Model of unidirectional block formation leading to reentrant ventricular tachycardia in the infarct border zone of postinfarction canine hearts

Abstract Background When the infarct border zone is stimulated prematurely, a unidirectional block line (UBL) can form and lead to double-loop (figure-of-eight) reentrant ventricular tachycardia (VT) with a central isthmus. The isthmus is composed of an entrance, center, and exit. It was hypothesize...

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Veröffentlicht in:Computers in biology and medicine 2015-07, Vol.62, p.254-263
Hauptverfasser: Ciaccio, Edward J, Coromilas, James, Ashikaga, Hiroshi, Cervantes, Daniel O, Wit, Andrew L, Peters, Nicholas S, McVeigh, Elliot R, Garan, Hasan
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container_issue
container_start_page 254
container_title Computers in biology and medicine
container_volume 62
creator Ciaccio, Edward J
Coromilas, James
Ashikaga, Hiroshi
Cervantes, Daniel O
Wit, Andrew L
Peters, Nicholas S
McVeigh, Elliot R
Garan, Hasan
description Abstract Background When the infarct border zone is stimulated prematurely, a unidirectional block line (UBL) can form and lead to double-loop (figure-of-eight) reentrant ventricular tachycardia (VT) with a central isthmus. The isthmus is composed of an entrance, center, and exit. It was hypothesized that for certain stimulus site locations and coupling intervals, the UBL would coincide with the isthmus entrance boundary, where infarct border zone thickness changes from thin-to-thick in the travel direction of the premature stimulus wavefront. Method A quantitative model was developed to describe how thin-to-thick changes in the border zone result in critically convex wavefront curvature leading to conduction block, which is dependent upon coupling interval. The model was tested in 12 retrospectively analyzed postinfarction canine experiments. Electrical activation was mapped for premature stimulation and for the first reentrant VT cycle. The relationship of functional conduction block forming during premature stimulation to functional block during reentrant VT was quantified. Results For an appropriately placed stimulus, in accord with model predictions: (1) The UBL and reentrant VT isthmus lateral boundaries overlapped (error: 4.8±5.7 mm). (2) The UBL leading edge coincided with the distal isthmus where the center-entrance boundary would be expected to occur. (3) The mean coupling interval was 164.6±11.0 ms during premature stimulation and 190.7±20.4 ms during the first reentrant VT cycle, in accord with model calculations, which resulted in critically convex wavefront curvature with functional conduction block, respectively, at the location of the isthmus entrance boundary and at the lateral isthmus edges. Discussion Reentrant VT onset following premature stimulation can be explained by the presence of critically convex wavefront curvature and unidirectional block at the isthmus entrance boundary when the premature stimulation interval is sufficiently short. The double-loop reentrant circuit pattern is a consequence of wavefront bifurcation around this UBL followed by coalescence, and then impulse propagation through the isthmus. The wavefront is blocked from propagating laterally away from the isthmus by sharp increases in border zone thickness, which results in critically convex wavefront curvature at VT cycle lengths.
doi_str_mv 10.1016/j.compbiomed.2015.04.032
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The isthmus is composed of an entrance, center, and exit. It was hypothesized that for certain stimulus site locations and coupling intervals, the UBL would coincide with the isthmus entrance boundary, where infarct border zone thickness changes from thin-to-thick in the travel direction of the premature stimulus wavefront. Method A quantitative model was developed to describe how thin-to-thick changes in the border zone result in critically convex wavefront curvature leading to conduction block, which is dependent upon coupling interval. The model was tested in 12 retrospectively analyzed postinfarction canine experiments. Electrical activation was mapped for premature stimulation and for the first reentrant VT cycle. The relationship of functional conduction block forming during premature stimulation to functional block during reentrant VT was quantified. Results For an appropriately placed stimulus, in accord with model predictions: (1) The UBL and reentrant VT isthmus lateral boundaries overlapped (error: 4.8±5.7 mm). (2) The UBL leading edge coincided with the distal isthmus where the center-entrance boundary would be expected to occur. (3) The mean coupling interval was 164.6±11.0 ms during premature stimulation and 190.7±20.4 ms during the first reentrant VT cycle, in accord with model calculations, which resulted in critically convex wavefront curvature with functional conduction block, respectively, at the location of the isthmus entrance boundary and at the lateral isthmus edges. Discussion Reentrant VT onset following premature stimulation can be explained by the presence of critically convex wavefront curvature and unidirectional block at the isthmus entrance boundary when the premature stimulation interval is sufficiently short. The double-loop reentrant circuit pattern is a consequence of wavefront bifurcation around this UBL followed by coalescence, and then impulse propagation through the isthmus. The wavefront is blocked from propagating laterally away from the isthmus by sharp increases in border zone thickness, which results in critically convex wavefront curvature at VT cycle lengths.</description><identifier>ISSN: 0010-4825</identifier><identifier>EISSN: 1879-0534</identifier><identifier>DOI: 10.1016/j.compbiomed.2015.04.032</identifier><identifier>PMID: 25966920</identifier><identifier>CODEN: CBMDAW</identifier><language>eng</language><publisher>United States: Elsevier Ltd</publisher><subject>Activation mapping ; Animals ; Biomedical research ; Boundaries ; Cardiac arrhythmia ; Disease Models, Animal ; Dogs ; Experiments ; Heart attacks ; Internal Medicine ; Isthmus ; Methods ; Models, Cardiovascular ; Myocardial Infarction - pathology ; Myocardial Infarction - physiopathology ; Other ; Propagation ; Standard deviation ; Tachycardia, Ventricular - pathology ; Tachycardia, Ventricular - physiopathology ; Unidirectional block ; Ventricular tachycardia ; Wavefront curvature</subject><ispartof>Computers in biology and medicine, 2015-07, Vol.62, p.254-263</ispartof><rights>Elsevier Ltd</rights><rights>2015 Elsevier Ltd</rights><rights>Copyright © 2015 Elsevier Ltd. All rights reserved.</rights><rights>Copyright Elsevier Limited Jul 2015</rights><rights>2015 The Authors. Published by Elsevier Ltd. 2015 Elsevier Ltd</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c595t-772604375cfa11e621dc4cfeff04ba0eec67b006781078f6acea4c227c25a4fe3</citedby><cites>FETCH-LOGICAL-c595t-772604375cfa11e621dc4cfeff04ba0eec67b006781078f6acea4c227c25a4fe3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/1686856955?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>230,315,782,786,887,3552,27931,27932,46002,64392,64394,64396,72476</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25966920$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ciaccio, Edward J</creatorcontrib><creatorcontrib>Coromilas, James</creatorcontrib><creatorcontrib>Ashikaga, Hiroshi</creatorcontrib><creatorcontrib>Cervantes, Daniel O</creatorcontrib><creatorcontrib>Wit, Andrew L</creatorcontrib><creatorcontrib>Peters, Nicholas S</creatorcontrib><creatorcontrib>McVeigh, Elliot R</creatorcontrib><creatorcontrib>Garan, Hasan</creatorcontrib><title>Model of unidirectional block formation leading to reentrant ventricular tachycardia in the infarct border zone of postinfarction canine hearts</title><title>Computers in biology and medicine</title><addtitle>Comput Biol Med</addtitle><description>Abstract Background When the infarct border zone is stimulated prematurely, a unidirectional block line (UBL) can form and lead to double-loop (figure-of-eight) reentrant ventricular tachycardia (VT) with a central isthmus. The isthmus is composed of an entrance, center, and exit. It was hypothesized that for certain stimulus site locations and coupling intervals, the UBL would coincide with the isthmus entrance boundary, where infarct border zone thickness changes from thin-to-thick in the travel direction of the premature stimulus wavefront. Method A quantitative model was developed to describe how thin-to-thick changes in the border zone result in critically convex wavefront curvature leading to conduction block, which is dependent upon coupling interval. The model was tested in 12 retrospectively analyzed postinfarction canine experiments. Electrical activation was mapped for premature stimulation and for the first reentrant VT cycle. The relationship of functional conduction block forming during premature stimulation to functional block during reentrant VT was quantified. Results For an appropriately placed stimulus, in accord with model predictions: (1) The UBL and reentrant VT isthmus lateral boundaries overlapped (error: 4.8±5.7 mm). (2) The UBL leading edge coincided with the distal isthmus where the center-entrance boundary would be expected to occur. (3) The mean coupling interval was 164.6±11.0 ms during premature stimulation and 190.7±20.4 ms during the first reentrant VT cycle, in accord with model calculations, which resulted in critically convex wavefront curvature with functional conduction block, respectively, at the location of the isthmus entrance boundary and at the lateral isthmus edges. Discussion Reentrant VT onset following premature stimulation can be explained by the presence of critically convex wavefront curvature and unidirectional block at the isthmus entrance boundary when the premature stimulation interval is sufficiently short. The double-loop reentrant circuit pattern is a consequence of wavefront bifurcation around this UBL followed by coalescence, and then impulse propagation through the isthmus. The wavefront is blocked from propagating laterally away from the isthmus by sharp increases in border zone thickness, which results in critically convex wavefront curvature at VT cycle lengths.</description><subject>Activation mapping</subject><subject>Animals</subject><subject>Biomedical research</subject><subject>Boundaries</subject><subject>Cardiac arrhythmia</subject><subject>Disease Models, Animal</subject><subject>Dogs</subject><subject>Experiments</subject><subject>Heart attacks</subject><subject>Internal Medicine</subject><subject>Isthmus</subject><subject>Methods</subject><subject>Models, Cardiovascular</subject><subject>Myocardial Infarction - pathology</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Other</subject><subject>Propagation</subject><subject>Standard deviation</subject><subject>Tachycardia, Ventricular - pathology</subject><subject>Tachycardia, Ventricular - physiopathology</subject><subject>Unidirectional block</subject><subject>Ventricular tachycardia</subject><subject>Wavefront curvature</subject><issn>0010-4825</issn><issn>1879-0534</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqNkk1v1DAQhiMEokvhLyBLXLhsGDt2Pi6VoCofUhEHQOJmOZNJ19usvdjJSsuf4C_jdJcWeoHTjDzPvPaM3yxjHHIOvHy1ztFvtq31G-pyAVzlIHMoxINsweuqWYIq5MNsAcBhKWuhTrInMa4BQEIBj7MToZqybAQssp8ffUcD8z2bnO1sIBytd2Zg7eDxmvU-bMx8wgYynXVXbPQsELkxGDey3ZxYnAYT2GhwtUcTOmuYdWxcUQq9CTiy1oeOAvvhHc03bX0cj6VZGY2zqbAiE8b4NHvUmyHSs2M8zb6-vfhy_n55-endh_PXl0tUjRqXVSVKkEWlsDecUyl4hxJ76nuQrQEiLKsWoKxqDlXdlwbJSBSiQqGM7Kk4zc4OutupTUvEm4kGvQ12Y8Jee2P13xVnV_rK77RURSGkSAIvjwLBf58ojnpjI9IwGEd-ippXwGVTF4X8N1rWdXorV01CX9xD134K6T9uqLJWZaNUouoDhcHHGKi_fTcHPRtEr_WdQfRsEA1SJ4Ok1ud_zn3b-NsRCXhzAChtf2cp6IiWHNLBHLrz9n9uObsngoN1Fs1wTXuKdzPpKDToz7NRZ59ylTIF34pfPsfqwA</recordid><startdate>20150701</startdate><enddate>20150701</enddate><creator>Ciaccio, Edward J</creator><creator>Coromilas, James</creator><creator>Ashikaga, Hiroshi</creator><creator>Cervantes, Daniel O</creator><creator>Wit, Andrew L</creator><creator>Peters, Nicholas S</creator><creator>McVeigh, Elliot R</creator><creator>Garan, Hasan</creator><general>Elsevier Ltd</general><general>Elsevier Limited</general><general>Elsevier</general><scope>6I.</scope><scope>AAFTH</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>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AL</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>JQ2</scope><scope>K7-</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0N</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>M7Z</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>7QO</scope><scope>5PM</scope></search><sort><creationdate>20150701</creationdate><title>Model of unidirectional block formation leading to reentrant ventricular tachycardia in the infarct border zone of postinfarction canine hearts</title><author>Ciaccio, Edward J ; Coromilas, James ; Ashikaga, Hiroshi ; Cervantes, Daniel O ; Wit, Andrew L ; Peters, Nicholas S ; McVeigh, Elliot R ; Garan, Hasan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c595t-772604375cfa11e621dc4cfeff04ba0eec67b006781078f6acea4c227c25a4fe3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Activation mapping</topic><topic>Animals</topic><topic>Biomedical research</topic><topic>Boundaries</topic><topic>Cardiac arrhythmia</topic><topic>Disease Models, Animal</topic><topic>Dogs</topic><topic>Experiments</topic><topic>Heart attacks</topic><topic>Internal Medicine</topic><topic>Isthmus</topic><topic>Methods</topic><topic>Models, Cardiovascular</topic><topic>Myocardial Infarction - pathology</topic><topic>Myocardial Infarction - physiopathology</topic><topic>Other</topic><topic>Propagation</topic><topic>Standard deviation</topic><topic>Tachycardia, Ventricular - pathology</topic><topic>Tachycardia, Ventricular - physiopathology</topic><topic>Unidirectional block</topic><topic>Ventricular tachycardia</topic><topic>Wavefront curvature</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ciaccio, Edward J</creatorcontrib><creatorcontrib>Coromilas, James</creatorcontrib><creatorcontrib>Ashikaga, Hiroshi</creatorcontrib><creatorcontrib>Cervantes, Daniel O</creatorcontrib><creatorcontrib>Wit, Andrew L</creatorcontrib><creatorcontrib>Peters, Nicholas S</creatorcontrib><creatorcontrib>McVeigh, Elliot R</creatorcontrib><creatorcontrib>Garan, Hasan</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</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>Nursing &amp; 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The isthmus is composed of an entrance, center, and exit. It was hypothesized that for certain stimulus site locations and coupling intervals, the UBL would coincide with the isthmus entrance boundary, where infarct border zone thickness changes from thin-to-thick in the travel direction of the premature stimulus wavefront. Method A quantitative model was developed to describe how thin-to-thick changes in the border zone result in critically convex wavefront curvature leading to conduction block, which is dependent upon coupling interval. The model was tested in 12 retrospectively analyzed postinfarction canine experiments. Electrical activation was mapped for premature stimulation and for the first reentrant VT cycle. The relationship of functional conduction block forming during premature stimulation to functional block during reentrant VT was quantified. Results For an appropriately placed stimulus, in accord with model predictions: (1) The UBL and reentrant VT isthmus lateral boundaries overlapped (error: 4.8±5.7 mm). (2) The UBL leading edge coincided with the distal isthmus where the center-entrance boundary would be expected to occur. (3) The mean coupling interval was 164.6±11.0 ms during premature stimulation and 190.7±20.4 ms during the first reentrant VT cycle, in accord with model calculations, which resulted in critically convex wavefront curvature with functional conduction block, respectively, at the location of the isthmus entrance boundary and at the lateral isthmus edges. Discussion Reentrant VT onset following premature stimulation can be explained by the presence of critically convex wavefront curvature and unidirectional block at the isthmus entrance boundary when the premature stimulation interval is sufficiently short. The double-loop reentrant circuit pattern is a consequence of wavefront bifurcation around this UBL followed by coalescence, and then impulse propagation through the isthmus. The wavefront is blocked from propagating laterally away from the isthmus by sharp increases in border zone thickness, which results in critically convex wavefront curvature at VT cycle lengths.</abstract><cop>United States</cop><pub>Elsevier Ltd</pub><pmid>25966920</pmid><doi>10.1016/j.compbiomed.2015.04.032</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record>
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source MEDLINE; Access via ScienceDirect (Elsevier); ProQuest Central UK/Ireland
subjects Activation mapping
Animals
Biomedical research
Boundaries
Cardiac arrhythmia
Disease Models, Animal
Dogs
Experiments
Heart attacks
Internal Medicine
Isthmus
Methods
Models, Cardiovascular
Myocardial Infarction - pathology
Myocardial Infarction - physiopathology
Other
Propagation
Standard deviation
Tachycardia, Ventricular - pathology
Tachycardia, Ventricular - physiopathology
Unidirectional block
Ventricular tachycardia
Wavefront curvature
title Model of unidirectional block formation leading to reentrant ventricular tachycardia in the infarct border zone of postinfarction canine hearts
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