Origin of the Giant R Wave in Acute Transmural Myocardial Infarction in the Pig

An increase in R wave amplitude and a diminution of S wave amplitude, together with ST segment elevation, have been described as very early electrocardiographic changes during clinical and experimental acute myocardial infarction. The genesis of these QRS changes remains unclear. We assessed the qua...

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Veröffentlicht in:Japanese Heart Journal 1989, Vol.30(6), pp.863-883
Hauptverfasser: CHANG, Winshih, AKIYAMA, Toshio, RICHESON, J. Franklin, FAILLACE, Robert T., SERRINO, Peter
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container_end_page 883
container_issue 6
container_start_page 863
container_title Japanese Heart Journal
container_volume 30
creator CHANG, Winshih
AKIYAMA, Toshio
RICHESON, J. Franklin
FAILLACE, Robert T.
SERRINO, Peter
description An increase in R wave amplitude and a diminution of S wave amplitude, together with ST segment elevation, have been described as very early electrocardiographic changes during clinical and experimental acute myocardial infarction. The genesis of these QRS changes remains unclear. We assessed the quantitative relationship between the local conduction delay and the formation of the giant R wave, using multiple epicardial, intramural unipolar, and bipolar electrodes in 30 open-chest pigs with acute transmural myocardial ischemia. Blood pressure, heart rate, serum electrolytes, hematocrit, and left ventricular size remained constant, or varied insignificantly throughout the experiments. In nonischemic pigs, transmural left ventricular activation occurred nearly simultaneously, and the activation time was not correlated with the net QRS potential. During acute ischemia, a giant R wave developed at all of the electrodes located within the ischemia region; R wave amplitude began to increase 1min after coronary artery ligation (p
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Franklin ; FAILLACE, Robert T. ; SERRINO, Peter</creator><creatorcontrib>CHANG, Winshih ; AKIYAMA, Toshio ; RICHESON, J. Franklin ; FAILLACE, Robert T. ; SERRINO, Peter</creatorcontrib><description>An increase in R wave amplitude and a diminution of S wave amplitude, together with ST segment elevation, have been described as very early electrocardiographic changes during clinical and experimental acute myocardial infarction. The genesis of these QRS changes remains unclear. We assessed the quantitative relationship between the local conduction delay and the formation of the giant R wave, using multiple epicardial, intramural unipolar, and bipolar electrodes in 30 open-chest pigs with acute transmural myocardial ischemia. Blood pressure, heart rate, serum electrolytes, hematocrit, and left ventricular size remained constant, or varied insignificantly throughout the experiments. In nonischemic pigs, transmural left ventricular activation occurred nearly simultaneously, and the activation time was not correlated with the net QRS potential. During acute ischemia, a giant R wave developed at all of the electrodes located within the ischemia region; R wave amplitude began to increase 1min after coronary artery ligation (p&lt;0.05), compared to control amplitude and peaked at 8min (p&lt;0.0001). The degree of conduction delay at a given site was correlated linearly with the local R wave amplitude (average of correlation coefficients±SEM at 1min, r=0.64±0.08, and at 8min, r=0.81±0.06). The magnitude of the R wave potential and the conduction delay were greater in regions deep inside the ischemic zone than in the border and normal areas (p&lt;0.0001), and were greater in subepicardial than in subendocardial areas (p&lt;0.05). In summary, during transmural ischemia, conduction is markedly slowed, and an orderly and discrete wavefront advances toward the center of the ischemic zone from lateral and subendocardial areas. When depolarization is complete in the rest of the heart, this slow activation front becomes temporally isolated and its progression gives rise to a giant R wave, which appears in recordings from overlying electrodes.</description><identifier>ISSN: 0021-4868</identifier><identifier>EISSN: 1348-673X</identifier><identifier>DOI: 10.1536/ihj.30.863</identifier><identifier>PMID: 2632838</identifier><identifier>CODEN: JHEJAR</identifier><language>eng</language><publisher>Tokyo: International Heart Journal Association</publisher><subject>Acute myocardial infarction ; Animals ; Biological and medical sciences ; Cardiology. Vascular system ; Coronary heart disease ; Electrocardiography ; Giant R wave ; Heart ; Heart Conduction System - physiopathology ; Medical sciences ; Myocardial conduction delay ; Myocardial Infarction - diagnosis ; Myocardial Infarction - physiopathology ; Myocardial ischemia ; QRS complex ; Swine</subject><ispartof>Japanese Heart Journal, 1989, Vol.30(6), pp.863-883</ispartof><rights>by International Heart Journal Association</rights><rights>1990 INIST-CNRS</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c574t-9fc6d30179d3f6b2760324199eacc8e756fc085528f7b0881b21be96382ca0e73</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,1877,4010,27900,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=6847710$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2632838$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>CHANG, Winshih</creatorcontrib><creatorcontrib>AKIYAMA, Toshio</creatorcontrib><creatorcontrib>RICHESON, J. Franklin</creatorcontrib><creatorcontrib>FAILLACE, Robert T.</creatorcontrib><creatorcontrib>SERRINO, Peter</creatorcontrib><title>Origin of the Giant R Wave in Acute Transmural Myocardial Infarction in the Pig</title><title>Japanese Heart Journal</title><addtitle>Jpn Heart J</addtitle><description>An increase in R wave amplitude and a diminution of S wave amplitude, together with ST segment elevation, have been described as very early electrocardiographic changes during clinical and experimental acute myocardial infarction. The genesis of these QRS changes remains unclear. We assessed the quantitative relationship between the local conduction delay and the formation of the giant R wave, using multiple epicardial, intramural unipolar, and bipolar electrodes in 30 open-chest pigs with acute transmural myocardial ischemia. Blood pressure, heart rate, serum electrolytes, hematocrit, and left ventricular size remained constant, or varied insignificantly throughout the experiments. In nonischemic pigs, transmural left ventricular activation occurred nearly simultaneously, and the activation time was not correlated with the net QRS potential. During acute ischemia, a giant R wave developed at all of the electrodes located within the ischemia region; R wave amplitude began to increase 1min after coronary artery ligation (p&lt;0.05), compared to control amplitude and peaked at 8min (p&lt;0.0001). The degree of conduction delay at a given site was correlated linearly with the local R wave amplitude (average of correlation coefficients±SEM at 1min, r=0.64±0.08, and at 8min, r=0.81±0.06). The magnitude of the R wave potential and the conduction delay were greater in regions deep inside the ischemic zone than in the border and normal areas (p&lt;0.0001), and were greater in subepicardial than in subendocardial areas (p&lt;0.05). In summary, during transmural ischemia, conduction is markedly slowed, and an orderly and discrete wavefront advances toward the center of the ischemic zone from lateral and subendocardial areas. When depolarization is complete in the rest of the heart, this slow activation front becomes temporally isolated and its progression gives rise to a giant R wave, which appears in recordings from overlying electrodes.</description><subject>Acute myocardial infarction</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Coronary heart disease</subject><subject>Electrocardiography</subject><subject>Giant R wave</subject><subject>Heart</subject><subject>Heart Conduction System - physiopathology</subject><subject>Medical sciences</subject><subject>Myocardial conduction delay</subject><subject>Myocardial Infarction - diagnosis</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Myocardial ischemia</subject><subject>QRS complex</subject><subject>Swine</subject><issn>0021-4868</issn><issn>1348-673X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1989</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kM9LwzAYhoMoc04v3oUexIPQmTRtkh5l6BxMJjLRW0jTZMvoj5m0wv57U1p6ST7yPvleeAC4RXCOEkyezP4wx3DOCD4DU4RjFhKKf87BFMIIhTEj7BJcOXeAEJGI4QmYRAT7gU3BZmPNzlRBrYNmr4KlEVUTfAbf4k8F_vlZto0KtlZUrmytKIL3Uy2FzY0fV5UWVjamrjqy-_1hdtfgQovCqZvhnoGv15ft4i1cb5arxfM6lAmNmzDVkuQYIprmWJMsogTiKEZpqoSUTNGEaAlZkkRM0wwyhrIIZSolmEVSQEXxDDz0e4-2_m2Va3hpnFRFISpVt47TNE69D-TBxx6UtnbOKs2P1pTCnjiCvLPHvT2OIfe0h--GrW1WqnxEB10-vx9y4aQotPcijRsxwmJKEfTYoscOrhE7NebCNkYWqmtEKYFdK-kPXz6mci8sVxX-B7dOjXY</recordid><startdate>1989</startdate><enddate>1989</enddate><creator>CHANG, Winshih</creator><creator>AKIYAMA, Toshio</creator><creator>RICHESON, J. Franklin</creator><creator>FAILLACE, Robert T.</creator><creator>SERRINO, Peter</creator><general>International Heart Journal Association</general><general>Japanese Heart Journal Association</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>1989</creationdate><title>Origin of the Giant R Wave in Acute Transmural Myocardial Infarction in the Pig</title><author>CHANG, Winshih ; AKIYAMA, Toshio ; RICHESON, J. Franklin ; FAILLACE, Robert T. ; SERRINO, Peter</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c574t-9fc6d30179d3f6b2760324199eacc8e756fc085528f7b0881b21be96382ca0e73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1989</creationdate><topic>Acute myocardial infarction</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cardiology. Vascular system</topic><topic>Coronary heart disease</topic><topic>Electrocardiography</topic><topic>Giant R wave</topic><topic>Heart</topic><topic>Heart Conduction System - physiopathology</topic><topic>Medical sciences</topic><topic>Myocardial conduction delay</topic><topic>Myocardial Infarction - diagnosis</topic><topic>Myocardial Infarction - physiopathology</topic><topic>Myocardial ischemia</topic><topic>QRS complex</topic><topic>Swine</topic><toplevel>online_resources</toplevel><creatorcontrib>CHANG, Winshih</creatorcontrib><creatorcontrib>AKIYAMA, Toshio</creatorcontrib><creatorcontrib>RICHESON, J. Franklin</creatorcontrib><creatorcontrib>FAILLACE, Robert T.</creatorcontrib><creatorcontrib>SERRINO, Peter</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>Japanese Heart Journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>CHANG, Winshih</au><au>AKIYAMA, Toshio</au><au>RICHESON, J. Franklin</au><au>FAILLACE, Robert T.</au><au>SERRINO, Peter</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Origin of the Giant R Wave in Acute Transmural Myocardial Infarction in the Pig</atitle><jtitle>Japanese Heart Journal</jtitle><addtitle>Jpn Heart J</addtitle><date>1989</date><risdate>1989</risdate><volume>30</volume><issue>6</issue><spage>863</spage><epage>883</epage><pages>863-883</pages><issn>0021-4868</issn><eissn>1348-673X</eissn><coden>JHEJAR</coden><abstract>An increase in R wave amplitude and a diminution of S wave amplitude, together with ST segment elevation, have been described as very early electrocardiographic changes during clinical and experimental acute myocardial infarction. The genesis of these QRS changes remains unclear. We assessed the quantitative relationship between the local conduction delay and the formation of the giant R wave, using multiple epicardial, intramural unipolar, and bipolar electrodes in 30 open-chest pigs with acute transmural myocardial ischemia. Blood pressure, heart rate, serum electrolytes, hematocrit, and left ventricular size remained constant, or varied insignificantly throughout the experiments. In nonischemic pigs, transmural left ventricular activation occurred nearly simultaneously, and the activation time was not correlated with the net QRS potential. During acute ischemia, a giant R wave developed at all of the electrodes located within the ischemia region; R wave amplitude began to increase 1min after coronary artery ligation (p&lt;0.05), compared to control amplitude and peaked at 8min (p&lt;0.0001). The degree of conduction delay at a given site was correlated linearly with the local R wave amplitude (average of correlation coefficients±SEM at 1min, r=0.64±0.08, and at 8min, r=0.81±0.06). The magnitude of the R wave potential and the conduction delay were greater in regions deep inside the ischemic zone than in the border and normal areas (p&lt;0.0001), and were greater in subepicardial than in subendocardial areas (p&lt;0.05). In summary, during transmural ischemia, conduction is markedly slowed, and an orderly and discrete wavefront advances toward the center of the ischemic zone from lateral and subendocardial areas. When depolarization is complete in the rest of the heart, this slow activation front becomes temporally isolated and its progression gives rise to a giant R wave, which appears in recordings from overlying electrodes.</abstract><cop>Tokyo</cop><pub>International Heart Journal Association</pub><pmid>2632838</pmid><doi>10.1536/ihj.30.863</doi><tpages>21</tpages><oa>free_for_read</oa></addata></record>
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subjects Acute myocardial infarction
Animals
Biological and medical sciences
Cardiology. Vascular system
Coronary heart disease
Electrocardiography
Giant R wave
Heart
Heart Conduction System - physiopathology
Medical sciences
Myocardial conduction delay
Myocardial Infarction - diagnosis
Myocardial Infarction - physiopathology
Myocardial ischemia
QRS complex
Swine
title Origin of the Giant R Wave in Acute Transmural Myocardial Infarction in the Pig
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