An Analysis of the Mechanical Disadvantage of Myocardial Infarction in the Canine Left Ventricle
An isotropic, initially spherical, membrane model of the infarcted ventricle satisfactorily predicts ventricular function in the infarcted heart when compared to clinical information and available ventricular models of higher complexity. Computations based on finite element solutions of this membran...
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Veröffentlicht in: | Circulation research 1980-11, Vol.47 (5), p.728-741 |
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creator | BOGEN, DANIEL K RABINOWITZ, STUART A NEEDLEMAN, ALAN MCMAHON, THOMAS A ABELMANN, WALTER H |
description | An isotropic, initially spherical, membrane model of the infarcted ventricle satisfactorily predicts ventricular function in the infarcted heart when compared to clinical information and available ventricular models of higher complexity. Computations based on finite element solutions of this membrane model yield end-diastolic and end-systolic pressure-volume curves, from which ventricular function curves are calculated, for infarcts of varying size and material properties. These computations indicate a progressive degradation of cardiac performance with increasing infarct size such that normal cardiac outputs can be maintained with Frank-Starling compensation and increased heart rate for acute infarcts no larger than 41% of the ventricular surface. The relationship between infarct stiffness and cardiac function is found to be complex and dependent on both infarct size and end-diastolic pressure, although moderately stiff subacute infarcts are associated with better function than extensible acute infarcts. Also, calculations of extensions and stresses suggest considerable disruption of the border zone contraction pattern, as well as elevated border zone systolic stresses. Circ Res 47728-741, 1980 |
doi_str_mv | 10.1161/01.res.47.5.728 |
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Computations based on finite element solutions of this membrane model yield end-diastolic and end-systolic pressure-volume curves, from which ventricular function curves are calculated, for infarcts of varying size and material properties. These computations indicate a progressive degradation of cardiac performance with increasing infarct size such that normal cardiac outputs can be maintained with Frank-Starling compensation and increased heart rate for acute infarcts no larger than 41% of the ventricular surface. The relationship between infarct stiffness and cardiac function is found to be complex and dependent on both infarct size and end-diastolic pressure, although moderately stiff subacute infarcts are associated with better function than extensible acute infarcts. Also, calculations of extensions and stresses suggest considerable disruption of the border zone contraction pattern, as well as elevated border zone systolic stresses. 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Computations based on finite element solutions of this membrane model yield end-diastolic and end-systolic pressure-volume curves, from which ventricular function curves are calculated, for infarcts of varying size and material properties. These computations indicate a progressive degradation of cardiac performance with increasing infarct size such that normal cardiac outputs can be maintained with Frank-Starling compensation and increased heart rate for acute infarcts no larger than 41% of the ventricular surface. The relationship between infarct stiffness and cardiac function is found to be complex and dependent on both infarct size and end-diastolic pressure, although moderately stiff subacute infarcts are associated with better function than extensible acute infarcts. Also, calculations of extensions and stresses suggest considerable disruption of the border zone contraction pattern, as well as elevated border zone systolic stresses. Circ Res 47728-741, 1980</description><subject>Animals</subject><subject>Disease Models, Animal</subject><subject>Dogs</subject><subject>Heart Rate</subject><subject>Heart Ventricles - physiopathology</subject><subject>Humans</subject><subject>Mathematics</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Stress, Physiological - physiopathology</subject><subject>Systole</subject><issn>0009-7330</issn><issn>1524-4571</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1980</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9UUuP0zAQthBoKQtnTkg5cUt2Jp7EzrEqu7BSV0i8rsZ1J9TgOoudsuq_x0srDqPR6HvM6BshXiM0iD1eATaJc0Oq6RrV6idigV1LNXUKn4oFAAy1khKeixc5_wRAku1wIS4UoUaJC_F9GatltOGYfa6msZp3XN2x29nonQ3VO5_t9o-Ns_3Bj_DdcXI2bX2BbuNok5v9FCsf_-lWRRS5WvM4V984zsm7wC_Fs9GGzK_O_VJ8vbn-svpQrz--v10t17Xr2h7qAcatJUWdJeq6Tg-oh74H146k2nIzbpyWrrdaOaVp5A0qkkQky6gIWnkp3p5879P0-8B5NnufHYdgI0-HbFRZo3GQhXh1Iro05Zx4NPfJ7206GgTzmKkBNJ-uPxtSpjMl06J4c7Y-bPa8_c8_h1hwOuEPU5g55V_h8MDJ7NiGeWfKD0ACtjUOGhDLVJdCkH8Bw2R_zQ</recordid><startdate>198011</startdate><enddate>198011</enddate><creator>BOGEN, DANIEL K</creator><creator>RABINOWITZ, STUART A</creator><creator>NEEDLEMAN, ALAN</creator><creator>MCMAHON, THOMAS A</creator><creator>ABELMANN, WALTER H</creator><general>American Heart Association, Inc</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>198011</creationdate><title>An Analysis of the Mechanical Disadvantage of Myocardial Infarction in the Canine Left Ventricle</title><author>BOGEN, DANIEL K ; RABINOWITZ, STUART A ; NEEDLEMAN, ALAN ; MCMAHON, THOMAS A ; ABELMANN, WALTER H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5260-90fda4745a4455589189660c2f4723291bc83c6a87c784feb17434443c7874023</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1980</creationdate><topic>Animals</topic><topic>Disease Models, Animal</topic><topic>Dogs</topic><topic>Heart Rate</topic><topic>Heart Ventricles - physiopathology</topic><topic>Humans</topic><topic>Mathematics</topic><topic>Myocardial Infarction - physiopathology</topic><topic>Stress, Physiological - physiopathology</topic><topic>Systole</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>BOGEN, DANIEL K</creatorcontrib><creatorcontrib>RABINOWITZ, STUART A</creatorcontrib><creatorcontrib>NEEDLEMAN, ALAN</creatorcontrib><creatorcontrib>MCMAHON, THOMAS A</creatorcontrib><creatorcontrib>ABELMANN, WALTER H</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>Circulation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>BOGEN, DANIEL K</au><au>RABINOWITZ, STUART A</au><au>NEEDLEMAN, ALAN</au><au>MCMAHON, THOMAS A</au><au>ABELMANN, WALTER H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>An Analysis of the Mechanical Disadvantage of Myocardial Infarction in the Canine Left Ventricle</atitle><jtitle>Circulation research</jtitle><addtitle>Circ Res</addtitle><date>1980-11</date><risdate>1980</risdate><volume>47</volume><issue>5</issue><spage>728</spage><epage>741</epage><pages>728-741</pages><issn>0009-7330</issn><eissn>1524-4571</eissn><abstract>An isotropic, initially spherical, membrane model of the infarcted ventricle satisfactorily predicts ventricular function in the infarcted heart when compared to clinical information and available ventricular models of higher complexity. Computations based on finite element solutions of this membrane model yield end-diastolic and end-systolic pressure-volume curves, from which ventricular function curves are calculated, for infarcts of varying size and material properties. These computations indicate a progressive degradation of cardiac performance with increasing infarct size such that normal cardiac outputs can be maintained with Frank-Starling compensation and increased heart rate for acute infarcts no larger than 41% of the ventricular surface. The relationship between infarct stiffness and cardiac function is found to be complex and dependent on both infarct size and end-diastolic pressure, although moderately stiff subacute infarcts are associated with better function than extensible acute infarcts. Also, calculations of extensions and stresses suggest considerable disruption of the border zone contraction pattern, as well as elevated border zone systolic stresses. 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source | MEDLINE; American Heart Association Journals; EZB-FREE-00999 freely available EZB journals; Journals@Ovid Complete |
subjects | Animals Disease Models, Animal Dogs Heart Rate Heart Ventricles - physiopathology Humans Mathematics Myocardial Infarction - physiopathology Stress, Physiological - physiopathology Systole |
title | An Analysis of the Mechanical Disadvantage of Myocardial Infarction in the Canine Left Ventricle |
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