4yczd5sH6Kg1fYSH-3iCvrx5_Xl5ll9cvj1fvrrIa8oUy2ssFBiialBCNg02GNtatQ0WZUkNcNxwRSkTAgMHW1PJqbHMMilbQQg09AS93L07resBGgvbW3o9BTeYsNHeOP23MrpO__TXmqmSc576n-77g_-1hjjrwUULfW9G8OuoJReipFWVwCf_gCu_DmO6TRMpMa4kZypRz3eUDT7GAO1hE4L11i-d_NKMa66TXwl__Of2B3hvUNLzne7iDDcH2YQrLWT6DP3-61L_EO-W6sOnj_o08c92fD2s_j_5Fv2er1Y</recordid><startdate>19810501</startdate><enddate>19810501</enddate><creator>Harmjanz, D</creator><creator>Reale, E</creator><general>BMJ Publishing Group Ltd and British Cardiovascular Society</general><general>BMJ Publishing Group LTD</general><scope>BSCLL</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>19810501</creationdate><title>Overcontraction and excess actin filaments. Basic elements of hypertrophic cardiomyopathy</title><author>Harmjanz, D ; Reale, E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b3484-b068ea18be867dd0a00cb8fd06223ae50d58334660e5ecb3753ac4c477f611ed3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1981</creationdate><topic>Actins - analysis</topic><topic>Adult</topic><topic>Cardiomyopathy, Hypertrophic - metabolism</topic><topic>Cardiomyopathy, Hypertrophic - pathology</topic><topic>Cardiomyopathy, Hypertrophic - physiopathology</topic><topic>Endocardium - ultrastructure</topic><topic>Heart Septum - ultrastructure</topic><topic>Humans</topic><topic>Male</topic><topic>Microscopy, Electron</topic><topic>Middle Aged</topic><topic>Myocardial Contraction</topic><topic>Myocardium - ultrastructure</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Harmjanz, D</creatorcontrib><creatorcontrib>Reale, E</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>British Heart Journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Harmjanz, D</au><au>Reale, E</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Overcontraction and excess actin filaments. Basic elements of hypertrophic cardiomyopathy</atitle><jtitle>British Heart Journal</jtitle><addtitle>Br Heart J</addtitle><date>1981-05-01</date><risdate>1981</risdate><volume>45</volume><issue>5</issue><spage>494</spage><epage>499</epage><pages>494-499</pages><issn>0007-0769</issn><issn>1355-6037</issn><eissn>1468-201X</eissn><eissn>2053-5864</eissn><abstract>Endomyocardial biopsies were taken from the right ventricular aspect of the interventricular septum in three patients with hypertrophic cardiomyopathy and were subjected to electronmicroscopical examination. Longitudinal sections confirmed already well-established findings. In the transverse sections disarray in the arrangement of the actin filaments and expansion of the myosin lattice, indicating clear overcontraction, were observed. The number of actin filaments varied from seven to 14 per hexagon; a number exceeding 12, however, was found in only one case. From our findings we conclude that overcontraction leads to a progressive deviation of the action filaments during systole caused by double overlap. The majority of these mechanisms results in a "self-impeding contraction" of the fibres. Functionally the excess of actin filaments may provide a balance between the unequal forces of contraction.</abstract><cop>England</cop><pub>BMJ Publishing Group Ltd and British Cardiovascular Society</pub><pmid>6894542</pmid><doi>10.1136/hrt.45.5.494</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Actins - analysis Adult Cardiomyopathy, Hypertrophic - metabolism Cardiomyopathy, Hypertrophic - pathology Cardiomyopathy, Hypertrophic - physiopathology Endocardium - ultrastructure Heart Septum - ultrastructure Humans Male Microscopy, Electron Middle Aged Myocardial Contraction Myocardium - ultrastructure |
title | Overcontraction and excess actin filaments. Basic elements of hypertrophic cardiomyopathy |
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