Comparison of hemodynamics, cardiac electrophysiology, and ventricular arrhythmia in an open- and a closed-chest porcine model of acute myocardial infarction
Ventricular fibrillation (VF) during acute myocardial infarction (AMI) is an important contributor to sudden cardiac death. Large animal models are widely used to study AMI-induced arrhythmia, but the mode of AMI induction ranges from thoracotomy and surgical ligation of a coronary vessel (open ches...
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Veröffentlicht in: | American journal of physiology. Heart and circulatory physiology 2020-02, Vol.318 (2), p.H391-H400 |
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description | Ventricular fibrillation (VF) during acute myocardial infarction (AMI) is an important contributor to sudden cardiac death. Large animal models are widely used to study AMI-induced arrhythmia, but the mode of AMI induction ranges from thoracotomy and surgical ligation of a coronary vessel (open chest) to minimally invasive techniques, including balloon occlusion (closed chest). How the choice of induction affects arrhythmia development is unclear. The aim of this study was to compare an open-chest and a closed-chest model with regard to hemodynamics, electrophysiology, and arrhythmia development. Forty-two female Danish Landrace pigs (20 open chest, 22 closed chest) were anesthetized, and occlusion of the mid-left anterior descending coronary artery was performed for 60 min. Opening the chest reduced blood pressure and cardiac output (Δ -22 mmHg, Δ -1.5 L/min from baseline, both
< 0.001 intragroup). Heart rate decreased with opening of the chest but increased with balloon placement (
< 0.001). AMI-induced ST elevation was lower in the open-chest group (
< 0.001). Premature ventricular contractions occurred in two distinct phases (0-15 and 15-40 min), the latter of which was delayed in the open-chest group (
= 0.005). VF occurred in 7 out of 20 and 12 out of 22 pigs in the open-chest and closed-chest groups, respectively (
= 0.337), with longer time-to-VF in the open-chest group (23.4 ± 1.2 min in open chest and 17.8 ± 1.4 min in closed chest;
= 0.007). In summary, opening the chest altered hemodynamic parameters and delayed the onset of ventricular arrhythmias. Hence, in the search for mechanisms and novel treatments of AMI-induced arrhythmia, caution should be taken when choosing between or comparing the results from these two models.
We demonstrated pronounced differences in hemodynamic parameters and time course of ventricular arrhythmias in regard to mode of infarct induction. Inducing myocardial infarction by thoracotomy and subsequent ligation decreased blood pressure and cardiac output and delayed the onset of ventricular arrhythmia, whereas balloon occlusion resulted in higher heart rates during infarct. |
doi_str_mv | 10.1152/ajpheart.00406.2019 |
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< 0.001 intragroup). Heart rate decreased with opening of the chest but increased with balloon placement (
< 0.001). AMI-induced ST elevation was lower in the open-chest group (
< 0.001). Premature ventricular contractions occurred in two distinct phases (0-15 and 15-40 min), the latter of which was delayed in the open-chest group (
= 0.005). VF occurred in 7 out of 20 and 12 out of 22 pigs in the open-chest and closed-chest groups, respectively (
= 0.337), with longer time-to-VF in the open-chest group (23.4 ± 1.2 min in open chest and 17.8 ± 1.4 min in closed chest;
= 0.007). In summary, opening the chest altered hemodynamic parameters and delayed the onset of ventricular arrhythmias. Hence, in the search for mechanisms and novel treatments of AMI-induced arrhythmia, caution should be taken when choosing between or comparing the results from these two models.
We demonstrated pronounced differences in hemodynamic parameters and time course of ventricular arrhythmias in regard to mode of infarct induction. Inducing myocardial infarction by thoracotomy and subsequent ligation decreased blood pressure and cardiac output and delayed the onset of ventricular arrhythmia, whereas balloon occlusion resulted in higher heart rates during infarct.</description><identifier>ISSN: 0363-6135</identifier><identifier>EISSN: 1522-1539</identifier><identifier>DOI: 10.1152/ajpheart.00406.2019</identifier><identifier>PMID: 31922881</identifier><language>eng</language><publisher>United States</publisher><subject>Action Potentials - physiology ; Animals ; Arrhythmias, Cardiac - physiopathology ; Coronary Vessels - physiopathology ; Disease Models, Animal ; Electrocardiography ; Electrophysiologic Techniques, Cardiac ; Female ; Heart - physiopathology ; Hemodynamics ; Myocardial Contraction ; Myocardial Infarction - physiopathology ; Swine ; Tachycardia, Ventricular - physiopathology ; Ventricular Premature Complexes - physiopathology</subject><ispartof>American journal of physiology. Heart and circulatory physiology, 2020-02, Vol.318 (2), p.H391-H400</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c350t-6ced48b7e4eda1e16173d04e8115a4313b78a7a6fb1c8a13404f69dc447202e03</citedby><cites>FETCH-LOGICAL-c350t-6ced48b7e4eda1e16173d04e8115a4313b78a7a6fb1c8a13404f69dc447202e03</cites><orcidid>0000-0002-6691-8581 ; 0000-0003-3558-8329 ; 0000-0001-6575-360X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3025,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31922881$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lubberding, Anniek F</creatorcontrib><creatorcontrib>Sattler, Stefan M</creatorcontrib><creatorcontrib>Flethøj, Mette</creatorcontrib><creatorcontrib>Tfelt-Hansen, Jacob</creatorcontrib><creatorcontrib>Jespersen, Thomas</creatorcontrib><title>Comparison of hemodynamics, cardiac electrophysiology, and ventricular arrhythmia in an open- and a closed-chest porcine model of acute myocardial infarction</title><title>American journal of physiology. Heart and circulatory physiology</title><addtitle>Am J Physiol Heart Circ Physiol</addtitle><description>Ventricular fibrillation (VF) during acute myocardial infarction (AMI) is an important contributor to sudden cardiac death. Large animal models are widely used to study AMI-induced arrhythmia, but the mode of AMI induction ranges from thoracotomy and surgical ligation of a coronary vessel (open chest) to minimally invasive techniques, including balloon occlusion (closed chest). How the choice of induction affects arrhythmia development is unclear. The aim of this study was to compare an open-chest and a closed-chest model with regard to hemodynamics, electrophysiology, and arrhythmia development. Forty-two female Danish Landrace pigs (20 open chest, 22 closed chest) were anesthetized, and occlusion of the mid-left anterior descending coronary artery was performed for 60 min. Opening the chest reduced blood pressure and cardiac output (Δ -22 mmHg, Δ -1.5 L/min from baseline, both
< 0.001 intragroup). Heart rate decreased with opening of the chest but increased with balloon placement (
< 0.001). AMI-induced ST elevation was lower in the open-chest group (
< 0.001). Premature ventricular contractions occurred in two distinct phases (0-15 and 15-40 min), the latter of which was delayed in the open-chest group (
= 0.005). VF occurred in 7 out of 20 and 12 out of 22 pigs in the open-chest and closed-chest groups, respectively (
= 0.337), with longer time-to-VF in the open-chest group (23.4 ± 1.2 min in open chest and 17.8 ± 1.4 min in closed chest;
= 0.007). In summary, opening the chest altered hemodynamic parameters and delayed the onset of ventricular arrhythmias. Hence, in the search for mechanisms and novel treatments of AMI-induced arrhythmia, caution should be taken when choosing between or comparing the results from these two models.
We demonstrated pronounced differences in hemodynamic parameters and time course of ventricular arrhythmias in regard to mode of infarct induction. Inducing myocardial infarction by thoracotomy and subsequent ligation decreased blood pressure and cardiac output and delayed the onset of ventricular arrhythmia, whereas balloon occlusion resulted in higher heart rates during infarct.</description><subject>Action Potentials - physiology</subject><subject>Animals</subject><subject>Arrhythmias, Cardiac - physiopathology</subject><subject>Coronary Vessels - physiopathology</subject><subject>Disease Models, Animal</subject><subject>Electrocardiography</subject><subject>Electrophysiologic Techniques, Cardiac</subject><subject>Female</subject><subject>Heart - physiopathology</subject><subject>Hemodynamics</subject><subject>Myocardial Contraction</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Swine</subject><subject>Tachycardia, Ventricular - physiopathology</subject><subject>Ventricular Premature Complexes - physiopathology</subject><issn>0363-6135</issn><issn>1522-1539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kc9u1DAQxi0EotvCEyAhHzk0W_-LkxzRClqkSlzgHM3aE-LKsYOdIOVheNd6u21Po9F833yj-RHyibM957W4gYd5REjLnjHF9F4w3r0huzIRFa9l95bsmNSy0lzWF-Qy5wfGWN1o-Z5cSN4J0bZ8R_4f4jRDcjkGGgc64hTtFmByJl9TA8k6MBQ9miXFedyyiz7-2a4pBEv_YViSM6uHRCGlcVvGyQF1oUxpnDFUTzKgxseMtjIj5oXOMRkXkJYg9KdMMOtS2i2e43xZMEAyi4vhA3k3gM_48blekd_fv_063FX3P29_HL7eV0bWbKm0QavaY4MKLXDkmjfSMoVt-RMoyeWxaaEBPRy5aYFLxdSgO2uUagQTyOQV-XLeO6f4dy1X9pPLBr2HgHHNvZBSi7prWlmk8iw1KeaccOjn5CZIW89Zf-LSv3Dpn7j0Jy7F9fk5YD1OaF89LyDkI_8BjqQ</recordid><startdate>20200201</startdate><enddate>20200201</enddate><creator>Lubberding, Anniek F</creator><creator>Sattler, Stefan M</creator><creator>Flethøj, Mette</creator><creator>Tfelt-Hansen, Jacob</creator><creator>Jespersen, Thomas</creator><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><orcidid>https://orcid.org/0000-0002-6691-8581</orcidid><orcidid>https://orcid.org/0000-0003-3558-8329</orcidid><orcidid>https://orcid.org/0000-0001-6575-360X</orcidid></search><sort><creationdate>20200201</creationdate><title>Comparison of hemodynamics, cardiac electrophysiology, and ventricular arrhythmia in an open- and a closed-chest porcine model of acute myocardial infarction</title><author>Lubberding, Anniek F ; Sattler, Stefan M ; Flethøj, Mette ; Tfelt-Hansen, Jacob ; Jespersen, Thomas</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c350t-6ced48b7e4eda1e16173d04e8115a4313b78a7a6fb1c8a13404f69dc447202e03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Action Potentials - physiology</topic><topic>Animals</topic><topic>Arrhythmias, Cardiac - physiopathology</topic><topic>Coronary Vessels - physiopathology</topic><topic>Disease Models, Animal</topic><topic>Electrocardiography</topic><topic>Electrophysiologic Techniques, Cardiac</topic><topic>Female</topic><topic>Heart - physiopathology</topic><topic>Hemodynamics</topic><topic>Myocardial Contraction</topic><topic>Myocardial Infarction - physiopathology</topic><topic>Swine</topic><topic>Tachycardia, Ventricular - physiopathology</topic><topic>Ventricular Premature Complexes - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lubberding, Anniek F</creatorcontrib><creatorcontrib>Sattler, Stefan M</creatorcontrib><creatorcontrib>Flethøj, Mette</creatorcontrib><creatorcontrib>Tfelt-Hansen, Jacob</creatorcontrib><creatorcontrib>Jespersen, Thomas</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>American journal of physiology. Heart and circulatory physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lubberding, Anniek F</au><au>Sattler, Stefan M</au><au>Flethøj, Mette</au><au>Tfelt-Hansen, Jacob</au><au>Jespersen, Thomas</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Comparison of hemodynamics, cardiac electrophysiology, and ventricular arrhythmia in an open- and a closed-chest porcine model of acute myocardial infarction</atitle><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle><addtitle>Am J Physiol Heart Circ Physiol</addtitle><date>2020-02-01</date><risdate>2020</risdate><volume>318</volume><issue>2</issue><spage>H391</spage><epage>H400</epage><pages>H391-H400</pages><issn>0363-6135</issn><eissn>1522-1539</eissn><abstract>Ventricular fibrillation (VF) during acute myocardial infarction (AMI) is an important contributor to sudden cardiac death. Large animal models are widely used to study AMI-induced arrhythmia, but the mode of AMI induction ranges from thoracotomy and surgical ligation of a coronary vessel (open chest) to minimally invasive techniques, including balloon occlusion (closed chest). How the choice of induction affects arrhythmia development is unclear. The aim of this study was to compare an open-chest and a closed-chest model with regard to hemodynamics, electrophysiology, and arrhythmia development. Forty-two female Danish Landrace pigs (20 open chest, 22 closed chest) were anesthetized, and occlusion of the mid-left anterior descending coronary artery was performed for 60 min. Opening the chest reduced blood pressure and cardiac output (Δ -22 mmHg, Δ -1.5 L/min from baseline, both
< 0.001 intragroup). Heart rate decreased with opening of the chest but increased with balloon placement (
< 0.001). AMI-induced ST elevation was lower in the open-chest group (
< 0.001). Premature ventricular contractions occurred in two distinct phases (0-15 and 15-40 min), the latter of which was delayed in the open-chest group (
= 0.005). VF occurred in 7 out of 20 and 12 out of 22 pigs in the open-chest and closed-chest groups, respectively (
= 0.337), with longer time-to-VF in the open-chest group (23.4 ± 1.2 min in open chest and 17.8 ± 1.4 min in closed chest;
= 0.007). In summary, opening the chest altered hemodynamic parameters and delayed the onset of ventricular arrhythmias. Hence, in the search for mechanisms and novel treatments of AMI-induced arrhythmia, caution should be taken when choosing between or comparing the results from these two models.
We demonstrated pronounced differences in hemodynamic parameters and time course of ventricular arrhythmias in regard to mode of infarct induction. Inducing myocardial infarction by thoracotomy and subsequent ligation decreased blood pressure and cardiac output and delayed the onset of ventricular arrhythmia, whereas balloon occlusion resulted in higher heart rates during infarct.</abstract><cop>United States</cop><pmid>31922881</pmid><doi>10.1152/ajpheart.00406.2019</doi><orcidid>https://orcid.org/0000-0002-6691-8581</orcidid><orcidid>https://orcid.org/0000-0003-3558-8329</orcidid><orcidid>https://orcid.org/0000-0001-6575-360X</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Action Potentials - physiology Animals Arrhythmias, Cardiac - physiopathology Coronary Vessels - physiopathology Disease Models, Animal Electrocardiography Electrophysiologic Techniques, Cardiac Female Heart - physiopathology Hemodynamics Myocardial Contraction Myocardial Infarction - physiopathology Swine Tachycardia, Ventricular - physiopathology Ventricular Premature Complexes - physiopathology |
title | Comparison of hemodynamics, cardiac electrophysiology, and ventricular arrhythmia in an open- and a closed-chest porcine model of acute myocardial infarction |
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