Re-entrant arrhythmias in simulations of the long-QT syndrome
In the congenital LQTS, repolarisation of the ventricles is prolonged and patients with LQTS are at an increased risk of ventricular arrhythmias. Four LQTS phenotypes have been identified LQT1, LQT2 and LQT4 affect potassium channels, and LQT3 affects sodium channels. The incidence of arrhythmias is...
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creator | Clayton, R.H. Bailey, A. Biktashev, V.N. Holden, A.V. |
description | In the congenital LQTS, repolarisation of the ventricles is prolonged and patients with LQTS are at an increased risk of ventricular arrhythmias. Four LQTS phenotypes have been identified LQT1, LQT2 and LQT4 affect potassium channels, and LQT3 affects sodium channels. The incidence of arrhythmias is higher in LOT1 but the incidence of lethal arrhythmias is higher in LQT3. The aim of the study was to compare re-entry in simulations of LQT1 and LQT3 myocardium. We modified the Oxsoft equations for the guinea pig ventricular cell to simulate 30 mm/spl times/30 mm 2 dimensional LQT1 and LQT3 preparations Although there was no difference in vulnerable period between normal, LQT1 and LQT3 simulations re-entrant wave meander was 3.6 times greater in LQT1 than normal, but only 1.3 times greater in LQT3 than normal. We propose that the greater meander in LQT1 explains the higher incidence of self terminating non-lethal arrhythmias in this phenotype. |
doi_str_mv | 10.1109/CIC.1999.825921 |
format | Conference Proceeding |
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Four LQTS phenotypes have been identified LQT1, LQT2 and LQT4 affect potassium channels, and LQT3 affects sodium channels. The incidence of arrhythmias is higher in LOT1 but the incidence of lethal arrhythmias is higher in LQT3. The aim of the study was to compare re-entry in simulations of LQT1 and LQT3 myocardium. We modified the Oxsoft equations for the guinea pig ventricular cell to simulate 30 mm/spl times/30 mm 2 dimensional LQT1 and LQT3 preparations Although there was no difference in vulnerable period between normal, LQT1 and LQT3 simulations re-entrant wave meander was 3.6 times greater in LQT1 than normal, but only 1.3 times greater in LQT3 than normal. We propose that the greater meander in LQT1 explains the higher incidence of self terminating non-lethal arrhythmias in this phenotype.</description><identifier>ISSN: 0276-6547</identifier><identifier>ISSN: 0276-6574</identifier><identifier>ISBN: 0780356144</identifier><identifier>ISBN: 9780780356146</identifier><identifier>DOI: 10.1109/CIC.1999.825921</identifier><language>eng</language><publisher>IEEE</publisher><subject>Anisotropic magnetoresistance ; Bioelectric phenomena ; Biomembranes ; Cardiology ; Cells ; Computational modeling ; Computer simulation ; Electrocardiography ; Equations ; Genetic mutations ; Heart rate ; Myocardium ; Stress</subject><ispartof>Computers in Cardiology 1999. Vol.26 (Cat. 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No.99CH37004)</title><addtitle>CIC</addtitle><description>In the congenital LQTS, repolarisation of the ventricles is prolonged and patients with LQTS are at an increased risk of ventricular arrhythmias. Four LQTS phenotypes have been identified LQT1, LQT2 and LQT4 affect potassium channels, and LQT3 affects sodium channels. The incidence of arrhythmias is higher in LOT1 but the incidence of lethal arrhythmias is higher in LQT3. The aim of the study was to compare re-entry in simulations of LQT1 and LQT3 myocardium. We modified the Oxsoft equations for the guinea pig ventricular cell to simulate 30 mm/spl times/30 mm 2 dimensional LQT1 and LQT3 preparations Although there was no difference in vulnerable period between normal, LQT1 and LQT3 simulations re-entrant wave meander was 3.6 times greater in LQT1 than normal, but only 1.3 times greater in LQT3 than normal. We propose that the greater meander in LQT1 explains the higher incidence of self terminating non-lethal arrhythmias in this phenotype.</description><subject>Anisotropic magnetoresistance</subject><subject>Bioelectric phenomena</subject><subject>Biomembranes</subject><subject>Cardiology</subject><subject>Cells</subject><subject>Computational modeling</subject><subject>Computer simulation</subject><subject>Electrocardiography</subject><subject>Equations</subject><subject>Genetic mutations</subject><subject>Heart rate</subject><subject>Myocardium</subject><subject>Stress</subject><issn>0276-6547</issn><issn>0276-6574</issn><isbn>0780356144</isbn><isbn>9780780356146</isbn><fulltext>true</fulltext><rsrctype>conference_proceeding</rsrctype><creationdate>1999</creationdate><recordtype>conference_proceeding</recordtype><sourceid>6IE</sourceid><sourceid>RIE</sourceid><recordid>eNqFkDtPwzAURi0BEqV0RmLyxJZiX7_igQFFPCpVQqAyR7fkhlpKnBK7Q_89lcLO9A3f0RkOYzdSLKUU_r5aVUvpvV-WYDzIM3YlXCmUsVLrczYT4GxhjXaXbJFS2AoAc7qdmbGHDyoo5hFj5jiOu2Pe9QETD5Gn0B86zGGIiQ8tzzvi3RC_i_cNT8fYjENP1-yixS7R4m_n7PP5aVO9Fuu3l1X1uC4CKJ0L8oQOGomtUUpp8OSRHLalK93WatBKNqVBgaCc8s0WsXRQOiuArDCG1JzdTd79OPwcKOW6D-mLug4jDYdUgztlMOD-BaWy2oOBE3g7gYGI6v0YehyP9ZRP_QKu12IB</recordid><startdate>1999</startdate><enddate>1999</enddate><creator>Clayton, R.H.</creator><creator>Bailey, A.</creator><creator>Biktashev, V.N.</creator><creator>Holden, A.V.</creator><general>IEEE</general><scope>6IE</scope><scope>6IH</scope><scope>CBEJK</scope><scope>RIE</scope><scope>RIO</scope><scope>7SC</scope><scope>8FD</scope><scope>JQ2</scope><scope>L7M</scope><scope>L~C</scope><scope>L~D</scope></search><sort><creationdate>1999</creationdate><title>Re-entrant arrhythmias in simulations of the long-QT syndrome</title><author>Clayton, R.H. ; Bailey, A. ; Biktashev, V.N. ; Holden, A.V.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-i234t-e9ea72d1af5333429e9ae7af8787b642431d85a0a23739dbaa87287602e6055e3</frbrgroupid><rsrctype>conference_proceedings</rsrctype><prefilter>conference_proceedings</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Anisotropic magnetoresistance</topic><topic>Bioelectric phenomena</topic><topic>Biomembranes</topic><topic>Cardiology</topic><topic>Cells</topic><topic>Computational modeling</topic><topic>Computer simulation</topic><topic>Electrocardiography</topic><topic>Equations</topic><topic>Genetic mutations</topic><topic>Heart rate</topic><topic>Myocardium</topic><topic>Stress</topic><toplevel>online_resources</toplevel><creatorcontrib>Clayton, R.H.</creatorcontrib><creatorcontrib>Bailey, A.</creatorcontrib><creatorcontrib>Biktashev, V.N.</creatorcontrib><creatorcontrib>Holden, A.V.</creatorcontrib><collection>IEEE Electronic Library (IEL) Conference Proceedings</collection><collection>IEEE Proceedings Order Plan (POP) 1998-present by volume</collection><collection>IEEE Xplore All Conference Proceedings</collection><collection>IEEE Electronic Library (IEL)</collection><collection>IEEE Proceedings Order Plans (POP) 1998-present</collection><collection>Computer and Information Systems Abstracts</collection><collection>Technology Research Database</collection><collection>ProQuest Computer Science Collection</collection><collection>Advanced Technologies Database with Aerospace</collection><collection>Computer and Information Systems Abstracts Academic</collection><collection>Computer and Information Systems Abstracts Professional</collection></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Clayton, R.H.</au><au>Bailey, A.</au><au>Biktashev, V.N.</au><au>Holden, A.V.</au><format>book</format><genre>proceeding</genre><ristype>CONF</ristype><atitle>Re-entrant arrhythmias in simulations of the long-QT syndrome</atitle><btitle>Computers in Cardiology 1999. Vol.26 (Cat. No.99CH37004)</btitle><stitle>CIC</stitle><date>1999</date><risdate>1999</risdate><spage>121</spage><epage>124</epage><pages>121-124</pages><issn>0276-6547</issn><issn>0276-6574</issn><isbn>0780356144</isbn><isbn>9780780356146</isbn><abstract>In the congenital LQTS, repolarisation of the ventricles is prolonged and patients with LQTS are at an increased risk of ventricular arrhythmias. Four LQTS phenotypes have been identified LQT1, LQT2 and LQT4 affect potassium channels, and LQT3 affects sodium channels. The incidence of arrhythmias is higher in LOT1 but the incidence of lethal arrhythmias is higher in LQT3. The aim of the study was to compare re-entry in simulations of LQT1 and LQT3 myocardium. We modified the Oxsoft equations for the guinea pig ventricular cell to simulate 30 mm/spl times/30 mm 2 dimensional LQT1 and LQT3 preparations Although there was no difference in vulnerable period between normal, LQT1 and LQT3 simulations re-entrant wave meander was 3.6 times greater in LQT1 than normal, but only 1.3 times greater in LQT3 than normal. We propose that the greater meander in LQT1 explains the higher incidence of self terminating non-lethal arrhythmias in this phenotype.</abstract><pub>IEEE</pub><doi>10.1109/CIC.1999.825921</doi><tpages>4</tpages></addata></record> |
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source | IEEE Electronic Library (IEL) Conference Proceedings |
subjects | Anisotropic magnetoresistance Bioelectric phenomena Biomembranes Cardiology Cells Computational modeling Computer simulation Electrocardiography Equations Genetic mutations Heart rate Myocardium Stress |
title | Re-entrant arrhythmias in simulations of the long-QT syndrome |
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