Long-term monitoring of the changes in signal-averaged ECG after coronary artery occlusion and intracoronary endothelin-1 injection in dogs
Myocardium undergoes functional changes in the infarcted region primarily due to ischemia. Following myocyte functional alterations of the noninfarcted myocardium are caused by remodelling and hypertrophy. We have monitored and compared changes in the electrocardiographical (ECG) image after coronar...
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Veröffentlicht in: | Physiological research 2006, Vol.55 (1), p.9-14 |
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description | Myocardium undergoes functional changes in the infarcted region primarily due to ischemia. Following myocyte functional alterations of the noninfarcted myocardium are caused by remodelling and hypertrophy. We have monitored and compared changes in the electrocardiographical (ECG) image after coronary artery occlusion (CAO, n=5) and intracoronary endothelin-1 (ET-1, n=3) administration during a 6-month period. In 3 dogs, the CAO was repeated 6 months after the first occlusion. Signal-averaged ECG (SA ECG) was recorded before the operation and 10 days, 1 month, 3 months and 6 months after myocardial infarction (MI). The modified Wigner distribution was used for spectrotemporal analysis of the SA ECG. Eight-hour Holter monitoring was performed in each dog before and after experimental MI. Spectrotemporal representations of the QRS complex were stabilized after the first 1-month period in the group of dogs after CAO. The same results were also observed after the repeated CAO. No arrhythmias were recorded 9 days after CAO. The spectrotemporal representations of the QRS complex after intracoronary ET-1 administration were not stabilized during the whole observed period. Very few arrhythmic events were recorded by Holter monitoring already 3 days after intracoronary ET-1 injection. Experimental MI induced by CAO caused a changed ECG image, which was stable from 1 month after MI induction till the end of the monitoring. However, the ECG image after ET-1 administration was not stable during the whole observed period. No arrhythmic events were recorded in either group 3 months postoperatively that could be caused by healthy myocardial status before the experimental MI induction. In clinical practice, however, ischemic heart disease usually precedes the MI. Arrhythmogenic substrate could thus be a consequence of combination of healthy status of the myocardium before MI and MI itself. |
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Following myocyte functional alterations of the noninfarcted myocardium are caused by remodelling and hypertrophy. We have monitored and compared changes in the electrocardiographical (ECG) image after coronary artery occlusion (CAO, n=5) and intracoronary endothelin-1 (ET-1, n=3) administration during a 6-month period. In 3 dogs, the CAO was repeated 6 months after the first occlusion. Signal-averaged ECG (SA ECG) was recorded before the operation and 10 days, 1 month, 3 months and 6 months after myocardial infarction (MI). The modified Wigner distribution was used for spectrotemporal analysis of the SA ECG. Eight-hour Holter monitoring was performed in each dog before and after experimental MI. Spectrotemporal representations of the QRS complex were stabilized after the first 1-month period in the group of dogs after CAO. The same results were also observed after the repeated CAO. No arrhythmias were recorded 9 days after CAO. The spectrotemporal representations of the QRS complex after intracoronary ET-1 administration were not stabilized during the whole observed period. Very few arrhythmic events were recorded by Holter monitoring already 3 days after intracoronary ET-1 injection. Experimental MI induced by CAO caused a changed ECG image, which was stable from 1 month after MI induction till the end of the monitoring. However, the ECG image after ET-1 administration was not stable during the whole observed period. No arrhythmic events were recorded in either group 3 months postoperatively that could be caused by healthy myocardial status before the experimental MI induction. In clinical practice, however, ischemic heart disease usually precedes the MI. Arrhythmogenic substrate could thus be a consequence of combination of healthy status of the myocardium before MI and MI itself.</description><identifier>ISSN: 0862-8408</identifier><identifier>EISSN: 1802-9973</identifier><identifier>DOI: 10.33549/physiolres.930743</identifier><identifier>PMID: 15857164</identifier><language>eng</language><publisher>Czech Republic: Institute of Physiology</publisher><subject>Animals ; Arrhythmias, Cardiac - diagnosis ; Arrhythmias, Cardiac - etiology ; Arrhythmias, Cardiac - physiopathology ; Coronary Disease - etiology ; Disease Models, Animal ; Dogs ; Electrocardiography, Ambulatory ; Endothelin-1 ; Heart - drug effects ; Heart - physiopathology ; Myocardial Infarction - diagnosis ; Myocardial Infarction - etiology ; Myocardial Infarction - physiopathology ; Risk Factors ; Signal Processing, Computer-Assisted ; Time Factors</subject><ispartof>Physiological research, 2006, Vol.55 (1), p.9-14</ispartof><rights>Copyright Institute of Physiology 2006</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-5193e2617b0c6675fc173b66c5f4218a0c1af327b637fb651ccdc37a620a0b353</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,864,4024,27923,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15857164$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hubka, P</creatorcontrib><creatorcontrib>Bernadic, M</creatorcontrib><creatorcontrib>Hulín, I</creatorcontrib><title>Long-term monitoring of the changes in signal-averaged ECG after coronary artery occlusion and intracoronary endothelin-1 injection in dogs</title><title>Physiological research</title><addtitle>Physiol Res</addtitle><description>Myocardium undergoes functional changes in the infarcted region primarily due to ischemia. Following myocyte functional alterations of the noninfarcted myocardium are caused by remodelling and hypertrophy. We have monitored and compared changes in the electrocardiographical (ECG) image after coronary artery occlusion (CAO, n=5) and intracoronary endothelin-1 (ET-1, n=3) administration during a 6-month period. In 3 dogs, the CAO was repeated 6 months after the first occlusion. Signal-averaged ECG (SA ECG) was recorded before the operation and 10 days, 1 month, 3 months and 6 months after myocardial infarction (MI). The modified Wigner distribution was used for spectrotemporal analysis of the SA ECG. Eight-hour Holter monitoring was performed in each dog before and after experimental MI. Spectrotemporal representations of the QRS complex were stabilized after the first 1-month period in the group of dogs after CAO. The same results were also observed after the repeated CAO. No arrhythmias were recorded 9 days after CAO. The spectrotemporal representations of the QRS complex after intracoronary ET-1 administration were not stabilized during the whole observed period. Very few arrhythmic events were recorded by Holter monitoring already 3 days after intracoronary ET-1 injection. Experimental MI induced by CAO caused a changed ECG image, which was stable from 1 month after MI induction till the end of the monitoring. However, the ECG image after ET-1 administration was not stable during the whole observed period. No arrhythmic events were recorded in either group 3 months postoperatively that could be caused by healthy myocardial status before the experimental MI induction. In clinical practice, however, ischemic heart disease usually precedes the MI. Arrhythmogenic substrate could thus be a consequence of combination of healthy status of the myocardium before MI and MI itself.</description><subject>Animals</subject><subject>Arrhythmias, Cardiac - diagnosis</subject><subject>Arrhythmias, Cardiac - etiology</subject><subject>Arrhythmias, Cardiac - physiopathology</subject><subject>Coronary Disease - etiology</subject><subject>Disease Models, Animal</subject><subject>Dogs</subject><subject>Electrocardiography, Ambulatory</subject><subject>Endothelin-1</subject><subject>Heart - drug effects</subject><subject>Heart - physiopathology</subject><subject>Myocardial Infarction - diagnosis</subject><subject>Myocardial Infarction - etiology</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Risk Factors</subject><subject>Signal Processing, Computer-Assisted</subject><subject>Time Factors</subject><issn>0862-8408</issn><issn>1802-9973</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</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>eNpdkd1KwzAYhoMobk5vwAMJHniWmZ_mp4cy5hQGnuhxSdO062iTmbTCrsGbNrqh4FH4yPO8fMkLwDXBc8Z4lt_vNvvY-i7YOM8Zlhk7AVOiMEV5LtkpmGIlKFIZVhNwEeMWYyqxZOdgQrjikohsCj7X3jVosKGHvXft4EPrGuhrOGwsNBvtGhth62BsG6c7pD9s0I2t4HKxgrpOHjQ-eKfDHuqQxj30xnRjWstB7aqkDkH_ItZVPgV3rUMkXW2tGb7BlF_5Jl6Cs1p30V4dzxl4e1y-Lp7Q-mX1vHhYI8MkHRAnObNUEFliI4TktSGSlUIYXmeUKI0N0TWjshRM1qXgxJgqmVpQrHHJOJuBu0PuLvj30cah6NtobNdpZ_0YCyFFTpRSCbz9B279GNI_xIISSolUPE8QPUAm-BiDrYtdaPv02oLg4qen4q-n4tBTkm6OyWPZ2-pPORbDvgD3k5Nh</recordid><startdate>2006</startdate><enddate>2006</enddate><creator>Hubka, P</creator><creator>Bernadic, M</creator><creator>Hulín, I</creator><general>Institute of Physiology</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>3V.</scope><scope>4T-</scope><scope>4U-</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>BYOGL</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>2006</creationdate><title>Long-term monitoring of the changes in signal-averaged ECG after coronary artery occlusion and intracoronary endothelin-1 injection in dogs</title><author>Hubka, P ; Bernadic, M ; Hulín, I</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-5193e2617b0c6675fc173b66c5f4218a0c1af327b637fb651ccdc37a620a0b353</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>Arrhythmias, Cardiac - diagnosis</topic><topic>Arrhythmias, Cardiac - etiology</topic><topic>Arrhythmias, Cardiac - physiopathology</topic><topic>Coronary Disease - etiology</topic><topic>Disease Models, Animal</topic><topic>Dogs</topic><topic>Electrocardiography, Ambulatory</topic><topic>Endothelin-1</topic><topic>Heart - drug effects</topic><topic>Heart - physiopathology</topic><topic>Myocardial Infarction - diagnosis</topic><topic>Myocardial Infarction - etiology</topic><topic>Myocardial Infarction - physiopathology</topic><topic>Risk Factors</topic><topic>Signal Processing, Computer-Assisted</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hubka, P</creatorcontrib><creatorcontrib>Bernadic, M</creatorcontrib><creatorcontrib>Hulín, I</creatorcontrib><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>Docstoc</collection><collection>University Readers</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>East Europe, Central Europe Database</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>Research Library Prep</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Nursing & Allied Health Premium</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><jtitle>Physiological research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hubka, P</au><au>Bernadic, M</au><au>Hulín, I</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Long-term monitoring of the changes in signal-averaged ECG after coronary artery occlusion and intracoronary endothelin-1 injection in dogs</atitle><jtitle>Physiological research</jtitle><addtitle>Physiol Res</addtitle><date>2006</date><risdate>2006</risdate><volume>55</volume><issue>1</issue><spage>9</spage><epage>14</epage><pages>9-14</pages><issn>0862-8408</issn><eissn>1802-9973</eissn><abstract>Myocardium undergoes functional changes in the infarcted region primarily due to ischemia. Following myocyte functional alterations of the noninfarcted myocardium are caused by remodelling and hypertrophy. We have monitored and compared changes in the electrocardiographical (ECG) image after coronary artery occlusion (CAO, n=5) and intracoronary endothelin-1 (ET-1, n=3) administration during a 6-month period. In 3 dogs, the CAO was repeated 6 months after the first occlusion. Signal-averaged ECG (SA ECG) was recorded before the operation and 10 days, 1 month, 3 months and 6 months after myocardial infarction (MI). The modified Wigner distribution was used for spectrotemporal analysis of the SA ECG. Eight-hour Holter monitoring was performed in each dog before and after experimental MI. Spectrotemporal representations of the QRS complex were stabilized after the first 1-month period in the group of dogs after CAO. The same results were also observed after the repeated CAO. No arrhythmias were recorded 9 days after CAO. The spectrotemporal representations of the QRS complex after intracoronary ET-1 administration were not stabilized during the whole observed period. Very few arrhythmic events were recorded by Holter monitoring already 3 days after intracoronary ET-1 injection. Experimental MI induced by CAO caused a changed ECG image, which was stable from 1 month after MI induction till the end of the monitoring. However, the ECG image after ET-1 administration was not stable during the whole observed period. No arrhythmic events were recorded in either group 3 months postoperatively that could be caused by healthy myocardial status before the experimental MI induction. In clinical practice, however, ischemic heart disease usually precedes the MI. Arrhythmogenic substrate could thus be a consequence of combination of healthy status of the myocardium before MI and MI itself.</abstract><cop>Czech Republic</cop><pub>Institute of Physiology</pub><pmid>15857164</pmid><doi>10.33549/physiolres.930743</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Arrhythmias, Cardiac - diagnosis Arrhythmias, Cardiac - etiology Arrhythmias, Cardiac - physiopathology Coronary Disease - etiology Disease Models, Animal Dogs Electrocardiography, Ambulatory Endothelin-1 Heart - drug effects Heart - physiopathology Myocardial Infarction - diagnosis Myocardial Infarction - etiology Myocardial Infarction - physiopathology Risk Factors Signal Processing, Computer-Assisted Time Factors |
title | Long-term monitoring of the changes in signal-averaged ECG after coronary artery occlusion and intracoronary endothelin-1 injection in dogs |
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